Complex regional pain syndrome type II as a complication of subclavian catheter insertion.
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Biomedical subjects
Publications and source records attributed to D Solanki.
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BACKGROUND: Isovolemic hemodilution has been suggested for blood conservation and to improve hemodynamic tolerance to abdominal aortic cross clamping. However, the hemodynamic effects of hemodilution during descending thoracic aortic cross clamping (DAC) have not been established. We evaluated them in anesthetized swine. METHODS: Hemodilution (n = 7) was produced by the isovolemic exchange of blood for 6% hetastarch to a target hematocrit of 20%. Hematocrit in control pigs (n = 7) remained at 30%. DAC was performed at the T9 level for 45 minutes. During a 60-minute reperfusion period, control pigs were infused with lactated Ringer's solution; shed blood was returned to hemodilution pigs, followed by lactated Ringer's. If hypotension occurred despite left atrial pressure of 10 mm Hg or greater, boluses of phenylephrine were given to keep mean arterial pressure above 60 mm Hg. RESULTS: Hemodilution caused a marked reduction in hematocrit and in global oxygen delivery (DO2). DAC produced a significant increase in proximal arterial pressure, cardiac index, and DO2 and oxygen consumption (VO2) was markedly reduced in both groups. A significant increase in systemic vascular resistance during DAC occurred only in control pigs. After reperfusion, vascular resistance was significantly lower than baseline in hemodilution pigs, requiring a sixfold greater dose of phenylephrine to avoid hypotension. A lower global DO2 and supply-limited VO2 were also observed in hemodilution pigs. CONCLUSIONS: Isovolemic hemodilution maintains hemodynamic stability during DAC. During lower torso reperfusion, however, hemodilution caused hemodynamic instability, decreased global DO2, and limited VO2, which may offset its potential benefits.
OBJECTIVE: We tested the hypothesis that the pharmacologic properties of a small volume of alpha alpha-cross-linked hemoglobin (alpha alpha Hb) could effectively resuscitate pigs subjected to hemorrhage. METHODS: Fourteen pigs hemorrhaged to a mean arterial pressure (MAP) of 40 mm Hg for 60 minutes were treated with a 4-mL/kg 2-minute infusion of 10 g/dL alpha alpha Hb or 7 g/dL human serum albumin, an oncotically matched control solution. RESULTS: The removal of blood (17 +/- 1.5 mL/kg) caused the typical physiologic responses to hemorrhagic hypovolemia. Infusion of alpha alpha Hb restored mean arterial pressure and coronary perfusion pressure, but cardiac output and mixed venous O2 saturation did not improve significantly. Pulmonary arterial pressure and pulmonary vascular resistance increased markedly and were higher than baseline levels after alpha alpha Hb. Infusion of human serum albumin produced only minor hemodynamic changes. Brain blood flow did improve to baseline values after alpha alpha Hb, but was the only tissue to do so. In the human serum albumin group, superior mesenteric artery blood flow recovered to baseline values, whereas brain blood flow did not. Blood flows to other tissues were similar in both groups. CONCLUSION: Small-volume infusion of alpha alpha Hb restored mean arterial pressure and brain blood flow, but pulmonary hypertension and low peripheral perfusion may offset benefits for trauma patients.
BACKGROUND: In order to test the hypothesis that inhaled nitric oxide (NO) reverses the pulmonary hypertension induced by alphaalpha-diaspirin crosslinked hemoglobin (alphaalphaHb), were studied anesthetized pigs that were administered with a total dose of 200 mg/kg of 10% alphaalphaHb. Inhaled NO (5 ppm) was administered for 10 min, and then discontinued for 10 min. This cycle was then repeated with 10 ppm inhaled NO. RESULTS: alphaalphaHb caused pulmonary arterial pressure (PAP) to increase from 27 +/- 1.7 to 40 +/- 3.0 mmHg (P<0.05) and dynamic lung compliance to decrease from 29+/- 1.5 to 23+/- 1.6 ml/cmH2O (P < 0.05). After both doses of inhaled NO, but particularly 10 ppm, PAP was reduced (P < 0.05) and lung compliance increased (P < 0.05) from the alphaalphaHb levels. When inhaled NO was discontinued PAP again increased and lung compliance decreased to levels significantly different from baseline (P < 0.05). CONCLUSION: We conclude that cell-free hemoglobin-induced pulmonary hypertension and decreased lung compliance can be selectively counteracted by inhaled NO.
PURPOSE: To evaluate FAM [5-FU (5-fluorouracil), doxorubicin, mitomycin C] chemotherapy as adjuvant therapy for patients with resected TNM stage I, II, or III gastric carcinoma. PATIENTS AND METHODS: One hundred ninety-three eligible patients were accrued from 1978 to 1991 in a phase III trial comparing six cycles (1 year) of postoperative FAM chemotherapy with observation only. RESULTS: The median follow-up on this study was 9.5 years. For all patients, no differences (log-rank analysis) in disease-free survival (p = 0.45) and overall survival (p = 0.57) between FAM therapy (93 cases) and surgery (100 cases) were observed. Quality of surgical resection affected survival irrespective of FAM use. Cases with curative resection, defined in a retrospective review of pathology and surgical reports as cases having no evidence of residual disease in the abdomen and tumor-free margins > 1 cm, had superior survival compared to cases not meeting these requirements (p < 0.001). FAM was well tolerated with 6% (five of 90) of cases demonstrating grade IV hematologic toxicity. There were two drug-related fatalities (one cardiomyopathy, one hematolytic uremic syndrome). CONCLUSION: FAM is not effective adjuvant therapy for TNM stage I, II, and III patients with resected gastric cancer. Future adjuvant studies must emphasize prospective surgical quality control to assure enrollment of appropriately staged and resected cases and wide participation to assure adequate case accrual over a reasonable period.
The pretreatment characteristics of 265 multiple myeloma patients treated between 1977 and 1983 were evaluated as potential prognostic factors for survival. Patients whose diagnosis was based on bone marrow plasmacytosis (greater than 30%) were noticed to have poorer survival (P less than 0.001). Although classification of patients according to stage has traditionally been used to identify prognostic groups, differences in survival were noted only between Stage III and Stage I or II patients using one of two common staging systems. Multivariate analysis using Cox's proportional hazards model identified the following prognostic factors in order of importance: plasmacytosis (hazard ratio [HR] = 2.2, 95% confidence interval [CI] = 1.49 to 3.27), hypercalcemia (HR = 1.68, CI = 1.22 to 2.32), hypoalbuminemia (HR = 1.51, CI = 1.15 to 1.99), alkaline phosphatase (HR = 1.62, CI = 1.18 to 2.23), hyperuricemia (HR = 1.46, CI = 1.09 to 1.96), and renal insufficiency (HR = 1.48, CI = 1.08 to 2.04). All patients were followed from 2 to 7.5 years and 130 (49%) survived over 2 years. Logistic regression analysis demonstrated that hyperuricemia, hypoalbuminemia, renal insufficiency, plasmacytosis, gender, alkaline phosphatase, and hypercalcemia were significant predictors of 2-year survival. Knowledge of these factors could be of value in predicting prognosis and planning therapy in patients with multiple myeloma.
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Cytogenetic studies in a 33-year-old male patient with chronic myelogenous leukemia of 7 years duration revealed a so-called i(17q) chromosome marker and other cytogenetic abnormalities during the early phase of blastic crisis which were not present at diagnosis. Careful morphologic examination of this marker using G- and C-banding techniques revealed it to be a dicentric chromosome with a very short intercentromeric area. The fact that the dicentric nature of this marker was not apparent with the conventional Giemsa stain emphasizes the usefulness of the C-banding technique in defining the origin of this important cytogenetic marker.
Delayed hemolytic transfusion reactions in eight persons were manifested solely or primarily by an apparently unexplained posttransfusion decrease in the hematocrit value. Alloantibodies were eventually found in all eight patients, but were sometimes undetectable for as long as 72 hours after the reaction. This did not preclude the occurrence of a new, acute hemolytic reaction. There were three instances of reversible renal failure complicating the reaction. In two patients, some or all of the antibodies became undetectable after four and nine months. In a third, the indirect antiglobulin reactions became considerably weaker after 12 months. Patients previously sensitized to RBC antigens should have available records inspected and a warning device (wristband or wallet card) provided to help prevent reactions caused by an anamnestic antibody rise.
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