Established ARDS Treated with a Sustained Course of Adrenocortical Steroids: TOTAL EXPERIENCE

Ten patients have been treated with a program of sustained ACS for established ARDS including the three described above (Table 1). In all patients, the initiating event(s) had resolved prior to the use of ACS. The ARDS had been present from four to 40 days before the ACS program was initiated (average-11 days). The etiologies of ARDS in our patients were sepsis, aspiration, and trauma (one patient each); cardiopulmonary arrest (two patients); and post-pump cardiopulmonary bypass (five patients). The ACS ther­apy was longer than three weeks in all surviving patients and a dosage of greater than 40 mg a day was employed for an average of 12 days. Patients 3 through 10 were all treated with uninterrupted courses of ACS (Table 1). Their responses to ACS were similar to that demonstrated in patient 3 (Fig 4) except for case 6 who died. After four to seven days of therapy, signifi­cant clinical improvement in ventilatory requirements, oxygenation, and chest roentgenograms were apparent in all patients. Nine Ga citrate scans were performed in eight patients. Significant uptake was observed in all scans (Table 1 and Fig 3).

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Established ARDS Treated with a Sustained Course of Adrenocortical Steroids: PATIENT PROFILES AND CLINICAL TECHNIQUES part 2

Case 2

One week following an acute myocardial infarction, a 37-year-old native American woman (Fig 2) required emergency replacement of the mitral valve for severe acute mitral regurgitation. The postoperative course was complicated by diffuse pulmonary infil­trates and prolonged ventilator dependence. By the seventh hospital day, there had been no improvement in the ARDS in spite of supportive measures. Hemodynamic measurements showed a wedge pressure of 19 mm Hg and pulmonary artery pressures of 43/29. A ^Ga citrate scan demonstrated significant pulmonary uptake of isotope at 48 hours (Fig 3). A rapidly tapering dose of ACS was given, and distinctive improvements in oxygenation and chest roentgenogram were observed. The patient was successfully weaned from mechanical ventilation and extubated. However, the patient, who had been improving daily, began to deteriorate without apparent reason.

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Established ARDS Treated with a Sustained Course of Adrenocortical Steroids: PATIENT PROFILES AND CLINICAL TECHNIQUES

Ten patients with established ARDS were cared for by the authors over an 18-month period and represent our total experience with ARDS treated with ACS since the index case (Table 1). The first two patients initially had a limited course of ACS, but subsequently completed a sustained course of greater than 21 days. Seven patients had uninterrupted courses of therapeutic ACS for greater than 21 days while one died during therapy.

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Established ARDS Treated with a Sustained Course of Adrenocortical Steroids

The word, “controversy,” is repeatedly used to describe the debate surrounding the use of ACS in patients suffering from ARDS. Prominent clinicians and scientists are on opposite sides of the issue quoting well-done work to support their views. Recent carefully performed studies have shown short-term, high-dose adrenocortical steroids do not improve ul­timate outcome. Our experience has led us to question further the use of these agents in this complicated problem. What is the effect of a longer course of therapy? Can patient selection identify a group or subset who may respond to this therapy? What are the implications of gallium uptake by ARDS lungs for pathogenesis and therapy?

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Echocardiographic Observations in Survivors of Acute Electrical Injury: DISCUSSION

There is little information available concerning the 104 cardiac sequelae in survivors of electrical shock. Electrocardiographic patterns typical of acute myo­cardial infarction have been reported immediately after resuscitation, but it has been suggested that in long-term survivors these resolve completely. To our knowledge, only one previous report has provided any direct information concerning cardiac function in such patients. Lewin et al reported the noninvasive car­diac findings in a 19-year-old who was successfully resuscitated following an electrical injury. An echocar­diogram performed at the time of cardiac enzyme elevation and striking ECG abnormalities demon­strated severe global left ventricular hypokinesis. However, a follow-up echocardiogram three days later showed significantly improved ventricular function, and a gated blood pool scan performed at that time demonstrated an ejection fraction of 69 percent. A repeat echocardiogram at one year was entirely nor­mal. In contrast, the two patients described herein had persistent abnormalities of left ventricular func­tion. In one, although there was a marked reduction in the extent of dysfunction noted initially, left ven­tricular apical dyskinesis persisted. In addition, two months later, a thallium scan demonstrated a fixed perfusion defect consistent with apical infarction. In the second patient, there was severe biventricular dysfunction that persisted until death at day 6.

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Echocardiographic Observations in Survivors of Acute Electrical Injury: CASE REPORTS

Case 1

A 25-year-old previously well man lost consciousness when he touched an electrical wire. At least ten minutes elapsed before cardiopulmonary resuscitation (CPR) was initiated. On arrival at the hospital he was successfully defibrillated after several DC countershocks but he never regained consciousness. Although physical examination subsequently revealed stable vital signs and normal results of cardiac examination, findings from neurologic examination and diagnostic testing were consistent with severe anoxic brain damage. The electrocardiogram (ECG) revealed sinus tachycardia with poor R-wave progression in V, through V_e. His creatine kinase value was 9,800 units/L with 5 percent MB. A two- dimensional echocardiogram revealed severe biventricular hypoki- nesis with left ventricular apical dyskinesis (Fig 1). The left ventricular ejection fraction calculated by gated blood pool scanning was 15 percent. A repeat echocardiogram four days later was unchanged. A rest thallium study revealed apical, inferior, and septal defects. The patients neurologic status deteriorated and he died six days later.

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Echocardiographic Observations in Survivors of Acute Electrical Injury

Although it is well known that cardiopulmonary arrest is the main cause of immediate death due to electrical injury, there is a paucity of information concerning the cardiovascular sequelae in survivors of the acute event. Enzyme changes consistent with myocardial necrosis have been reported. However, these may be difficult to interpret in the context of extensive noncardiac muscular damage at the time of the original injury and/or during resuscitation. Electrocardiographic patterns of myocardial infarction have also been described immediately following the electrical insult. These typically normalize dramatically and in long-term survivors have been reported to be totally reversible. Similarly, the single previous case report describing left ventricular function following acute electrical injury also suggested that there is total recovery of left ventricular function.

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