Sudden Death and Staged Therapy for Hemodynamic Stabilization in Patients Enrolled in a Heart Transplantation Program

To investigate the impact of staged therapy for advanced heart failure on therapeutic endpoints, 236 consecutive patients (coronary artery disease/dilated cardiomyopathy in 61/175 patients, left ventricular ejection fraction 14%± 5%, New York Heart Association Class IIl/IIIIV in 102/79/55 patients, respectively) with advanced heart failure were prospectively followed. One hundred thirtyseven patients enrolled from January 1989 to December 1991 were treated conventionally with digoxin, furosemide, and low dose angiotension converting enzyme (ACE) inhibition. Patients refractory to this therapy underwent urgent heart transplantation. Ninetynine patients enrolled from January 1992 to August 1993 underwent staged therapy: stage 1: maximal tolerated ACE inhibition; stage 2: therapy with PGE₁ for preand afterload reduction to achieve hemodynamic stabilization; or stage 3: refractory patients bridged to heart transplantation with continuous outpatient dobutamine. Sudden death was defined as death within 1 hour of symptoms if heart failure symptoms remained stable over the previous 7 days. Conventionally treated patients were followed for 10 ± 9 months; patients who underwent staged therapy for 9 ±5 months. In the group of patients that underwent standard therapy, 39 of 137 (28%) patients died: 5 (13%) deaths occurred suddenly, and death due to progressive pump failure occurred in the remaining 34 (87%) patients. In the group of patients that underwent staged therapy, 25 of 99 (25%) patients died: 13 (52%) deaths occurred suddenly, and 12 (48%) deaths occurred due to progressive pump failure. Thus, patients who underwent staged therapy were at increased risk for sudden death (P = 0.01, relative risk 3.4, 95% confidence interval 1.2–9.7) but were at lower risk for death from pump failure (P = 0.009, relative risk 0.44, 95% confidence interval 0.22–0.84). In patients who underwent therapy with continuous outpatient PGE₁ (n = 7) or dobutamine (n= 21), risk for sudden death (P = NS by log rank test) did not increase. In conclusion, staged therapy significantly reduced death from pump failure; however, patients who could be stabilized and considered too well for heart transplantation were at increased risk for sudden death. Thus, overall survival did not improve. Of note, outpatient dobutamine did not increase the risk for sudden death.     

Lymphoproliferative responses to Borrelia burgdorferi in circumscribed scleroderma

Summary Humoral immune responses to Borrelia hurgdorferi (Bb) have been reported to occur in certain patients with circumscribed scleroderma (CS) (morphoea). Together with the isolation of spiro-chaetes from CS skin biopsies, this finding was taken to suggest Bb as the aetiological agent of CS. Since there is cellular immunoreactivity to Bb in patients with chronic Lyme borreliosis (LB). Bb-specific lymphocytic responses were tested in patients with CS. For this purpose, peripheral blood mononuclear cells from CS patients and. as controls, from patients with various manifestations of LB, and from healthy volunteers without any evidence of Bb infection, were exposed to Bb organisms for 5 days and then assayed for DNA synthesis. Stimulation indices (SI)> 10 were scored positive. By performing lymphocyte proliferation tests we found: (i) that not only patients with various manifestations of LB but also a considerable percentage of seropositive (five of 13 = 38%) and seronegative (six of 26 = 23%) CS patients exhibit an elevated Bb-induced lymphocyte proliferation; (ii) that the magnitude of the cellular response seen in CS patients is comparable to that encountered in patients with established Bb manifestations; and (iii) that, within a given patient, antibiotic therapy can result in a significant reduction of this response. These results support a causative role of Bb in at least some CS patients. Bb-induced lymphocyte responses were also seen in both seropositive and seronegative erythema chronicum migrans patients. These findings show that the pattern of Bb-specific immune responses is more complex than previously thought, and underscore the importance of lymphocyte function assays in evaluating the diagnosis of potential Bb infection in seronegative patients.     

REACTIVE ARTHRITIS: UROGENTTAL SWAB CULTURE IS THE ONLY USEFUL DIAGNOSTIC METHOD FOR THE DETECTION OF THE ARTHRITOGENIC INFECTION IN EXTRA-ARTICULARLY ASYMPTOMATIC PATIENTS WITH UNDIFFERENTIATED OLIGOARTHRITIS

Reactive arthritis (ReA) is a scronegative oligoarthritis triggeredby a preceding extra-articular infection. While evidence ofa microbial infection is mandatory for establishing the diagnosisof ReA, the sensitivity of bacteriological and serological testshas not been determined in patients without symptoms of infection.In a retrospective study, we evaluated the usefulness of urogenitalswab cultures, serology and stool culture to identify infectionsin 234 patients with undifferentiated oligoarthritis. One hundredand forty-four patients complaining about joint pain who hadno sign or history of inflammatory arthritis served as controls.Urogenital swab cultures showed a microbial infection in 44%of the patients with oligoarthritis (15% Chlamydia, 14% Mycoplasma,28% Ureaplasma), whereas in the control group only 26% had apositive result (4% Chlamydia, 7% Mycoplasma, 21% Ureaplasma)(P < 0.001). A Chlamydia IgG-antibody titre     

PLASMA CONCENTRATIONS OF NORADRENALINE AND ADRENALINE AND PLASMA RENIN ACTIVITY DURING EXTRADURAL BLOCKADE IN DOGS

Anaesthetized dogs (pentobarbitone 25 mg kg^–1+ 3 mg kg^–1h^–1) with a Teflon catheter inserted to the femoral arteryfor pressure and heart rate measurement and blood sampling werestudied. Eitradural puncture was carried out at L7-S1 underx-ray control and 2% lignocaine (1 ml min^–1) infused forapproximately 10 min. During extradural block a decrease inarterial pressure was accompanied by a simultaneous decreasein plasma noradrenaline concentration (NA) and a compensatoryincrease in plasma renin activity (PRA), which became significant15 min after commencing the block when the arterial pressurewas at the minimum. Dihydroergotamine (DHE) led to a rapid reversalof the hypotension with no change in heart rate and a decreasein PRA. Hypovolaemia (blood loss 5 ml kg^–1) was inducedbefore and during block, respectively, in two further experimentalgroups. Increased NA and PRA were found under hypovolaemia withoutextradural block, but only PRA increased with hypovolaemia anda block. The effects of DHE in the later studies were comparableto those observed in the initial study.     

Overfeeding Macronutrients to Critically Ill Adults: Metabolic Complications

Metabolic complications from overfeeding critically ill patients are serious and sometimes fatal. Nutrition care is best provided through repeated evaluation of patients’ responses to feeding. Nutrition support may need to be modified over time to maintain metabolic stability and promote recovery. This article describes the etiology of 10 metabolic complications of overfeeding. Guidelines for recommending macronutrients are discussed, as are factors that could increase the risk of overfeeding. Patients who are very small, very large, or very old are particularly vulnerable to overfeeding. Overfeeding protein has led to azotemia, hypertonic dehydration, and metabolic acidosis. Excessive carbohydrate infusion has resulted in hyperglycemia, hypertriglyceridemia, and hepatic steatosis. High-fat infusions have caused hypertriglyceridemia and fat-overload syndrome. Hypercapnia and refeeding syndrome have also been caused by aggressive overfeeding. Dietitians can prevent or curtail the metabolic complications of overfeeding by identifying patients at risk, providing adequate assessment, coordinating interdisciplinary care plans, and delivering timely and appropriate monitoring and intervention. Dietitians need to document complications, interventions, and the outcomes of their clinical care to evaluate the appropriateness of existing nutrition guidelines. J Am Diet Assoc. 1998;98:795-806.