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Biomedical subjects

R M Hardaway

Publications and source records attributed to R M Hardaway.

At least 19 recordsLinked to original sources
PubMed1992

Organ damage in shock, disseminated intravascular coagulation, and stroke.

Disseminated intravascular coagulation (DIC) may cause multiple organ failure. Although DIC may cause capillary occlusion in any and all organs, the lungs, liver, kidneys, gut, heart and brain are particularly affected. Focal brain necrosis can also be caused by DIC. Fibrinolytic therapy will often restore significant blood flow to the capillaries of the lungs. This results in significant increase in lung function because the lung is more resistant to actual necrosis and will resume function once circulation is restored. Administration of fibrinolytic therapy will also prevent liver and kidney failure if started within four hours after trauma. This therapy, when given in low doses intravenously over a twenty-four hour period, has little effect on the coagulation mechanism, and abnormal bleeding, therefore, has not been a concern. It is speculated that if plasminogen activators are effective and safe for treating the intravascular clots of DIC, then perhaps they would be effective in treating other types of intravascular coagulation in the brain, such as various types and degrees of stroke.

Aged↗
PubMed1990

A new treatment for traumatic shock and ARDS.

Trauma causes more years of lost life than any other cause of death. Traumatic shock and sepsis are the most common late causes of death following trauma. Traumatic shock and sepsis cause multiple organ failure. The most common organ to fail is the lung, which develops Adult Respiratory Distress Syndrome (ARDS). ARDS can be caused by Disseminated Intravascular Coagulation (DIC) with microscopic clots in the lungs. Trauma causes hemolysis and the red cell stroma may initiate DIC. Plasminogen activators, which causes lysis of blood clot, can lyse pulmonary microthrombi and prevent the onset of ARDS even when given several hours after the trauma.

Animals↗
PubMed1990

Prevention of adult respiratory distress syndrome with plasminogen activator in pigs.

Death from traumatic shock has been associated with loss of blood externally or internally. However, many patients die after trauma, even though blood volume restoration is adequate. Death is often due to pulmonary failure (adult respiratory distress syndrome [ARDS]). Death and ARDS have been associated with disseminated intravascular coagulation (DIC) and microclots in the lungs. Dissolution of the microclots after trauma can be achieved by activation of endogenous plasmin. Nine pigs were anesthetized for 48 h. Trauma was administered by 60 standard blows to each thigh resulting in a bruise of muscle but no skin, bone, or major vessel injury. Nutrition and respiration were maintained at normal levels. All nine pigs died with severe lung pathology and low PaO2. Ten other traumatized pigs were treated with a plasminogen activator iv 4 h after trauma. Five of these were treated with tissue plasminogen activator (tPA) and five with urokinase. All treated pigs survived 48 h and maintained a normal PaO2. Autopsy showed minimal lung pathology.

Animals↗
PubMed1987

Influence of steroids on hemorrhagic and traumatic shock.

A hemorrhagic-traumatic shock model in 20 domestic pigs (Sus scrofa) was used to evaluate the pharmacologic effect of methylprednisolone in preventing disseminated intravascular coagulation (DIC). Pairs of animals were anesthetized with thiopental and both femoral arteries cannulated. Four ml/kg-1 of blood were withdrawn, frozen, thawed, and returned to the animal. One femoral artery cannula was connected to a blood pressure monitor for arterial systolic, diastolic, and mean pressures along with heart rate and ECG. The other catheter was used to bleed the animal down to and maintain a mean arterial pressure of 50 mm Hg for 2 hours. Blood samples were taken during the control period before bleeding, and at the end of the 2-hour shock period. Blood samples were analyzed for prothrombin time, partial thromboplastin time, fibrinogen level, and platelet count. The combination of hemorrhagic shock and hemolysis produced DIC and a fatal shock. Pharmacologic doses (30 mg/kg-1) of methylprednisolone significantly prevent the DIC.

Adrenal Cortex Hormones↗
PubMed1982

Pulmonary artery pressure versus pulmonary capillary wedge pressure and central venous pressure in shock.

Evidence is presented from 43 dogs and 30 patients that under conditions of severe hemorrhagic, traumatic or septic shock, there may be partial obstruction of the pulmonary microcirculation due to disseminated intravascular coagulation (DIC) particularly in the pulmonary venules. This may cause the left atrial pressure to fall and the pulmonary artery pressure to rise, in some cases drastically. Pulmonary edema may result. This dangerous rise in pulmonary artery pressure is not reflected by the wedged pulmonary artery catheter which will monitor only the status of the left heart. Central venous pressure (CVP) may remain within normal limits even after pulmonary artery pressure has risen to dangerous levels with the development of pulmonary edema. It is only with right ventricle failure against the high pulmonary pressure that CVP rises. It is concluded that pulmonary artery pressure measurements are very important in monitoring intravenous fluid administration in severe shock. Wedged pulmonary artery pressures monitor the left heart but may be misleading if taken alone. Central venous pressure gives a delayed response to fluid overload.

Aged↗
PubMed1980

Mechanism of traumatic shock.

Although many attempts have been made to demonstrate the existence of a shock-producing toxin, little success has been attained. Traumatic shock is generally believed to be caused by simple loss of blood. Evidence is presented that tissue trauma causes hemolysis. Although hemoglobin is harmless, the stroma of the broken red cells is a clotting stimulant which, in the presence of the slow capillary flow of hemorrhagic shock, sustains a continuing disseminated intravascular coagulation. This disseminated intravascular coagulation produces a clotting defect, morbidity and death. The condition is not responsive to intravenously administered fluids but is responsive to fibrinolysin therapy.

Animals↗
PubMed1979

Importance of capillary perfusion.

Perfusion is more critical than oxygen in the maintenance of cell viability. A high hematocrit or high fibrinogen level increases blood viscosity and predisposes to disseminated intravascular coagulation. It is recommended that a hematocrit of about 30 be maintained in periods of circulatory stress such as shock or extracorporeal circulation.

Animals↗
PubMed1979

The danger of hemolysis in shock.

Intravascular hemolysis is sometimes harmful and often fatal. Other times it is harmless. Dogs were paired and subjected to hemorrhagic shock. One of the pair was given 2 ml/kg of autologous hemolyzed blood before bleeding. The other of the pair was given 2 ml/kg of heparinized autologous blood. All of the animals given heparinized blood survived, whereas, all of the animals given hemolyzed blood died. The animals given hemolyzed blood developed coagulation changes indicative of Disseminated Intravascular Coagulation (DIC), whereas, the dogs given nonhemolyzed blood did not. It is concluded that hemolysis in the presence of shock (slow capillary flow) causes DIC and death. Hemorrhagic shock alone or hemolysis alone was harmless.

Animals↗
PubMed1979

Monitoring of the patient in a state of shock.

Patients in a state of shock require careful monitoring to carry out intelligently appropriate treatment. Many methods of monitoring are available. Some are required for all patients in a state of shock, some are only required in severe or refractory shock, some are of little value, some are valuable but difficult or expensive and some are confusing and may mean the opposite of what they seem to indicate.

Animals↗
PubMed1979

Treatment of shock.

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Acid-Base Equilibrium↗
PubMed1978

Viet Nam wound analysis.

A statistical study is reported of 17,726 wounded American soldiers in Viet Nam over 15 months from March 1966 to July 1967. Causes, location, treatment, and results were analyzed for various regions, organs, and tissues. Results of treatment were remarkably good, the best in the history of military surgery. Major problems of resuscitation and treatment of local tissue injury which had not before been treated on a large scale were treated with excellent results.

Abdominal Injuries↗
PubMed1976

The effect of hemorrhagic shock on disseminated intravascular coagulation.

Experiments tend to confirm the hypothesis that a thromboplastic substance in the blood stream causes little DIC if blood flow is normal. However, if the same quantity of thromboplastic material is present in a slow capillary flow, it will produce DIC and possible death, with a marked clotting defect.

Animals↗