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Nasal toxicity of cocaine: a hypercoagulable effect?

Nasal insufflation of cocaine injures the nasal mucosa and can perforate the septum. Cocaine-induced vasoconstriction resulting in ischemia is one of the methods that may be responsible for this damage. We are determining whether cocaine also produces a hypercoagulable state that may compound factors which have been previously established to cause damage to the nasal mucosa and septum. This study uses Modified Recalcification Time (MRT), a test developed in our laboratory that has the ability to measure the overall coagulation process. Our study revealed no connection between cocaine and enhanced platelet function or monocyte-released tissue factor. The coagulation process was unaffected by the addition of the drug, so we conclude that cocaine does not cause a hypercoagulable state and cannot assist in the explanation regarding the ischemic changes of the nasal septum.

Blood Coagulation↗

Abrupt versus gradual withdrawal of vitamin K antagonist treatment in patients with venous thromboembolic disease: assessment of hypercoagulability and clinical outcome.

BACKGROUND: It is yet unclear whether vitamin K antagonist treatment should be stopped abruptly or gradually after an episode of venous thromboembolism. The mode of withdrawal might influence a potential development of a hypercoagulable state, which could influence the risk for recurrent disease. METHODS: We prospectively studied 37 consecutive patients in whom acenocoumarol was discontinued either abrupt (18) or gradually (19) (2/3 and 1/3 of the initial dose for one week). Blood sampling was performed at various time points up to 18 days after complete withdrawal and was analysed for INR, prothrombin fragment F1 + 2 and D-dimer. All patients were clinically followed-up for the assessment of the association between hypercoagulability and occurrence of disease such as recurrent venous thromboembolism or malignancy. RESULTS: An approximately fourfold increase was observed (median increase from 0.3 to 1.3 nmol/l) in the F1 + 2 levels after both abrupt and gradual withdrawal and in the D-dimer concentrations in the abrupt withdrawal group (0.10 to 0.44 mg/l), while those in whom acenocoumarol was discontinued gradually showed a less pronounced increase of the D-dimer levels (0.11 to 0.29 mg/L) (not significant). During follow-up one recurrent venous thromboembolic event occurred in each group, and a diagnosis of cancer was made four times. All these patients had the highest D-dimer concentrations measured in the entire study group. CONCLUSIONS: This study indicates the potential for a hypercoagulable state after acenocoumarol discontinuation, which was not prevented by tapering the acenocoumarol dose. D-dimer, measured 2 to 3 weeks after acenocoumarol withdrawal, might be an important tool to identify patients at risk for recurrent venous thromboembolism and/or for the presence of an underlying malignancy.

Acenocoumarol↗

Hemostatic problems and thromboembolic complications in nephrotic children.

A hypercoagulable state and the risk of thromboembolism in both arterial and venous circulation is a relatively frequent and serious feature of nephrotic syndrome (NS) in children and adults. The aim of this study was to evaluate the coagulation states of children with NS before and after corticosteroid (CS) therapy and to compare the results with a healthy control group. The first group consisted of 49 nephrotic children (30 boys and 19 girls) with a mean age of 6. 5+/-4.9 years (range 1-16 years). The control group included 17 healthy children (9 boys and 8 girls). At the time of admission, all patients were evaluated for the presence of clinical thromboembolism, hematological and biochemical indicators of a hypercoagulative state, and renal disease. This was repeated after CS treatment. Deep vein thrombosis was observed in 2 nephrotic patients who had very low plasma antithrombin III (AT III) levels and fibrinogen levels above 750 mg/dl. Thus, the prevalence of thromboembolism was 4% in our pediatric nephrotic population. The mean AT III level of the study group was 68.2+/-23.4% at the onset of the disease, which was significantly lower than the level of the control group (84.0+/-7. 6%). Plasma AT III levels increased to 74.4+/-15.3% after CS treatment, which correlated with the serum albumin levels. However, there was no correlation with urinary protein excretion. Protein C levels were higher than controls during all stages of the disease in both steroid-responsive and -unresponsive patients. The mean protein S level was similar in both groups. Plasma fibrinogen and cholesterol levels were significantly higher in the study group but decreased to within normal limits with remission. Our study suggests that thromboembolic complications are not infrequent in children with NS, and may be related to low plasma AT III and albumin and high fibrinogen and cholesterol levels.

Adolescent↗

HIV and thrombosis: a review.

The array of clinicopathologic factors associated with acquired immune deficiency syndrome (AIDS) patients continues to increase and surprise many physicians. The recent literature contains reports of thrombotic episodes occurring in patients with human immunodeficiency virus (HIV) infection. Various abnormalities predisposing to a hypercoagulable state have also been reported in AIDS patients including the presence of antiphospholipid antibodies and the lupus anticoagulant; deficiencies of protein C, protein S, heparin cofactor II, and antithrombin and increased levels of von Willebrand factor, and d-dimers. These abnormalities correlate with the severity of HIV-associated immunosuppression as measured by the CD4 cell counts and with the presence of concurrent infectious or neoplastic diseases. The authors reviewed the medical literature and describe various abnormalities predisposing to a hypercoagulable state in AIDS patients along with the management of such complications. This issue is important because deep venous thrombosis (DVT), pulmonary embolus (PE), or thrombosis at other sites can develop in patients with AIDS who are ambulatory and have no known risk factors for pathologic thrombus formation, providing another challenge in an already difficult clinical situation. This also provides a strong rationale for careful prospective studies focusing on the prevalence and risk factors involved in the development of thromboembolic complications in patients with AIDS.

AIDS-Related Opportunistic Infections↗

[Diagnosis of predictive state of disseminated intravascular coagulation].

The early stage of the state in which coagulation or fibrinolytic pathway is activated has been difficult to be estimated. Recently, it has become possible to detect an early stage of DIC (pre-DIC) due to the development of highly sensitive methods which quantitate so called "molecular markers". Molecular markers can be classified into three groups: 1) activation fragments of coagulation proteins (e.g. F1+2); 2) protease and its inhibitor complex (e.g. TAT, IXa-AT-III, Xa-AT-III and PIC); 3) degradation products (e.g. FPA, FPB beta, SFMC and D-dimer). Among them, F1+2, TAT, FPA and SFMC reflect in vivo thrombin generation, while PIC, FPB beta and D-dimer reflect in vivo plasmin generation. IXa-AT-III and Xa-AT-III may be useful markers to detect hypercoagulable states in an earlier stage of underlying various disorders. Measurement of circulating levels of the zymogens and protease inhibitors is unable to detect small changes caused by low grade DIC or localized thrombotic events. Monitoring plasma levels of molecular markers, however, gives us more specific and accurate information regarding the onset and time course of hypercoagulable states and enable us to diagnose DIC at an early stage and to evaluate the effect of treatment for patients with DIC, specifically.

Antithrombin III↗

[The experimental study of blood coagulation and fibrinolysis in acute portal vein occlusion].

Influence of acute portal vein occlusion on blood coagulation and fibrinolysis have not been fully clarified. In this experimental study in mongrel dogs, 1) changes of blood coagulation and fibrinolysis in portal vein and peripheral vein, 2) histological changes in small intestine and 3) activity of plasminogen activator in small intestine were investigated periodically after acute portal vein ligation with or without heparinized hydrophilic catheter-bypass between portal and femoral vein. All five dogs died 81-130 minutes (mean 105 minutes) after portal vein ligation. On the other hand, all five bypassed dogs survived in good condition for more than four hours. Acute portal venous congestion caused hypercoagulable state in portal system and apparent DIC occurred in portal system 10 minutes after portal vein ligation. Activity of tissue plasminogen activator which was observed mostly in the endothelial cells of vessels in submucosal layers of small intestine decreased rapidly and disappeared within 20 minutes after portal vein ligation. To the contrary, with the use of the catheter-bypass procedure, no significant changes of blood coagulation and fibrinolysis were observed. These results indicate clearly that portal venous congestion is the trigger of hypercoagulable state in portal system, which progresses to irreversible DIC in 20 minutes. With the use of the catheter-bypass procedure, portal vein shut-down is performed without any abnormal coagulation and fibrinolysis in portal bed and systemic circulation.

Animals↗

Platelet adhesiveness, plasma fibrinogen, and fibrinolytic activity in young patients with ischaemic stroke.

Cerebral thromboembolic stroke in the young is uncommon. Disturbances in the n ormally existing dynamic equilibrium between coagulation and fibrinolysis may play a major role in the pathogenesis of such episodes. In a search for a possible hypercoagulable state platelet adhesiveness by the method of Eastham, plasma fibrinogen and euglobulin clot lysis times were estimated in 46 patients. A group of 15 normal subjects matched for age and sex were also studied for comparison. Significant increase in platelet adhesiveness (P less than 0.001) and plasma fibrinogen (P less than 0.001) was noted in the patients when compared with the normal subjects. Absence of corresponding increases in fibrinolytic activity in the patients suggests disturbed equilibrium between coagulation and fibrinolysis. The possibility of a hypercoagulable state in these cases is discussed.

Adult↗

Cerebral infarction associated with protein C deficiency following allogeneic bone marrow transplantation.

Hypercoagulable states associated with deficiencies in circulating anticoagulant protein C occur after chemotherapy for a variety of malignant diseases. Protein C deficiency also occurs following bone marrow transplantation (BMT) and may be responsible for a variety of transplantation-associated complications. We report the case of a child who suffered a stroke associated with low protein C antigen and activity occurring 11 months after allogeneic BMT. Protein C levels recovered spontaneously by 18 months after BMT. We speculate that the protein C deficiency and and resultant hypercoagulable state led to the stroke, and the deficiency of this anticoagulant was a sequela of the transplant.

Bone Marrow Transplantation↗

Rapid quantitative evaluation of plasma D-dimer levels in thrombotic states using an automated latex photometric immunoassay.

To evaluate a recently developed latex photometric immunoassay (LPIA) that which can measure 40 samples quantitatively within 30 minutes, we measured D-dimer levels in blood samples obtained from patients with disseminated intravascular coagulation (DIC). Linearity of D-dimer determination was shown over the range from 0.5 to 36 micrograms/ml, and recovery studies demonstrated 94 to 108% recovery. The intra-assay and inter-assay coefficients of variation ranged from 0.6 to 11.3% at plasma D-dimer levels of 0.54 to 30.1 micrograms/ml. No interference by lipids, bilirubin, haemoglobin, rheumatoid factor, or gamma-globulin was noted. The normal D-dimer range was less than 0.5 microgram/ml in healthy ambulatory subjects, while the level in elderly subjects with atherosclerosis (14%) or in immobilized subjects (38%) was well above this limit. There was a strong correlation between plasma and serum D-dimer levels (r = 0.993). D-dimer levels measured by this LPIA showed a good correlation with those determined using two kinds of ELISA. The LPIA D-dimer levels were elevated in some subjects with diseases predisposing to DIC, but remained below 10.0 micrograms/ml. On the other hand, the LPIA D-dimer levels in DIC subjects were almost always above 10.0 microgramS/ml. Our study showed that a hypercoagulable state should be suspected when the LPIA D-dimer level is greater than 0.5 microgram/ml and that DIC should be diagnosed when the level is greater than 10.0 micrograms/ml in the presence of an appropriate underlying disease. This LPIA system can rapidly evaluate the presence of a hypercoagulable state as accurately as any ELISA, and thus seems potentially valuable for both emergency and routine laboratory use.

Adult↗

Pulmonary thromboembolism in AIDS patient with chronic venous insufficiency, pulmonary tuberculosis and breast cancer: a case report and pathophysiology review.

Recent literature reports thrombotic episodes occurring in patients with HIV infection associated with other abnormalities including neoplasms and infections predisposing to a hypercoagulable state. We report a 47-year-old woman who developed pulmonary thromboembolism in association with HIV infection, pulmonary tuberculosis and breast cancer. She was treated with rifampin, isoniazid, pyrazinamide; heparin, phenprocoumon, zidovudine, lamivudine and efavirenz. Acid fast bacilli were visualized in a sputum smear and three months after, Mycobacterium tuberculosis was isolated from lymph node biopsy during a episode of immune reconstitution. The isolated mycobacteria showed sensitivity to all first-line drugs. HIV infection, breast cancer and pulmonary tuberculosis have several mechanisms that induce hypercoagulable state and can lead to thromboembolic complications. Pulmonary thromboembolism in this patient was a diagnostic challenge because of all the other severe diseases that she experienced at the same time.

Acquired Immunodeficiency Syndrome↗

[Plasma thrombomodulin levels in elderly subjects].

Plasma levels of thrombomodulin (TM), fibrinogen, antithrombin III (ATIII) and thrombin ATIII complex (TAT) were studied in healthy young subjects (group A), healthy elderly subjects (group B) and patients with level of TM in group B tended to be higher than that in group A. Levels of TM, fibrinogen and TAT in group C suggested the presence of a hypercoagulable state. When group C was further divided into those with and without diabetes mellitus (DM), the TM level in the former tended to be higher than that in the latter. Furthermore, among the patients with DM, those with diabetic retinopathy showed significantly higher levels of TM than those without retinopathy. Thus, high TM levels indicate the presence of endothelial injury. In groups B and C, TM correlated positively with fibrinogen, and negatively with ATIII, which also indicates that a high TM level is related to a hypercoagulable state. In conclusion, the TM level is considered to be a potential marker of the presence of endothelial injury.

Adult↗

Deep Venous Thrombosis and Pulmonary Embolism.

Venous thromboembolic disease, including deep venous thrombosis (DVT) and pulmonary embolism (PE), is an under-diagnosed and under-appreciated medical problem that results in significant patient morbidity and mortality. Inadequate venous thromboprophylaxis in surgical as well as medically ill patients results in DVT and PE that negatively impact patient outcomes and increase health-care costs. A high index of clinical suspicion combined with an evidence-based use of diagnostic tests helps identify patients with acute thrombosis. Failure to accurately and promptly diagnose and treat DVT and PE can result in excess morbidity and mortality due to postthrombotic syndrome, pulmonary hypertension, and recurrent thrombosis. Conversely, unnecessary anticoagulation provides risk in the absence of any tangible benefit. The immediate commencement of parenteral anticoagulant therapy with intravenous unfractionated heparin or a subcutaneous low molecular weight heparin (LMWH) upon presentation with DVT or PE (often even before objective diagnosis confirmation) is necessary to minimize propagation, embolization, and recurrence rates. We favor weight-based LMWH therapy in most of our patients with DVT because of the ability to treat exclusively or primarily in the outpatient setting. We still admit patients with PE for a minimum duration of 2 days for close observation. Subsequent conversion to oral anticoagulation with warfarin (target INR of 2.0 to 3.0 in most patients) should include an overlap with parenteral therapy of at least 4 to 5 days and until a stable target INR has been achieved. A minimum of 3 to 6 months of anticoagulation is recommended following a first episode of idiopathic DVT and any PE. A shorter course of therapy may be sufficient following a situational (eg, after surgery and postpartum) or calf DVT. Long-term, and at times lifelong, therapy should be considered in patients with thrombosis in the setting of a persistent acquired or inherited hypercoagulable state. Thrombolytic therapy probably should be reserved for young patients with iliofemoral DVT, any patient with a threatened limb due to impending venous limb gangrene, and those with PE who have objective evidence of cardiopulmonary compromise. Unfavorable risk-to-benefit and cost-to-benefit ratios make more extensive use of thrombolytics undesirable. The prevention of the postthrombotic syndrome with fitted, graduated compression garments and age- and gender-appropriate cancer screening are indicated in all patients with DVT in an attempt to minimize morbidity and mortality. Hypercoagulable state testing is indicated when the results of individual tests will significantly impact the choice of anticoagulant, intensity of therapy, therapeutic monitoring, family screening, family planning, prognosis determination, and most of all, duration of therapy.

Journal Article↗

Effects of a selective thromboxane A2 synthetase inhibitor on immune complex glomerulonephritis.

It has been reported that agents which block the prostaglandin system inhibit the development of glomerulonephritis. However, the mechanisms of these effects are not clear. We studied the effect of a selective thromboxane A2 (TxA2) synthetase inhibitor, 1-benzylimidazole (BIm), on the immune complex glomerulonephritis produced by bovine serum albumin (BSA) in New Zealand white rabbits. As the BSA nephritis developed, there was no change of creatinine (Cr), serum urea nitrogen (SUN), or creatinine clearance (Ccr), but urinary protein excretion increased almost 3-fold. Coagulation and fibrinolytic studies suggested a hypercoagulable state and increased fibrinolytic activity. Platelet aggregation showed the reduction of maximum aggregation induced by ADP and collagen. Histological examination by light microscopy, immunofluorescence, and electron microscopy revealed glomerular polymorphonuclear leukocyte (PMN) infiltration, mononuclear cell (MON) proliferation, and fibrin deposition. In 70% of the rabbits, IgG and C3 deposits were seen by immunofluorescence mainly in mesangial areas. The administration of BIm to BSA nephritis had no effects on Cr, SUN or Ccr, but it significantly lessened the proteinuria. The study of coagulation and fibrinolytic activity suggested a less hypercoagulable state, and more efficient fibrinolysis occurred than in the group without BIm. BIm tended to normalize platelet aggregation. It also lessened the histological PMN infiltration (p less than 0.05), MON proliferation (p less than 0.01), and fibrin deposition (p less than 0.05). These data suggest that TxA2 may play an important pathogenetic role in the development and progression of glomerulonephritis.

Adenosine Diphosphate↗

Factor VII coagulant activity (VIIc) and hypercoagulability in chronic renal disease and dialysis: relationship with dyslipidaemia, inflammation, and factor VII genotype.

BACKGROUND: Factor VII coagulant activity (VIIc) is implicated in cardiovascular disease (CVD) risk in the general population. VIIc is correlated with hyperlipidaemia and influenced by a polymorphism of the factor VII gene and could contribute to thrombotic risk in patients with renal disease. METHODS: We studied VIIc in 100 patients with chronic renal disease or on maintenance dialysis and examined its relationship with dyslipidaemia, a marker of coagulation activation prothrombin fragment F1+2 (F1+2), the acute-phase reactant and coagulation factor fibrinogen, a mediator of the inflammatory response interleukin-6 (IL6), and the factor VII R353Q polymorphism. RESULTS: VIIc (186+/-58 vs 140+/-37, % standard, P<0.0001) and F1+2 (0.51 vs 0.30 nM, median, P<0.0001) were increased in the patients with renal disease compared with the control group, consistent with a hypercoagulable state. Patients and controls heterozygous for the factor VII R353Q polymorphism, had 35% lower VIIc than homozygotes for the R353 allele, indicating that the Q353 allele could confer genetic protection from thrombotic risk. There was a significant correlation between VIIc and F1+2 (r=0.26, P<0.05), total and VLDL cholesterol, and triglycerides, but the correlation with lipids did not differ by genotype. VIIc and F1+2 also correlated with increased concentration of IL6 and fibrinogen, and inversely with albumin, suggesting that a persistent inflammatory response could contribute to a hypercoagulable state, possibly via cytokine induced activation of the endothelium, or by induction of monocytes to express tissue factor. Patients with CVD complications or a history of myocardial infarction did not have higher VIIc or F1+2 than those without CVD. CONCLUSIONS: VIIc was significantly increased in renal disease states and strongly influenced by a common polymorphism of the factor VII gene, but the increase in VIIc and its correlation with lipids was not genotype specific. VIIc correlated with evidence of increased coagulation activation and persistence of an inflammatory response. A persistent inflammatory response and the dyslipidaemia of renal disease may contribute to coagulation activation and increased cardiovascular risk. Prospective studies are required to evaluate increased VIIc as a thrombotic risk factor in chronic renal disease.

Adult↗

Mesenteric vein thrombosis associated with a familial deficiency of free protein S.

Signs and symptoms of an acute intra-abdominal emergency developed in a 26-year-old man; this emergency prompted surgical exploration. It was discovered that he had a devitalized small bowel as a result of mesenteric vein thrombosis. An extensive evaluation for hypercoagulable states disclosed that he had a normal total protein S concentration, but by assay and on crossed immunoelectrophoresis studies, he had a decreased concentration of free protein S. A family study demonstrated protein S deficiency in his father and in a sister. On a subsequent determination, the propositus had a decreased concentration of total protein S. This case illustrates the association of protein S deficiency with mesenteric thrombosis and serves to caution that a single determination of total protein S is not an adequate evaluation when the index of suspicion for a hypercoagulable state is high.

Adult↗

Anatomic distribution of venous thrombosis in patients with antiphospholipid antibody: imaging findings.

OBJECTIVE: Antiphospholipid antibodies are immunoglobulins that cross-react with phospholipid within cell membranes. These antibodies have been associated with a hypercoagulable state manifested by early stroke, frequent arterial and venous thromboses, recurrent fetal loss, thrombocytopenia, and livedo reticularis (antiphospholipid syndrome). The purpose of this study was to determine the anatomic distribution of venous thrombosis in patients with antiphospholipid antibodies as seen on imaging examinations. MATERIALS AND METHODS: We retrospectively reviewed the laboratory results of patients tested for antiphospholipid antibodies at a tertiary referral center during the period January 1992 to April 1994. This review revealed 228 patients with antiphospholipid antibodies. We excluded patients with systemic lupus erythematosus or any other medical condition associated with a hypercoagulable state and patients over 65 years old. Thirty-one of the remaining 73 patients had undergone imaging studies of the CNS or non-CNS venous system. Radiologic studies (contrast angiography or venography, MR angiography or venography, or Doppler sonography) were examined for the presence of venous thrombosis. Nineteen patients--11 men and eight women, 18-62 years old (average age, 38 years)--with venous thromboses were identified. RESULTS: Twelve patients had non-CNS thrombosis alone, three had CNS thrombosis alone, and four had both CNS and non-CNS thromboses. Locations of non-CNS thromboses included deep veins of the legs (nine occurrences), pulmonary vessels (five), and large veins in the thorax or abdomen (six). Three of these patients had documented thromboses at other sites. Twelve patients had recurrent thrombotic events (six with multiple recurrences), including five with arterial thromboses and two with both venous and arterial thromboses and stroke. Among patients with CNS involvement, five had documented thromboses (four dural sinus, one arterial) and two had arterial distribution strokes demonstrated by CT. Two patients with only non-CNS thromboses had either seizures or migraines. CONCLUSION: Deep veins of the leg were the most common site of venous thrombosis. The thoracic and abdominal venous system and the dural sinuses--unusual sites of thrombosis in the general population--are other common sites. Antiphospholipid antibodies should be suspected when thromboses are found in these locations in the absence of other known risk factors, or when found in combination with arterial thromboses or CNS ischemic disease in young or middle-aged patients.

Adolescent↗

Saphenous vein thrombophlebitis (SVT): a deceptively benign disease.

PURPOSE: The association between deep vein thrombosis (DVT) and the hypercoagulable state is a well-established entity. However, the association between saphenous vein thrombophlebitis and coagulation abnormalities has not been investigated. Although thrombosis of varicose veins typically runs a benign course, phlebitis of the saphenous system may propagate to the deep system or saphenofemoral junction that requires more aggressive therapy. Given the potential similarity in clinical outcome between saphenous vein thrombophlebitis (SVT) and DVT, we have investigated the coagulation profile of patients presenting with isolated SVT. METHODS: Seventeen consecutive patients who presented to our vascular laboratory with isolated SVT had a coagulation profile performed that included antithrombin III (AT III), protein C (PC), protein S (PS) antigen and activity levels, activated protein C (APC) resistance, factor V DNA mutation, and coagulation factors II and X. All patients had duplex scans performed on both the superficial and deep venous systems. Patients with SVT only were treated with nonsteroidal antiinflammatory drugs (NSAIDs) and warm soaks as outpatients, whereas those patients found to have DVT or a clot at the saphenofemoral junction were fully anticoagulated with heparin and coumadin therapy. All 17 patients had at least one repeat coagulation profile performed up to 5 months after their SVT occurrence to ensure that the results of hypercoagulability were not transient. RESULTS: Ten (59%) of the 17 patients with SVT had abnormal coagulation profiles on initial presentation. All 10 patients who were hypercoagulable had repeat tests and 6 (35%) remained abnormal. Four patients who had abnormal results converted to normal values. Seven patients with normal coagulation profiles on initial presentation had repeat tests and all remained normal. CONCLUSION: The incidence of the hypercoagulable state in patients with SVT is high. Thirty-five percent of patients with isolated SVT had consistently abnormal coagulation profiles. Patients with SVT may be prone to the development of DVT or saphenofemoral junction thrombophlebitis and should be closely followed after the initial diagnosis of hypercoagulability.

Adult↗

Placental emboli from a fetus papyraceous.

A syndrome in monozygotic twins that consists of a macerated twin fetus (fetus papyraceous) and a live-born twin with various anatomical defects has been described. The etiology is thought to be placental transfer of emboli or thromboplastic material through vascular shunts. Thromboplastic material precipitates disseminated intravascular coagulation (DIC) in the fetus, with a resultant hypercoagulable state due to relative fetal antithrombin III deficiency. Two cases of this syndrome will be discussed. The case of a live-born twin with intestinal atresia, who developed in utero with a fetus papyraceous, is reported. Emboli were demonstrated in vascular shunts of the diamniotic-monochorionic placenta. The hypothesis of intestinal atresia as a result of a vascular accident is reviewed. Another case involving a live-born twin with congenital skin defects, who developed in utero with a fetus papyraceous, is also reported. The skin defects were a congenital disruption from fetal DIC with resultant hypercoagulable state. Several other manifestations of the placental emboli syndrome will be discussed and the vascular etiology of the disruptions explained.

Adult↗