[Silver amalgam. 2. Reflection on cavity preparation for amalgams].
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Biomedical subjects
Publications and source records attributed to F Roth.
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The increasing use of central venous catheters requires knowledge of possible hazards. Complications such as pneumothorax, hemothorax, hematomas in the chest wall or mediastinum and pulmonary emboli caused by the catheter are easily seen on plain chest films. Cardiac tamponade, perforation of vessels, air emboli and thrombosis have to be considered as a possible cause in case of sudden deterioration of a patient.
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Attention is drawn to the incidence rate of the various types of obliterations of the carotid artery in the extracranial area. The evaluation is based on 242 carotid stenoses from a total of 1283 angiograms. Over and above this, the paper presents initial results of computertomography in 15 patients with obliterations of the carotid arteries in the cervical region.
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An investigation has been conducted into clinical signs and concomitant ultrastructural alterations in the peripheral nerves of 4 patients who developed polyneuropathy and, in part, encephalopathy following gentamicin therapy. The ultrastructural analysis of the nerve biopsy afforded evidence of an induced lysosomal abnormality comparable to the changes observed in gentamicin nephrotoxicity. As in nephrotoxicity, the neurotoxic effect seems to be reversible.
The increase of the inflationary lung volume created by a respiratory maneuver is critical for preventing postoperative alveolar collapse. We measured this volume as achieved with IPPB or incentive spirometry (IS) in 20 postoperative surgical patients. Using IPPB, with gas flow and peak airway pressures carefully adjusted for each patient, a value of 2240 +/- 630 cc (mean +/- 1 SD) was obtained compared to 1960 +/- 650 cc with IS. This difference is highly significant (p less than 0.0005 by the Wilcoxon test). We conclude that IPPB, by careful application, and with monitoring of tidal volumes, is likely to provide better prophylaxis of postoperative pulmonary complications, particularly in patients with compromised lung function and in an intensive care unit, where enough trained personel are available.
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Spontaneous respiration in the presence of upper airway obstruction causes considerable negative intra alveolar pressure which may lead to pulmonary oedema "ex vacuo". Four cases are presented of spontaneously breathing patients who sustained upper airway obstruction lastin from one to several hours, leading to manifest pulmonary oedema. The pathogenesis of pulmonary oedema ex vacuo is discussed on the basis of alteration of physiological parameters such as capillary, alveolar and pleural pressures, as well as the properties of lung liquid exchange. In contrast, pulmonary oedema occurring after re-expansion of a collapsed lung is reported in one patient. No negative intraalveolar pressure could be incriminated in this case since the patient was ventilated using intermittent positive pressure from the beginning of lung expansion. We tend to attribute the evolution of this second kind of pulmonary oedema to capillary damage, resulting from hypoperfusion of the atelectatic areas, altered alveolar surface lining layer, infection and other cases. The therapeutic measures used in pulmonary oedema "exvacuo" are briefly mentioned.
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In nine patients, undergoing repeat operations because of severe intra-abdominal infection developing after major abdominal surgery, serum potassium concentrations were monitored during induction of anaesthesia. Four patients showed an increase of serum potassium ranging from 2.5 to 3.1 mmol/litre above baseline values within 3-6 min after suxamethonium 100 mg i.v. In five patients there was no change. The four patients demonstrating an increase had suffered from pyrexia and leucocytosis for at least 2 weeks. The other five had signs of infection for no more than 9 days. It is concluded that patients with signs of severe intra-abdominal infection lasting longer than 1 week represent an additional category susceptible to suxamethonium-induced hyperkalaemia. They should receive only non-depolarizing muscle relaxants. When the use of suxamethonium is unavoidable, the injection of a non-depolarizing muscle relaxant before the administration of suxamethonium is recommended.
A serious danger to the circulation following the administration of suxamethonium is known to occur in patients reacting with an abnormal release of potassium. So far the following groups of patients have been found to be at an increased risk: burns, multiple trauma, tetanus, neurological disorders, uraemia. As a result of our investigations patients with severe intraabdominal infections are also to be regarded as at risk. Four of ten patients with this diagnosis have shown an increase of serum-potassium of more than 2.5 mequiv/l following suxamethonium injection in spite of a prophylactic small dose of nondepolarizing relaxant. The predisposing factors are high fever of over a week's duration and a leucocytosis of more than 10,000/cu. mm. A possible hypothesis and pathogenesis of the abnormal efflux of potassium is discussed. Prophylaxis consists of using only nondepolarizing relaxants in these cases. When there is a special indication for suxamethonium the potassium increase can be lessened if the patient is given a small dose of nondepolarizing relaxant prior to the administration of suxamethonium.
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