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Biomedical subjects

A Larcan

Publications and source records attributed to A Larcan.

At least 73 records · Page 4Linked to original sources
PubMed1988

[Treatment using plasma exchange of massive acute hemolysis. 15 cases].

Fifteen patients admitted to an intensive care unit for massive acute hemolysis (MAH), defined by a free hemoglobinemia of more than 60 mumol/l, were treated by plasma exchange (PE) after a mean period following onset of 48.5 39 hours. The aim of plasma exchange therapy was to obtain early purification of hemoglobin and other substances released by red cell lysis and to prevent serious complications of MAH such as shock and RVHF or acute renal failure. Treatment by PE produced a decrease in initial hemoglobinemia of 76%, this level then remaining stable. The PE also appeared effective in the prevention and treatment of shock and RVHF, but much less so for installed acute renal failure. Comparison of results with those of a previous series of 16 patients with MAH treated by exsanguino-transfusion showed that PE was more effective, simpler to perform and less aggressive for early treatment of MAH, if rigorous conditions are applied.

Adult↗
PubMed1987

[Asphyxic pulmonary edema caused by upper airway obstruction in adults].

A case of pulmonary oedema following acute pharyngo-laryngeal obstruction is reported. The case is compared with the results of the literature. The haemodynamic data suggested a non-cardiogenic effect, with low pulmonary arterial occlusion pressure of 1 mmHg and right-to-left shunting. Positive end-expiratory pressure was used with success. The mechanisms underlying such oedema are not well known, and may include disturbances in the balance of transpulmonary forces or hypoxia. However the outcome is usually favourable.

Adult↗
PubMed1987

[Physiopathological approach to pathological hyperlactatemia in the diabetic patient. Value of blood metformin].

Type B lactic acidosis, or pathological hyperlactatemia (PHL), is defined by an arterial lactate level greater than 5 mmol X l-1. It is a known and severe complication of diabetes mellitus treated with biguanide hypoglycaemic agents, particularly phenformin which was taken off the French pharmaceutical market in 1977. Metformin, which remains the only biguanide hypoglycaemic agent currently prescribed in France, may also lead to this complication. However it does so less frequently and mostly in the diabetic presenting with renal failure. A few well studied cases showed that PHL could be correlated with excessive metformin blood levels, i.e. a toxic mechanism. In order to find out whether this toxic mechanism was the real cause of PHL in diabetics treated with metformin, a systematic study of metformin blood levels was carried out in 20 such patients. They had all been admitted to a critical care unit presenting with PHL. The results of this study led us to distinguish between two groups of patients. The seven patients of the first group had high metformin blood levels (4.3 to 65.8 micrograms X l-1). In these, renal excretion or extrarenal dialysis lowered or normalized their hyperlactatemia, and six of the seven recovered from PHL. In the second group, with thirteen patients, metformin blood levels were within the normal therapeutic range (0.225 to 3 micrograms X l-1) for seven patients and close to zero for the other six. This second group received the same treatment as the first one. Only three patients recovered, the others all died.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Lactic↗
PubMed1987

[Thrombogenic thrombopenia related to heparin. Clinical, biological and therapeutic results. Apropos of 32 cases].

Heparin induced thrombocytopenia is characterized by often dramatic evolution of thrombotic arterial and venous complications. These occurred or are worsened in curative or preventive heparin therapy and the treatment remains delicate. The authors report 32 observations of thrombocytopenia complicated with thromboembolic events; seven deaths are to mention. The tests of platelet aggregation with standard heparin and platelets poor patient's plasma confirm the diagnosis in 28 cases of 30 very early studied and in 2 cases around the 6th day only after the stop of standard heparin. The choice of anticoagulant therapy is carried out the negative tests of platelet aggregation with low molecular weight heparin (L.M.W.H.) (CY 216, CY 222 Choay, PK 10109 Pharmuka). In L.M.W. heparin therapy, clinical and biological improvement is obtained in 26 cases of 30 treated cases. In three cases, the rapid climbing of platelet countings is not present although negative tests of platelet aggregation with selected L.M.W.H. In one case, after a initial climbing of platelet countings, the thrombocytopenia recurs rapidly with L.M.W. heparin after a operation. The immediate or secondary passage with K-antivitamins, platelet antiaggregant stabilized medium and long term's evolution.

Adult↗
PubMed1987

[Use of a low molecular weight heparin, CY 222, in the treatment of consumption coagulopathy].

UNLABELLED: Among the different treatments used for consumption coagulopathies, the most contested is classical heparin because of the risk of worsening of a hemorrhagic syndrome. A low molecular weight heparin was evaluated to determine possible improvement of this risk. METHODS: Treatment with CY 222 (Choay) was administered over 2 years to 29 patients (mean age 40 years, range 15-74) with coagulation coagulopathies. Diagnosis was based on the presence of 3 of the following 5 signs: platelets less than 150,000/mm, fibrinogen less than 2 g/l, QT less than 50%, ethanol test positive, PDF greater than 20 micrograms/ml. Etiology could be classed in 3 groups: gravido-puerperal (12 cases), medical disorders (15 cases), post-traumatic (2 cases). Dosage was 150 U/kg every 18 hours subcutaneously. The usual symptomatic treatment included: transfusion of red cells, frozen fresh plasma, platelets and antithrombin III as necessary. A hemorrhage syndrome was present in 16 cases. The course of the disease was evaluated on clinical findings and surveillance of hemostasis parameters; anti-Xa activity was determined in 15 patients. RESULTS: Hemorrhage was arrested and biological values normalized in 22 patients (76%) including 15 (52%) survivors. In the 7 cases where the coagulopathy was not improved, the hemorrhagic syndrome persisted in 4. In the 22 successful outcomes, the hemostasis was corrected within 48 to 72 hours, with the exception of the thrombopenia, which persisted up to the 6th day. Mean anti-Xa activity was 0.32 +/- 0.16 anti-Xa U/ml. CONCLUSION: Results of this preliminary, non-randomized study show CY 222 to be as effective as heparin in the treatment of consumption coagulopathies.

Adult↗
PubMed1987

[Fractionated heparins. The clinician's viewpoint].

Currently the rapid development of low molecular weight heparins offers the following questions: assessment of such heparins in prophylaxis of thrombo-embolic disease in surgical or medical procedures; comparison with prior, double-blinded, randomized methods of reference like Kakkar's in general, abdominal, genital, neoplastic and especially orthopedic surgery; search of the most effective standardized dose with no reliable biologic data (usual assays are rather complex and concern more activity than efficacy); respect of absolute contraindication but usefulness of these treatments in relative contraindication of high molecular weight heparin; duration, regimen and outcome measures. The most important standpoint concerns the standardized dosage with few or no reliable biologic tests; thus these dosages cannot be adjusted to coagulation assays.

Blood Coagulation Disorders↗
PubMed1986

[Acute respiratory distress syndrome in adults in colchicine poisoning].

Two cases of adult respiratory distress syndrome were treated in a series of 26 patients suffering from colchicine overdose. The syndrome appeared between the 24th and 72nd hours. It was characterized by the presence of interstitial as well as alveolar oedema seen on chest roentgenograms. Haemodynamic investigation showed a hyperkinetic state with moderate precapillary pulmonary arterial hypertension. In addition, multivisceral phenomena were observed in all cases. Post-mortem examination revealed interstitial and alveolar pulmonary oedema with haemorrhagic or macrophagic alveolitis often accompanied by hyaline membrane. The physiopathology of ARDS occurring in colchicine poisoning appeared to involve such different factors as infection, the presence of a state of shock and disseminated intravascular coagulopathy. The direct toxic action of colchicine on pneumocyte microtubules and the inhibition of surfactant production were a probable cause. The responsibility of colchicine in leukocyte aggregation remains to be determined.

Adult↗
PubMed1986

[Severe thrombopenia associated with treatment with pentosan polysulfate].

Two cases of severe thrombocytopaenia associated with acute thrombo-embolic manifestations during treatment by pentosan polysulphate, a low molecular weight heparinoid, are reported. Plasma samples from both patients caused in vitro aggregation in the presence of pentosan polysulphate. Interruption of the drug led to the recovery of the platelet count. The hypothesis of an immunoallergic mechanism similar to heparin associated thrombocytopaenia is supported. Furthermore, it seemed likely to be found with all the polysulphated X glycosaminoglycans. During treatment by pentosan polysulphate, platelet count should be monitored to avoid this potentially life-threatening syndrome.

Drug Hypersensitivity↗