Meig's or Pseudomeig's syndrome?

The triad of ascites, hydrothorax in association with a benign ovarian tumor is defined as Meig's syndrome. It is a rare clinical entity. A case of a 62 year-old woman whith dyspnoe, abdominal discomfort and ascites is presented. Clinical and ultrasonographic findings revealed extended palpable pelvic mass originating from the ovaries and ascites as well as hydrothorax of the left lung by chest radiography. The treatment method was surgical intervention. Cytomorphologic studies were positive for malignacy and adenocarcinoma cells were confirmed. The pathogenesis of the pleural and ascites fluids and the importance of CA-125 are discussed (Fig. 2, Ref. 21).

Polymyositis in a patient with recurring ovarian cancer and history of unrelated breast cancer.

BACKGROUND: Polymyositis (PM) is an idiopathic inflammatory myopathy. Occasionally, it may present as a paraneoplastic syndrome and it is strongly associated with ovarian and weakly with breast cancer. We present here a case of a 60-year-old patient with sequential breast and ovarian (second primary) carcinomas followed by PM as a paraneoplastic disorder. CASE REPORT: The patient had been diagnosed with stage I breast carcinoma 3 years ago and had been treated with conservative surgery followed by radiotherapy and six cycles of chemotherapy (CMF). One and a half year later an ovarian carcinoma was diagnosed for which the patient underwent abdominal hysterectomy oophorectomy and omentectomy. The pathological report characterized it as second primary. Adjuvant chemotherapy with carboplatin and taxol was administered. Fourteen months after the initial laparotomy, the patient was re-operated due to ovarian carcinoma recurrence which was involving all lesser pelvis organs. After a successful radical removal of the recurrence the patient developed a fully expressed PM. This case serves to remind that this disease can occur as a paraneoplastic disorder.

Regional effects of dobutamine in endotoxic shock.

beta-2-Adrenergic agents can increase mesenteric blood flow under normal conditions. However, the effects of dobutamine on regional blood flow in sepsis are less well defined since diverging results had been obtained in some studies due to the differences in animal models. In this fluid-resuscitated hyperdynamic endotoxic dog model, we studied the effects of dobutamine on mesenteric, renal, and femoral perfusion. Twenty-one dogs were anesthetized with pentobarbital and paralyzed. Cardiac output was determined by thermodilution, whole body oxygen consumption (VO2) by indirect calorimetry, and regional blood flow by electromagnetic flow probes. Gut tonometry was also assessed. After 2 mg/kg endotoxin administration, the dogs were randomized to receive fluids (to achieve a pulmonary artery balloon-occluded pressure around 10 mm Hg) either alone (n = 7) or combined with a dobutamine infusion at a rate of 5 microgram/kg x min (n = 7) or 10 microgram/kg x min (n = 7). After fluid resuscitation, cardiac index increased (from 57 +/- 28 to 258 +/- 112 ml/kg x min, P < 0.001) but then slightly decreased with time in the control group, but further increased (to 436 +/- 85 ml/kg x min, P < 0.001) and remained elevated in the dobutamine-treated animals. Whole body oxygen delivery (DO2) followed a similar course. Whole body VO2 increased after endotoxin and fluid resuscitation (from 4.9 +/- 1.3 to 6.3 +/- 1.1 ml/kg x min, P < 0.01), especially in the dobutamine-treated animals (to 6.7 +/- 2.1 ml/kg x min, P < 0.01). Mesenteric DO2 increased after fluid administration (from 11.6 +/- 6.7 to 56.3 +/- 31.9 ml/min, P < 0.01) and further increased with dobutamine (to 91.7 +/- 42.5 ml/min, P < 0.01). It decreased with time in all groups. Mesenteric VO2 remained unchanged but gastric intramucosal pH (pHi) continuously decreased with time in the control group (from 7.41 +/- 0.24 to 6.80 +/- 0.17, P < 0.01) while dobutamine prevented the decrease in pHi (7.08 +/- 0.29). Renal DO2 and renal VO2 decreased with time slightly and similarly in the three groups (from 34.8 +/- 13.8 to 22.9 +/- 10 ml/min and 4.0 +/- 1.6 to 2.8 +/- 1.0 ml/min, respectively) but urine output increased only in the dobutamine-treated animals (from 2.0 +/- 1.5 to 6.9 +/- 7.0 ml/min, P < 0.01). Femoral DO2 decreased with time in the control groups but increased in the dobutamine-treated animals. Femoral VO2 remained stable. No statistical differences were found between 5 and 10 microgram/kg x min dobutamine. In this hyperdynamic endotoxic shock model, administration of a limited dose of dobutamine could be useful to increase mesenteric blood flow and urine output.

Regional arteriovenous differences in P(CO2) and pH can reflect critical organ oxygen delivery during endotoxemia.

The goal of this study was to assess whether serial measurements of regional veno-arterial PcoC2 (VAPco2) and arteriovenous pH (AVpH) differences reflect the onset of tissue hypoxia in various organs during endotoxemia. In 12 anesthetized, mechanically ventilated dogs, ultrasonic flow probes were placed around superior mesenteric, renal, and femoral arteries to measure regional blood flow. The corresponding veins were cannulated for blood sampling. Oxygen uptake (V02) was determined from exhaled gas analysis, and oxygen delivery (D02) was calculated as the product of thermodilution cardiac output and arterial oxygen content. Six dogs served as controls, and six received Escherichia coli endotoxin. Cardiac tamponade was induced to reduce D02. Systemic, mesenteric, and femoral critical D02 (DO2crit) were higher in the endotoxic than in the control group (systemic: 12.1 + or - 2.2 vs. 7.9 + or - 2.6 mL/kg min; mesenteric: 8.2 + or - 2.5 vs. 4.1 + or - .6 mL/100 g tissue-min; femoral: 8.3 + or - 2.3 vs. 4.6 + or - .9 mL/min; all p < .05). Systemic and regional critical oxygen extraction ratio (O2ERcrit) were lower in the endotoxic than in the control group (systemic: 45.1 + or - 9.7 vs. 74.1 + or - 9.1%; mesenteric: 37.1 + or - 15.4 vs. 71.1 + or - 7.4%; renal: 30.7 + or - 24.6 vs. 53.9 + or - 28.7%; femoral: 48.1 + or - 9.2 vs. 75.3 + or - 6.9%; all p < .05). With and without endotoxin, systemic and regional DO2crit calculated from V02, VAPco2, or AVpH were similar. In conclusion, systemic and regional VAPco2 and AVpH gradients can reflect hypoxic threshold in the presence, as in the absence, of endotoxemia.

Correlation of serial blood lactate levels to organ failure and mortality after trauma.

To define the value of serial measurements of blood lactate levels after trauma, the present study investigated the correlation between blood lactate, mortality, and organ failure in 129 trauma patients, including 100 intensive care unit (ICU) survivors and 29 ICU fatalities. On admission, injury severity score (ISS) was higher and Glasgow coma score (GCS), revised trauma score (RTS), and trauma revised ISS (TRISS) were lower in the nonsurvivors than in the survivors. Serial arterial blood lactate levels were measured on admission and at least three times a day until normalization. Both initial lactate and highest lactate levels were higher in the nonsurvivors than in the survivors. Organ failure developed in 84 (65%) of the 129 patients. Patients with organ failure had significantly lower RTS and TRISS. Initial lactate and highest lactate levels were significantly higher in patients with organ failure than without organ failure (3.4 [0.7 to 12.7] versus 2.4 [0.4 to 7.6] mEq/L and 4.1 [0.7 to 12.7] versus 2.8 [0.4 to 8.9] mEq/L, respectively, both P < .01). The duration of hyperlactatemia averaged 2.2 days in the former but 1.0 day in the latter patients (P < .01). The data therefore indicate that not only the initial or the highest lactate value but also the duration of hyperlactatemia can be correlated with the development of organ failure. These observations stress the importance of the initial resuscitation in the prevention of organ failure. Serial blood lactate measurements are reliable indicators of morbidity and mortality after trauma.

Effects of methylene blue on oxygen availability and regional blood flow during endotoxic shock.

OBJECTIVE: We hypothesized that methylene blue, by inhibiting the activation of soluble guanylate cyclase mediated by nitric oxide, may reverse systemic hypotension, enhance myocardial function, and improve peripheral distribution of blood flow during endotoxic shock. DESIGN: Randomized, controlled, acute intervention study. SETTING: University intensive care laboratory. SUBJECTS: Twenty-one healthy, anesthetized, mongrel dogs, weighing 26 +/- 4 kg. INTERVENTIONS: Groups 1 (n = 7) and 2 (n = 7) received endotoxin (2 mg/kg iv) alone combined with increasing doses of 2.5, 5, 10, and 20 mg/kg iv of methylene blue. Each dose was administrated for 30 mins with a free interval of 30 mins. Group 3 (n = 7) served as a control group, receiving the same doses of methylene blue in the absence of endotoxin. All animals were given normal saline to keep cardiac filling pressures constant. Blood flow probes were placed around the superior mesenteric, renal, and femoral arteries to measure regional blood flow by ultrasonic technique. Data were collected every 30 mins during the study. MEASUREMENTS AND MAIN RESULTS: After endotoxemia, methylene blue increased systemic and pulmonary arterial pressure and vascular resistances in a dose-dependent manner up to 10 mg/kg, but had no effect on cardiac index. At the highest dose, methylene blue decreased arterial pressure and systemic vascular resistance. At doses of methylene blue of < or = 10 mg/kg, mesenteric and femoral blood artery flow increased. At the highest dose of 20 mg/kg, femoral artery blood flow further increased, but mesenteric blood flow decreased. Renal artery blood flow was unaffected by methylene blue. In the absence of endotoxin, methylene blue at doses of 2.5 or 5 mg/kg did not alter mean arterial pressure, but reduced cardiac index, indicating an increase in systemic vascular resistance. In contrast, the higher doses of 10 or 20 mg/kg of methylene blue decreased mean arterial pressure and systemic vascular resistance. However, pulmonary arterial pressure and pulmonary vascular resistance increased in a dose-dependent manner. Mesenteric and renal artery blood flow decreased but femoral blood flow increased. As in the presence of endotoxin, methylene blue induced dose-related increases in oxygen uptake and oxygen extraction ratio, but did not alter oxygen delivery. Methylene blue largely attenuated the endotoxin-induced increase in plasma nitrite concentrations. CONCLUSIONS: Low and moderate doses of methylene blue can significantly increase arterial blood pressure but not cardiac index during endotoxic shock. Methylene blue infusion may selectively increase mesenteric blood flow. High doses of methylene blue can worsen systemic hypotension, myocardial depression, and pulmonary hypertension after endotoxemia.

Tirilazad mesylate (U-74006F) inhibits effects of endotoxin in dogs.

The present study explored the effects of a potent antioxidant, the 21-aminosteroid U-74006F, on the systemic and regional hemodynamics and the oxygen extraction capabilities during endotoxic shock. Twenty-four anesthetized dogs were randomized into three groups. Group 1 (n = 8) served as control. Group 2 (n = 8) and group 3 (n = 8) received 2 mg/kg iv of Escherichia coli endotoxin, followed 30 min later by saline infusion. Group 3 was given U-74006F as an intravenous bolus of 80 micrograms/kg followed by an infusion of 10 micrograms.kg-1.min-1, and group 2 received an equivalent volume of vehicle. Tamponade was induced 30 min later to study the oxygen extraction capabilities of the animals. Compared with the endotoxin-alone group, the U-74006F-treated dogs maintained higher mean arterial pressure, cardiac index, stroke volume index, and left ventricular stroke work index and lower pulmonary vascular resistance. They also showed a higher fractional blood flow to mesenteric and renal beds. Endotoxin administration increased whole body critical oxygen delivery (DO2crit) from 7.7 +/- 2.4 to 12.0 +/- 1.9 ml.kg-1.min-1 (P < 0.05), but U-74006F decreased DO2crit to 7.8 +/- 2.0 ml.kg-1.min-1 (P < 0.05 vs. endotoxin alone). Endotoxin decreased critical oxygen extraction ratio (O2ERcrit) from 75.0 +/- 12.7 to 44.3 +/- 8.7% (P < 0.05), but U-74006F increased O2ERcrit to 64.1 +/- 11.2% (P < 0.05 vs. endotoxin alone). U-74006F also decreased endotoxin-induced elevation of mesenteric and renal DO2crit and markedly increased regional O2ERcrit. Systemic and regional blood lactate concentrations were lower in the U-74006F-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)