Prolonged somatic survival of clinically brain-dead adult patient.

A 43-year-old woman suffered clinical brain death after severe head injury. The patient met the criteria for the diagnosis of clinical brain death on Day 3. Aggressive hemodynamic and respiratory managements coupled with triple hormone therapy were performed at the family's request, resulting in continued cardiac activity for a prolonged period. Spinal reflexes and automatisms were observed until cardiac arrest. Ventilatory support was discontinued on Day 168, when cardiac death was confirmed, and her kidneys and eyeballs were removed for transplantation. The patient survived for 165 days after the diagnosis of clinical brain death, which is an extremely prolonged period of somatic support for an adult patient after brain death. An extensive and informed discussion on the end-of-life treatment of clinically brain-dead patients is urgently required in Japan to establish treatment guidelines for such patients.

Beta2-Adrenergic agonists suppress rat autoimmune myocarditis: potential role of beta2-adrenergic stimulants as new therapeutic agents for myocarditis.

BACKGROUND: The therapeutic potential of beta2-adrenergic receptor (AR) agonists in the treatment of autoimmune diseases has been reported. However, the role of these drugs in the myocardial structure-induced autoimmune process, which is thought to play a crucial role in the progression of myocarditis to subsequent complications, has not been elucidated. METHODS AND RESULTS: Experimental autoimmune myocarditis (EAM) was induced in rats by immunization with cardiac myosin. On daily administration from day 0 after immunization, the beta2-selective AR agonists formoterol or salbutamol ameliorated EAM on day 21 and increased myocardial interleukin-10/interferon-gamma mRNA levels. Propranolol, a nonselective beta-AR antagonist, aggravated EAM on day 21 and decreased mRNA levels, whereas metoprolol, a beta1-selective AR antagonist, showed no effect. These results were reflected in vivo by the proliferation of cardiac myosin-primed lymph node cells from drug-treated rats. In vitro addition of beta2-selective AR agonists inhibited the activation of cardiac myosin fragment-specific myocarditogenic T lymphocytes, and this effect was reversed by ICI118,551, a beta2-selective AR antagonist. Furthermore, treatment with 2 different beta2-selective AR agonists starting on day 14 also ameliorated EAM on day 21. CONCLUSIONS: beta2-AR stimulation suppressed the development of EAM by inhibiting cardiac myosin-specific T-lymphocyte activation in lymphoid organs and by shifting the imbalance in Th1/Th2 cytokine toward Th2 cytokine. Furthermore, it also ameliorated established myocardial inflammation. beta2-AR-stimulating agents may represent important immunomodulators of the cardiac myosin-induced autoimmune process and have potential as a new therapy for myocarditis.

Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis.

OBJECTIVES: We assessed the significance of serum cytokine levels in patients with fulminant myocarditis. BACKGROUND: Although many investigations have demonstrated the crucial role of cytokines in the development of myocarditis, it remains uncertain whether serum levels of cytokines enable one to predict the prognosis of human myocarditis, especially concerning cardiogenic shock (CS) requiring a mechanical cardiopulmonary support system (MCSS). METHODS: We studied 22 consecutive patients with fulminant myocarditis and compared them with 15 patients with acute myocardial infarction (AMI) requiring MCSS. The patients with myocarditis were classified into three groups: eight patients with CS requiring MCSS on admission (group 1); six patients who unexpectedly lapsed into CS requiring MCSS more than two days after catecholamine had been initiated (group 2); and eight patients without MCSS (group 3). Furthermore, 14 patients with myocarditis requiring MCSS were divided into a fatal group (n = 5) and a survival group (n = 9). Biochemical markers, including serum cytokine levels and hemodynamic variables on admission, were analyzed. RESULTS: Serum levels of interleukin (IL)-10 and tumor necrosis factor-alpha, but not other cytokines, were significantly higher in myocarditis than in AMI. Only serum levels of IL-10 were significantly higher in group 1 and 2 than in group 3 (49.1 +/- 37.5/20.7 +/- 17.6 pg/ml vs. 2.4 +/- 1.1 pg/ml; p = 0.0008/0.0012). Serum IL-10 levels were also significantly higher in the fatal group than in the survival group with myocarditis (74.0 +/- 27.0 pg/ml vs. 16.4 +/- 8.8 pg/ml; p = 0.003). CONCLUSIONS: Serum IL-10 levels on admission enabled one to predict subsequent CS requiring MCSS and mortality of fulminant myocarditis patients.

[Case of infected subdural hematoma diagnosed by diffusion-weighted imaging].

An 80-year-old man who had undergone total gastrectomy and splenectomy for gastric cancer 13 years ago presented with headache, drowsiness, and high fever 1 month after a traffic accident. Brain CT scans revealed bilateral subdural fluid collections. Diffusion-weighted imaging (DWI) showed mixed high and low signal intensities in the left subdural fluid, and contrast-enhanced MR imaging revealed capsule enhancement of the left subdural fluid collection. The patient was diagnosed with left subdural empyema, and 2 burr-holes were drilled for drainage and irrigation. Operative findings revealed a neomembrane underneath the dura mater. Old hematoma and yellowish-white purulent fluid were present within the neomembrane. This confirmed the diagnosis of infected subdural hematoma (ISH). Abscess culture results were positive for Escherichia coli. The patient's symptoms resolved postoperatively with subsequent antibiotic therapy. However, 4 months after the operation, he suddenly died of severe sepsis and disseminated intravascular coagulation following cholecystitis, which was possibly associated with splenectomy. The clinical presentation, diagnosis, and treatment of an unusual case of ISH have been discussed. We emphasize that DWI and enhanced MR imaging may be useful for diagnosing ISH, and serial DWI evaluations may help in monitoring the therapeutic response in ISH.

Recurrent fulminant viral myocarditis with a short clinical course.

A 75-year-old man recovered from an episode of acute influenza. A myocarditis with a normalized level of serum cardiac troponin T, but less than 2 weeks after recovery, he rapidly fell into cardiogenic shock and died of fulminant myocarditis. The autopsied heart showed marked inflammatory cell infiltration that mainly consisted of mononuclear cells positive for CD8, suggesting that the second bout of myocarditis was caused by viral re-infection.