Biomedical subjects
Publications and source records attributed to A Sari.
A case of radiographic type I benign osteopetrosis with syringohydromyelia is presented. MRI revealed diffuse sclerosis of the bone marrow in the thick cranial bones and narrowing of the foramen magnum and subarachnoid spaces, especially in the posterior cranial fossa, and syringohydromyelia.
OBJECTIVE: To assess the utility of percutaneous catheter drainage in the management of tuberculous and nontuberculous psoas abscesses associated without any bony involvement or with minimal bony lesions that could not cause vertebral instability. MATERIALS AND METHOD: Eleven patients with psoas, iliopsoas and pelvic abscesses were drained under computed tomography and ultrasonography guidance. RESULTS: There were 15 (10 tuberculous, 5 pyogenic) abscesses in 11 patients. Six of the tuberculous abscesses and one of the pyogenic abscess were associated with vertebral involvement. Vertebral lesions were located in one or two vertebrae without causing any serious disturbance in the vertebral stabilization. In one case, the abscess was bilateral. Nine cases were drained under computed tomography guidance, while two cases were drained under both computed tomography and ultrasonography guidance. One session drainage was sufficient for abscess resolution in uniloculated cases. In the two of four multiloculated cases, catheter drainage was performed twice. Relapse of the abscess was found in only one patient. The mean abscess volume was 520 ml and mean drainage duration was 12 days. None of the cases required surgery. CONCLUSION: Percutaneous drainage, chemotherapy and additional external brace application with the cases associated with bony lesion may be used for treatment of tuberculous and nontuberculous unilocule and multiloculated abscesses.
The present study was undertaken to investigate the possible relationships between the magnitude of autopositive end-expiratory pressure (auto-PEEP) and measured PaO2 during one-lung ventilation (OLV). Forty-one adults received OLV anesthesia using a tidal volume of 8 mL/kg and a respiratory rate of 12 breaths/min. Auto-PEEP was quantified using an end-expiratory port occlusion method. During two-lung ventilation (2LV), auto-PEEP was observed in 18 of 41 patients and ranged from 0.5 to 2.5 cm H2O. During OLV, auto-PEEP was observed in 34 of 41 patients and ranged from 0.5 to 10 cm H2O. The mean (+/- SD) value of auto-PEEP was significantly higher during OLV than during 2LV (3.2 +/- 3.3 cm H2O versus 0.5 +/- 0.7 cm H2O, P < 0.0001). Auto-PEEP during OLV correlated inversely with preoperative forced expiratory volume in 1 s/forced vital capacity (y = 12.5 - 0.13x, r = -.05, P < 0.005). During OLV, there was no significant correlation between auto-PEEP and measured PaO2. These findings confirm that many patients do not exhale completely to functional residual capacity during OLV.
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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.
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.