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A Larcan

Publications and source records attributed to A Larcan.

At least 91 records · Page 5Linked to original sources

[Uterine rupture causing acute defibrination syndrome. Apropos of 3 cases].

The authors report three cases of rupture of the uterus during delivery, complicated by an acute defibrination syndrome. Death resulted in two cases. The sequence of rupture of the uterus----shock----pathological condition of coagulation----great increase in the shock occurred in all three patients. This sequence could only be arrested in one of the three patients who had a total hysterectomy. Partial hysterectomy in the other two was ineffective. These three case histories suggest that total hysterectomy after even partial correction of the haemorrhagic state can be the best treatment in this very serious condition.

Adult↗

[Fat embolism].

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Embolism, Fat↗

[Acute choriocapillaris occlusion in pregnancy and puerperium. Toxemias, thrombotic microangiopathies].

Six cases of gravidic toxemia (4) and thrombotic thrombocytopenic purpura (Moschowitz's disease) in puerperium with choriocapillaris occlusion, were examined. At the acute stage, the vision is improved, ophthalmoscopy of the fundus revealed cystlike bullous exudative subretinal with retinal detachment, yellowish spots (of retinal pigment epithelium) and often minimal localized arteriolar narrowing. The evolution included retina application pigmentary disturbances and Elschnig's spots. Fluorescein angiography showed delayed filling of the capillaris and dye leakage in the subretinal space (first hypofluorescence and late hyperfluorescence). There are various stages of ischaemic involvement but in all cases visual symptoms may be due to central obstructive choroidopathy with delayed filling and occlusion. The retinal detachment in toxemia or Moschowitz disease in pregnancy in secondary to microcirculatory choroidal damage (short ciliary vessels essentially) with rupture of blood retinal barrier. Other constatations are made in disseminated intravascular coagulation, periarteritis nodosa, accelerated nephrosclerosis, hemolytic uremic syndrome in puerperium, and these suggested possible relationship between the various conditions.

Choroid↗

[Acute edema of the lung in eclampsia].

In 6 cases of eclampsia in the course of pre and post-partum, we could observe neurological disorders associated with acute pulmonary oedema with acute respiratory distress occurring 5 to 72 hours after the first convulsive crisis. Hemodynamic check-up provided various results: 3 cases corresponded to A.P.O resulting from a lesion, with normal capillary pressure. In 3 other cases, there was hemodynamic oedema (overloading with high flow and hypervolemia in one case, myocardial incompetence with hypovolemia in an other case revealed by test filling in a third case). There were clinical signs of left ventricular failure in 4 case. Post-mortem investigations (5 cases) revealed unimportant ultrastructural alterations of myocardium only in 2 cases. Pulmonary histopathological investigations (5 cases) were the investigations carried out in case of oedema resulting from lesions with interstitial and alveolar oedema, hyaline membranes, alteration of pneumocytes, and intra-capillary thrombi. Mendelson's syndrome which was always discussed could be eliminated. The syndrome of respiratory distress was certainly connected with more or less generalized microcirculatory disorders (microembolism with hyperpermeability) connected with hemostasis disorders and cerebral manifestations.

Acute Disease↗

[Blood rheology in Raynaud's disease].

The part played by blood rheological factors in any vasomotor phenomenon is still difficult to define, in relation to its onset, maintenance and possible worsening. A high viscosity may contribute towards a difficulty in flow and viscosity is known to vary in an inverse manner with temperature. Many studies have been published reporting results of rheological investigations in Raynaud's syndromes, but whereas the majority describe both blood and plasma hyperviscosity, others report negative results or those that are interpretable with difficulty. A recent study in 49 patients with Raynaud's syndromes confirmed the presence of elevated blood and plasma viscosity values, particularly in Raynaud's syndromes secondary to other disorders and in digital arteritis. Elevated viscosity levels in "essential" Raynaud's syndromes were significant at low speeds only, suggesting the association of a disorder of erythrocyte aggregation with the properly termed vasomotor disturbance.

Blood Viscosity↗

[Rheologic activation of blood platelets. Preliminary study].

A Couette type coaxial cylinder viscosimeter was used to evaluate the influence of deformation rates up to 20,000/s on blood platelets, in the presence or absence of red cells. Plasma lactate dehydrogenase and haemoglobin levels were determined in order to assess cell lysis and the estimation of beta-thromboglobulin (beta-TG) was considered to be an index of platelet activation. Results for whole blood revealed a change in red cells from 10,000/s upwards, which increased as the rate rose. At the same time, beta-TG rose slowly from the lowest deformation rates then considerably, in relation with the liberation of erythrocytic substances. The rise in LDH and beta-TG levels in platelet rich plasma (PRP) remained small up to 7,000/s approximately, then increased very rapidly, suggesting earlier mechanical and biochemical activation than in whole blood.

Beta-Globulins↗

[Morphologic aspects of intravascular disseminated coagulation. Apropos of 100 cases].

The authors report a morphological study of one hundred cases of disseminated intravascular coagulation (D.I.C.) of various origins. In each case laboratory findings demonstrated an authentic consumption coagulopathy. In all cases organ biopsies were performed either in vitro (rarely), or mainly immediately after death or at autopsy. Optic microscopy was performed for all of them (3 stains were chosen: hemalum eosin saffron, Mallory's phosphotungstic acid hematoxylin stain, P.A.S.). For a smaller number of cases ultrastructural microscopy and immunofluorescence were performed. As far as microscopic findings are concerned, the authors insist particularly upon intravascular microthrombi (fibrinous type and hyalin type). Haemorrhages and particularly necrosis, because of multiple origin, are not detailed. The repartition of these microthrombi is particularly detailed (in connection with the different organs, etiologies, clinical and/or biological findings, treatments). A review of literature is reported.

Adolescent↗

[Blood hyperviscosity syndromes. Classification and physiopathological understanding. Therapeutic deductions].

Blood has a number of rheological properties which partially determine flow, especially at capillary level, and its capacity to deliver oxygen. It is non-Newtonian, pseudoplastic, thixotropic and viscoelastic. Viscosity can be studied with different types of viscosimeters (coaxial cylinder or capillary viscosimeters). It can be defined by the ratio of stress of deformation to rate of deformation. Viscosity depends on macrorheological parameters: hematocrit, serum proteins, especially fibrinogen and globulins, and also on microrheological parameters: degree of aggregation and red blood cell deformability. Viscosity rises when the temperature falls and decreases with the radius of the tube through which the blood flows (Fahraeus-Linqvist effects). Blood viscosity is studied clinically at different temperatures, and, above all, at different rates of deformation by carefully recording the hematocrit. Plasma viscosity, fibrinogen, albumia and immunoglobulin levels, the viscosity of blood cell suspensions in normal saline must also be taken into consideration. Special investigations (rheoscopy, filtrability) provide information about red cell aggregation and deformability. Hyperviscosity syndromes are observed with: --raised hematocrit (polycythemia and pseudopolycythemia), --conditions with raised serum proteins or changes in their composition (especially hyperfibrinogenemia, raised immunoglobulins, low albumin levels); inflammatory syndromes, dysglobulinemias (Fahey's syndrome of plasma hyperviscosity), --low temperature (hypothermia), --increased red cell aggregability (shock, fat embolism), --reduced red cell deformability due to various congenital and acquired conditions (sickle cell anemia, renal failure, hyperlipoproteinemia, thrombosis, diabetes). Conversely, hypoviscosity may occur with a low hematocrit, hypoproteinemia, hypofibrinogenemia, and hyperthermia. Increased viscosity results in a slowing of blood flow, stagnation of its constituents and in ischemia. Therapeutic interventions may be considered on the different components of the hyperviscosity syndrome: hemodilation, plasmapheresis, dispersion of aggregants, agents acting on red cell deformability.

Blood Viscosity↗

[Acute central neurologic complications and the pregnancy-puerperal status. 105 cases in an intensive care unit. Contribution to the study of the relation between pregnancy toxemia and cerebral vascular accidents].

Central neurological pathology in the course of puerperium was studied in 105 observations. One could distinguish: --meeting pathology (tumoral, metabolic, infectious processes) 12 cases, --cerebral vascular accidents (arterial, venous...) 30 cases, These two groups corresponded to a pathology without any obvious connection with gravidic toxemia. --eclamptic or not eclamptic toxemia with encephalopathy: 21 cases, --finally, toxemia associated to or complicated with focused neurological syndromes: 42 cases. Concerning cerebral vascular accidents, one could verify the importance of hemorrhagical accidents (13 cases: 3 subdurhematoma, 4 sub-arachnoid hemorrhages, 6 intra-cerebral hematoma (2 of them corresponded to previous affections revealed by the hemorrhage) (angioma, chorioepithelioma, metastases) and thrombo-embolic accidents (16 cases) corresponding especially to arterial thromboses, the frequency of which seems more important than the frequency of venous thromboses. Any generalized or focused central neurological accident sets the problem of toxemia but is not obligatory toxemic. An associated disorder of hemostasis (hypercoagulability, consumption coagulopathy) has to be searched for.

Acute Disease↗