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Biomedical subjects

C H Mielke

Publications and source records attributed to C H Mielke.

At least 19 recordsLinked to original sources
PubMed1989

Surgical treatment of adolescent idiopathic scoliosis. A comparative analysis.

Three hundred and fifty-two patients had a one-stage posterior spinal arthrodesis between 1960 and 1984 using one of four types of instrumentation: a Harrington distraction rod, Harrington distraction and compression rods, Harrington distraction and compression rods with a device for transverse traction, and a Harrington distraction rod with sublaminar wires. All of the patients were female (age-range, eleven to nineteen years), and all had idiopathic scoliosis with a single right or double thoracic curve. The minimum length of follow-up was two years. No significant difference was found among the four groups relative to the amount of correction that was obtained at operation or maintained two years after operation. An average of 13.5 per cent of correction was lost during follow-up in the patients who were treated with postoperative immobilization, and an average of 27 per cent was lost in the patients who were treated with sublaminar wires without immobilization. The use of a straight Harrington rod reduced normal thoracic kyphosis, the addition of a compression rod corrected hyperkyphosis, and the use of a rod with sublaminar wires corrected thoracic hypokyphosis or thoracic lordosis.

Adolescent↗
PubMed1983

Influence of aspirin on platelets and the bleeding time.

Aspirin influences the bleeding time, presumably through the inhibition of prostaglandin biosynthesis and the resultant platelet secretion reaction. This can be measured by prolongation of the bleeding time and changes in platelet function results. Despite these changes, bleeding is rarely a problem in patients who have normal hemostatic mechanisms. To investigate this, we have studied the technical variables associated with the determination of the bleeding time. Both venostasis and direction of the incision play a major role in the bleeding time prolongation induced by aspirin. When a bleeding time determination is performed with vertical incision without venostasis, there is almost no detectable prolongation of the bleeding time. These studies support our previous observations that aspirin has a mild influence on primary hemostasis.

Animals↗
PubMed1979

Heparin bleeding due to qualitative platelet dysfunction.

On two separate occasions, a 26-year-old white woman bled from arterial puncture wounds while receiving heparin for thromboembolic disease. Bleeding time was prolonged after heparin administration at the time that she was ill and bled, and when she was re-challenged 2 years later. Heparin may produce bleeding as a result of a qualitative platelet dysfunction.

Adult↗
PubMed1978

Altered factor VIII complexes in patients with acute respiratory insufficiency.

Acute respiratory failure is an often-fatal syndrome of multiple etiologies in which altered factor VIII may be a marker of endothelial disease. 12 women with overwhelming viral pneumonia were studied with serial factor VIII antigen, procoagulant activity, and von Willebrand's factor assays. Antigen levels were elevated (range: 86--1644%) out of proportion to procoagulant activity (range: 35--521% by a one-stage assay), and factor VIII antigen to activity ratios were as high as 16:1. Von Willebrand's factor was normal but correlated best with procoagulant activity. All patients had abnormal antigen patterns on crossed immunoelectrophoresis, with increases in protein of both fast and slow mobility. These changes in factor VIII correlated with the patient's clinical courses.

Acute Disease↗
PubMed1977

Impairment by heparin of primary haemostasis and platelet [14C]5-hydroxytryptamine release.

Heparin was administered to 34 normal subjects by intravenous injection (100 mu/kg) and the template bleeding time was significantly increased both 10 min and 120 min following injection. Before heparin the bleeding time was 5-3 +/- 1.0 min (mean +/- 1 SD); 10 min after injection it was 9.8 +/- 5.6 min (P less than 0.001); and 120 min after injection it was 7.2 +/- 3.9 min (P less than 0.001). Increases in the bleeding time were unrelated to changes in platelet count, and independent of heparin's effect on plasma coagulation. In blood drawn 10 min and 120 min following heparin injection, there was significantly less [14C]5-HT released from platelet-rich plasma (PRP) in response to collagen, 0.41 mM epinephrine and 8 micron ADP, although in vitro addition of heparin (0.1 mu/ml, 0.5 mu/ml and 2.5 mu/ml) to baseline PRP of three subjects did not depress [14C]5-HT release. Our experiments suggest that intravenous administration of a therapeutic dose of heparin can cause a significant reversible inpairment of platelet haemostatic properties, possibly by an indirect mechanism.

Adult↗
PubMed1977

Colchicine toxicity: a multisystem disease.

A 23-year-old black man survived a life-threatening multisystem disturbance resulting from a large single dose of colchicine administered intraurethrally for condyloma acuminata. Gastroenteritis and probable pancreatitis rapidly evolved into severe respiratory failure, marked neuromuscular problems, alopecia, and complete bone marrow aplasia. Within two months he had completely recovered. This patient demonstrates that colchicine should be used with extreme caution, if at all, for the therapy of condyloma acuminata.

Adult↗
PubMed1976

Role of platelets in hemostasis and thrombosis.

Platelets interact with the coagulation factors in a complex way to arrest bleeding or generate thrombi. Recently, the platelet's relationship to endothelial alteration and atheroma production has received renewed attention. At present, tests of platelet function better define "hypocoagulable" rather than "hypercoagulable" states.

Blood Coagulation↗
PubMed1975

The effect of somatostatin on coagulation and platelet function in man.

Preliminary evidence has suggested that somatostatin might interfere with platelet function in the baboon. Because this agent is currently being administered experimentally to human beings, we studied its effect on coagulation and platelet function in man. In five subjects, a four-hour infusion of somatostatin (500 micrograms per hour) had no definite effect on platelet count, leukocyte count, hematocrit, platelet adhesiveness and aggregation, bleeding time, partial thromboplastin time, prothrombin time, and fibrinogen levels. A similar infusion for 18 hours in three subjects was likewise without effect. These studies indicate that somatostatin does not affect coagulation and platelet function in man and that its prolonged administration lacks ostensible toxicity.

Adenosine Diphosphate↗
PubMed1975

Blood platelets and extracorporeal circulation; kinetic studies on dogs on cardiopulmonary bypass.

Platelet kinetics and functions were studied in dogs during extracorporeal circulation. A transient platelet sequestration in the liver occurs during the bypass. This reversible disappearance is accompanied by a loss of the ability of platelets to adhere or aggregate. The platelets which return to the circulation have normal functions and a normal life span. The irreversible damage is mainly due to the direct blood-gas interface. Impairment of lung function by platelet aggregates is discussed and the importance of an in vivo model to study the factors which affect the platelets, such as antiaggregating agents, is pointed out.

Animals↗
PubMed1975

Platelets, hemostasis, and thromboembolism during treatment of acute respiratory insufficiency with extracorporeal membrane oxygenation.

Twenty-eight patients were supported with long-term extracorporeal membrane oxygenation as a treatment for acute respiratory insufficiency. Clinical, laboratory, and autopsy data concerning platelets, hemostasis, and thromboembolic disease are presented for the periods during and after bypass. During bypass, a "foreign-surface coagulopathy" was encountered which consisted of abnormal bleeding plus frequent, generalized, small and large vessel thromboembolic events. The abnormal bleeding is attributed to heparin, thrombocytopenia, and a qualitative platelet defect. Possible causes of the thromboembolic events including disseminated intravascular coagulation are also discussed, and speculations are offered concerning clinical management and directions for future investigation.

Adolescent↗