CT-guided drainage of multilocular pelvic and gluteal tuberculous abscesses.
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Biomedical subjects
Publications and source records attributed to A Sari.
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OBJECTIVE: To investigate the effect of PaCO2 on cerebral blood flow (CBF) in chronic obstructive pulmonary disease (COPD). DESIGN: Before-after trial. SETTING: General ICU in a regional hospital. PATIENTS: 7 patients undergoing mechanical ventilation because of an exacerbation of COPD. INTERVENTION: CBF and cerebral metabolic rate of oxygen (CMRO2) of COPD were measured before and after hyperventilation and were compared by those of normal patients. CBF was measured by the Kety-Schmidt technique using 15% N2O. MEASUREMENTS/RESULTS: Hyperventilation produced a significant reduction in CBF in COPD with no concomitant change in CMRO2. CMRO2 in COPD was significantly lower than those in normal patients. The regression equation was shifted significantly more to the right in COPD. CONCLUSION: The sensitivity of CBF in CO2 remained but CMRO2 was reduced markedly in COPD patients.
Combined effects of inversed ratio ventilation (IRV) with positive end-expiratory pressure (PEEP) on cardiorespiratory function were examined in 24 patients with acute respiratory failure. Patients were divided into two groups: the IRV group (n = 12) who showed no significant increase in Pa(O)(2) with a 6 cmH(2)O of PEEP and PEEP group (n = 12) who were ventilated mechanically with PEEP only at maximum level of 10 cmH(2)O. In IRV group step-wise prolongation of the I : E ratio from 1 : 1.9 to 2.6 : 1 or 4 : 1 was applied as a Pa(O)(2) was improved and in PEEP group also level of PEEP was increased from 0, 5 to 10 cmH(2)O after one hour period irrespective of Pa(O)(2). Inversed ratio ventilation and PEEP increased significantly Pa(O)(2)/F i(O)(2), the increase being observed 6 hrs (I : E = 2 : 1) and 2 hrs (10 cmH(2)O) after starting IRV or PEEP. Further improvement of oxygenation was not observed in IRV even if I : E ratio was prolonged up to 2.6 : 1 or 4 : 1. These results suggested that combinations of IRV with PEEP were effective and an I : E ratio of 2 : 1 may be optimal, and IRV is advantageous compared to PEEP, but will take more long time to improve oxygenation than PEEP.
Dopamine improves renal function and renal blood flow by increasing cardiac output but its effect to ameriolate postoperative liver dysfunction has not yet been defined. Effect of 3-5 microg.kg(-1).min(-1) dopamine was studied in 22 patients who had total gastrectomy (dopamine group), and was compared with 22 patients who underwent the same operation and without dopamine infusion (control group). Liver function was evaluated from serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) values. Although postoperative SGOT and SGPT values in both groups were increased significantly higher than the preoperative values, the increases in SGOT (40 +/- 14 IU) and SGPT (32 +/- 15 IU) values in the dopamine group were significantly less than those in the control group (67 +/- 27 IU, 43 +/- 19 IU) ( P < 0.05, P < 0.01).In conclusion, these results suggested that this observation might be explained by amelioration of the postoperative liver dysfunction by infusion of dopamine. Dopamine infusion at a small dose during upper abdominal surgery is beneficial for liver function.
We investigated the effects of inversed ratio ventilation by altering the inspiratory:expiratory (I:E) ratio and assessing the time course changes in the intrapulmonary shunting (Qs/Qt) in 14 patients with acute respiratory failure. Stepwise prolongation of the I:E ratio from 1:1.9 to 2:1 and then to 2.6 or 4:1 was applied when PEEP failed to raise the PaO2 above 80 mmHg while breathing oxygen. A significant decrease in Qs/Qt was observed following prolongation of the I:E ratio from 1:1.9 (Qs/Qt = 45 +/- 9%) to 2:1 (Qs/Qt = 29 +/- 9%) but not with further prolongation of the I:E ratio (Qs/Qt = 27 +/- 7%). Improvement of the pulmonary ventilation/perfusion imbalance became more marked with continued IRV and a significant increase in PaO2 was observed at 6 h after initiating prolongation of the inspiratory time (P less than 0.05). There were no significant changes in hemodynamics, PaCO2, or peak inspiratory pressure during IRV. This ventilatory pattern may be indicated when PEEP fails to improve PaO2, but prolongation of the inspiratory time above an I:E ratio of 2:1 did not produce a greater improvement in Qs/Qt and further increases in PaO2 did not occur after more than 10 h of IRV in our 14 patients.
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The authors studied the effects of hypocapnic-hyperventilation on cerebral blood flow (CBF) (study 1) and on cerebral oxygenation (study 2) during mechanical ventilation in 8 patients, 4 with hepatic (HE) and 4 with septic encephalopathy (SE). In study 1, a positive linear relationship between CBF(y) and PaCO2 (x) was observed (y = 2.44x - 55.5, r = 0.6276, P less than 0.01, n = 18). In the study 2, hypocapnic-hyperventilation produced a reduction in CBF below the level required to meet the demand in 4 of 8 patients. A good linear relationship was observed between CBF/CMRO2 (CMRO2 = cerebral oxygen consumption, y) and jugular venous PO2 (PjVO2, x) (y = 0.99x - 15.53, r = 0.8962, P less than 0.01, n = 18). It is concluded that cerebrovascular reactivity to CO2 was preserved in these patients, therefore, intentional or inadvertant hyperventilation may produce cerebral ischemia. Moreover, JPVO2 may be useful in monitoring cerebral oxygenation in such patients.
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This study evaluated the reliability of cerebral blood flow equivalent (CBFE), which was calculated as the reciprocal of cerebral arteriovenous oxygen content difference (C(av)DO2) as a monitor during barbiturate therapy in patients with cerebral ischemic insults. A barbiturate (thiamylal) was administered at a rate of 3 mg . kg-1 . hr-1 for 2-5 days to four patients who had suffered cardiac arrest, four with acute focal ischemia, two with postoperative brain edema after neurosurgery, and one with brain damage due to asphyxia. Four of the 11 patients completely recovered neurologically (recovery group), and others had neurological sequelae or died (nonrecovery group). The mean value of CBFE in the recovery group decreased significantly with barbiturate therapy to 13 +/- 1 ml blood/ml O2 from 39 +/- 3 ml blood/ml O2 but did not decrease in the nonrecovery group. We conclude that CBFE can be useful for monitoring the effect of barbiturate therapy in ischemic brain insults.
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A 29-year old healthy woman suddenly developed hypovolemic shock, anasarca, pleural effusion, and ascites in the postpartum period. Plasma leakage was thought to be caused by generalized increased capillary permeability. She was treated successfully with massive plasma transfusions, administration of norepinephrine, and early institution of respiratory support. The patient has not developed a similar episode during 1 yr of follow-up.
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Cerebral circulation and metabolism during Althesin anaesthesia were studied in seven healthy patients. Althesin was given in a single dose of 0.1 ml/kg and thereafter infused at a constant rate of 0.3 ml/kg/h. During Althesin infusion, the cerebral blood flow (CBF), the cerebral metabolic rate for oxygen (CMRo2) were 29 +/- 10 ml/100 g/min and 1.7 +/- 0.4 ml/133 g/min, respectively. These values were significantly different from those obtained in awake subjects in our laboratory (CBF: 46 +/- 7 ml/100 g/min; CMRo2: 3.1 +/- 0.6 ml/100 g/min). During CBF measurement, the mean cerebral perfusion pressure, cerebral vascular resistance (CVR) and arterial carbon dioxide tension (PaCO2) were 89 +/- 16 mm Hg, 3.4 +/- 1.3 mm Hg/ml/100 g/min, and 36 +/- 9 mm Hg, respectively. The relationship between CBF and PaCO2 were studied and it was found that during Althesin anaesthesia reactivity of cerebral vessels to the alteration of PaCO2 was maintained. It is concluded that Althesin caused cerebral metabolic depression which was accompaned by a decrease in CBF and an increase in CVR.
The effects of diazepam, clomipramine, and chlorpromazine upon cerebral metabolism and blood flow were examined separately in 18 dogs. After the administration of diazepam or clomipramine, cerebral cortical oxygen consumption (CMRO2) decreased significantly by a maximum of 17% and 13% of control within 10 minutes and 15 minutes, and returned to control at 120 minutes and 90 minutes, respectively. Chlorpromazine, however, decreased by a maximum of 10% of control, a level which continued throughout the period of observation. It was observed that reduction in CMRglucose was followed by the reduction in CMRO2 at an interval during the early stages of CMRO2 depression. Diazepam produced a significant decrease in CBF accompanied by reduction in CMRO2, but neither clomipramine nor chlorpromazine had any effect on CBF in spite of reduction in CMRO2. Reduction in CMRO2 both with diazepam and clomipramine was accompanied by slow wave activities of EEG, but with chlorpromazine reduction in CMRO2 was accompanied with less pronounced slow wave activities. It was concluded that the three drugs examined were cerebral metabolic depressants.