[The diagnostic and therapeutic value of computerized tomography of the chest in intensive care].
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Biomedical subjects
Publications and source records attributed to D Mathieu.
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A retrospective, multi-institutional study was carried out on a series of 50 histologically proved benign hepatic tumors. The 27 hepatic adenomas (HAs) and 23 cases of focal nodular hyperplasia (FNH) were studied with ultrasonography (US) and dynamic computed tomography (CT). Angiography was performed in 26 cases (15 HAs, 11 FNHs); scintigraphy was not used because of its cost. US scans proved nonspecific. CT scans demonstrated hemorrhage in five HAs and were useful in characterizing tumoral vascularity and any intratumoral features such as necrosis or central fibrous scar. The presence of arterial vessels (five patients) in the projection of this central fibrous scar is suggestive of FNH. Dynamic CT scans did not show the type of tumor in most cases. In cases with lesions greater than 3 cm for which doubt as to the diagnosis persists, combined use of morphologic data, scintigraphy, dynamic CT scanning, and angiography can guide the therapeutic decision: surgery or follow-up CT study after use of oral contraceptives is stopped.
The computed tomographic (CT) findings in six patients with periportal tuberculous adenitis were reviewed retrospectively to analyze the main morphologic features of the disease. In all patients, hypodense lymph nodes were observed close to the porta hepatis, with peripheral enhancement seen after administration of contrast material. In one patient, this hypodense adenopathy was associated with homogeneous, normally enhancing lymph nodes. These different features on the CT scans could signify the evolving pathologic stages of the disease, with early noncaseating granulomas and subsequent caseation necrosis. Recognition of these hypodense lymph nodes, especially in patients at risk, should help optimize the correct diagnosis of periportal tuberculous adenitis.
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The comparative study of the results of detection of bacteriuria in 214 samples did not show an evidence of major discrepancies between the classical reference technique on solid media and the AUTOBAC technique on liquid media. The AUTOBAC provides a reliable and rapid test for bacteriuria which saves time and material for the laboratory. Although it has raised considerable interest, it should be used with caution in aplasic or immunodeficient patients in whom the classical criteria of urinary infection cannot be rigourously applied.
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The results of dynamic computed tomography (CT) in 13 patients with intracardiac filling defects and one with a pericardial lipoma are presented. The intracardiac filling defects were due to thrombus in five cases, myxoma in three, hydatid cysts in three, haemangiopericytoma in one and sarcoma in one. These kinds of lesions are well identified by CT which seems to be superior to echocardiography in the characterisation of the components and in the evaluation of the malignant spreading masses.
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The plasma and cellular changes seen during the use of extracorporeal circulatory circuits define the system's degree of haemocompatibility. Heparin is still very much used to prevent activation of the blood clotting mechanisms and to reduce their effects. The fall in concentration of the clotting factors and their inhibitors is usually moderate; it is due to haemodilution, particularly important in cardiac surgery and during plasma exchanges. Fibrinolysis is often activated. In cardiac surgery, it is seen in nearly 20% of cases straight after the end of the ECC, and in nearly 80% of cases during the ECC. In all cases of resin haemoperfusion, there is an early transitory fibrinolytic burst, seen only rarely during haemodialysis and plasma exchanges. This phenomenon is usually well controlled by the natural inhibitors; it can be prevented by antifibrinolytic drugs. Cellular changes show the same trends during cardiac surgery, haemoperfusion and haemodialysis. Thrombopaenia is seen within a few minutes starting of ECC. It is caused by platelet activation, with aggregate formation; these are then trapped by the microcirculation. Leukopaenia occurs at the same time, later followed by rebound; complement activation could be the main cause by forming aggregates of polymorphonuclear cells and monocytes. Intravascular mechanical haemolysis reaches significant levels only in a few cardiac surgical procedures. The great speed of activation of the plasma and platelet enzyme systems by the ECC circuits explains these early changes. They are not only due to direct effects of the physiological circulatory characteristics and to contact with artificial surfaces, but also to plasma-cell interactions and to the patients' reaction to these first alterations.
Portal thrombosis was diagnosed on computed tomography (CT) in 10 patients and confirmed by sonography. CT demonstrated decreased density of the portal vessels in 9 patients with peripheral arterial concentration of contrast material surrounding the intraluminal thrombus. In 1 patient, a fresh thrombus was seen as an increase in intraluminal density on the pre-contrast scan. The involved vessels were generally enlarged. Three patients had follow-up scans, which revealed a cavernoma in 2 and complete patency of the portal vein and its branches following anticoagulant therapy in 1. In the latter patient, localized abnormal intra-hepatic blood flow suggested infarction of portal origin as the result of clot migration.
Sixteen portal cavernomas were examined with dynamic computed tomography (CT) and confirmed by sonography. Characteristic features included loss of the normal vascular structure and the presence of sinuous collateral pathways which were enhanced during the portal phase. Fifteen patients exhibited transient differences in hepatic attenuation and peripheral arterial concentration of contrast material. Increased arterial flow in the poorly perfused territories is suggested as a cause of these hemokinetic abnormalities.
Forty hepatic abscesses were examined with dynamic computed tomography (CT). A "double target sign," consisting of a hypodense central area surrounded by first a hyperdense ring and then a hypodense zone, seems to be highly suggestive of abscess formation. In 12 cases, the hepatic parenchyma surrounding the lesion demonstrated transient hyperdensity after contrast injection, possibly due to localized hepatic venous obstruction secondary to acute hepatic inflammation. This is similar to the appearance of an arterioportal fistula.
Most patients with severe, acute pulmonary embolism (PE) have arterial hypoxemia. To further define the respective roles of ventilation to perfusion (VA/Q) mismatch and intrapulmonary shunt in the mechanism of hypoxemia, we used both right heart catheterization and the six inert gas elimination technique in seven patients with severe, acute PE (mean vascular obstruction, 55 percent) and hypoxemia (mean PaO2, 67 +/- 11 mm Hg). None had previous cardiopulmonary disease, and all were studied within the first ten days of initial symptoms. Increased calculated venous admixture (mean QVA/QT 16.6 +/- 5.1 percent) was present in all patients. The relative contributions of VA/Q mismatching and shunt to this venous admixture varied, however, according to pulmonary radiographic abnormalities and the time elapsed from initial symptoms to the gas exchange study. Although all patients had some degree of VA/Q mismatch, the two patients studied early (ie, less than 48 hours following acute PE) had normal chest x-ray film findings and no significant shunt; VA/Q mismatching accounted for most of the hypoxemia. In the others a shunt (3 to 17 percent of cardiac output) was recorded along with radiographic evidence of atelectasis or infiltrates and accounted for most of the venous admixture in one. In all patients, a low mixed venous oxygen tension (27 +/- 5 mm Hg) additionally contributed to the hypoxemia. Our findings suggest that the initial hypoxemia of acute PE is caused by an altered distribution of ventilation to perfusion. Intrapulmonary shunting contributes significantly to hypoxemia only when atelectasis or another cause of lung volume loss develops.
The indications for hyperbaric oxygen therapy (HBO) in the treatment of acute carbon monoxide (CO) poisoning are discussed far too little in the literature. Depending on the author reasons for referral to a hyperbaric center include the carboxyhemoglobin level, change in state of consciousness or neurological abnormalities. In our opinion, HBO should be used on much wider indications than is usual, not only because of the rapid relief from symptoms it provides but mainly because it may prevent severe delayed sequelae. During a period of 9 months 230 patients with CO poisoning were admitted to our intensive care unit; 203 were treated with HBO and 27 with normobaric oxygen. Our indications for HBO treatment were: coma, pathological neurological findings or loss of consciousness during CO exposure irrespective of normal clinical findings on admission. Four patients died and the others were discharged 12 hours to 25 days after the incident. Seven patients had minor neurological problems within two weeks of discharge and which disappeared within one month. Two patients were re-hospitalized for neuropsychiatric sequelae and recovered in 3 and 6 months respectively. Neither the clinical status upon admission nor COHb predicted the outcome of the poisoning. Referral to a HBO center should be considered when: --the patient is comatose --there are abnormal clinical findings --patients have been unconsciousness during exposure, irrespective of whether they are conscious on admission and have normal clinical status.