PubMed Health⌕ Search

Biomedical subjects

A Glatzl

Publications and source records attributed to A Glatzl.

9 recordsLinked to original sources
PubMed1989

[Catheter epidural analgesia in serial rib fractures].

According to our results, permanent epidural anaesthesia was significantly superior to systemic opioid treatment in patients with serial rib fractures. The main advantages were not only continuous pain relief despite the fact that the nonepidural control group required more than twice the dosage of morphine derivatives; also, the respiratory and pain-related recovery time was reduced. Another advantage was the selective effect (due to the local application) on respiratory pain and therefore on respiration as a whole. Deep breathing and expectoration were easier, so that the use of respirators and other artificial breathing aids could be avoided or at least reduced in duration in some cases. This makes the method particularly suitable for use in the management of polytraumatized patients. The standard dose was a mixture of 3.3 mg morphine and 37.5 mg bupivacaine (= 1/3 ampoule morphine + 15 ml Carbostesin 0.25%) every 12 h. When morphine was temporary contraindicated (frequently the final diagnosis in the case of an "acute abdomen" delayed the administration of morphine) the use of bupivacaine alone provided a satisfactory result for a certain time (we never observed tachyphylaxis). Additional systemic pain relievers were only necessary when the patient was suffering from pain caused by other injuries beyond the area of effectiveness of the epidural catheter (the only obvious disadvantage of the local application technique). On the other hand, epidural anaesthesia enabled us to treat a patient's lower-leg fracture by interlocking nailing, while adding only 0.01 mg fentanyl (= 2 ml Fentanyl Janssen) and 1.2 mg flunitrazepam (Rohypnol).

Adult↗
PubMed1980

Electron-microscopic investigation of lung biopsies in patients with post-traumatic respiratory insufficiency.

Lung biopsies were taken from patients during the course of post-traumatic respiratory insufficiency, from 3 hours to 19 days after the onset of shock. Electron-microscopic investigations revealed that the initial phases of cellular damaged were followed by both endothelial and epithelial changes, including atelectasis, lymphatic dilation, and interstitial as well as interalveolar fibrin extravasation. Interstitial edema and extravascular migration of granulocytes, lymphocytes and mast cells are followed by fibroblastic proliferation and, as an end result, fibrosis of the alveolar septa. As a result, fibroblasts replace capillaries at the surface, where gas exchange takes place. The capillaries are forced into the depths of the interstitial tissues. At the same time, the alveolar surface becomes covered with thick-walled proliferating epithelial cell layers, which also renders gas exchange increasingly difficult. Lung function is thereby reduced.

Endothelium↗
PubMed1980

[Acute post-traumatic lung failure - morphological evaluation (author's transl)].

We investigated morphological findings of human biopsy material taken from lung and muscle, as well as lung tissue taken from animals in hypovolatemic-traumatic shock experiments. This was an attempt to reproduce, by way of an experimental setup with animals, the morphological changes which were formely found in the biopsies. Our morphological results lead to the assumption that the posttraumatic progressive lung failure without direct lung trauma can be divided into two major phases which are of decisive importance for the clinical development. 1. Early changes: Massive leucostasis of polymorphonuclear granulocytes with partial degranulation in the lung. In additon, a swelling of the endothelium cells, fat globules and a beginning interstitial edema were observed. In none of the cases were microthrombi found. 2. The actual "shock lung or fat embolism syndrome" which can be diagnosed also clinically 24 to 72 hours after the trauma. Morphologically predominating here are the interstitial edema and the fibrosis secondary to this and which manifests itself clinically in a disturbed gas exchange. This is accompanied by serious changes in the alveolar epithelium, deposits rich in protein as well as an increased occurence of phagocytizing macrophages in the alveoli. The early morphological changes in shock lung can most likely be influenced by therapeutical measures (such as a prompt shock treatment, a balanced restoration of the loss in blood volume and an early artificial ventilation). In this way, also the feared shock lung syndrome can be avoided. In an experimental setup with animals these early changes, especially the leucostasis, can easily by reproduced. This has become possible by the experience gained from the human lung biopsies. By way of this animal experiment new methods of treatment can be tested which might lead to a clinical progress in the prophylaxis as well as in the treatment of the progressive post-traumatic lung failure.

Animals↗
PubMed1977

[Comparative studies on the ultrastructure of human lung and sceletal muscle in shock. II (author's transl)].

The ultrastructure of skeletal muscle biopsies was investigated and compared to lung biopsy material of the same patient in shock. We found almost complete conformity of ultrastructural changes in the micro-vascular system. Capillary endothelia of both tissue types react in a similar way with a more or less distinct swelling of endothelial cells and rarefaction of cell structures as well as constriction of the vascular lumina. Despite an intact structure of the capillary endothelia there is development of oedema in the perivascular areas with escape of plasma components, erythrocytes and granulocytes into the muscle interstitium. Finally, more distant tissue regions are becoming oedematous. While mainly lysosomal enzymes from the large number of infiltrating granulocytes, as well as fatty globules, are made responsible for the damage in the shock lung, the damage of the capillary region in the sceletal musculature is almost certainly caused by hypoxia. We consider muscle biopsy a suitable method to obtain a better knowledge of the microcirculatory situation and of the reaction of ultrastructures in shock.

Biopsy↗
PubMed1976

[Ultrastructure of the human lung in shock (author's transl)].

The material investigated was obtained by lung puncture with the aid of the Hausser needle. The puncture technique as well as the preparation of the biopsy material for electronmicroscopic diagnostics are described. The most outstanding criterion in all biopsies examined is the large number of polymorphonuclear, mainly neutrophile granulocytes in the capillary and precapillary arterioles. In contrast, hardly any platelets were found in pulmonary vessels. Also, our investigation of the material revealed no intravascular fibrin deposits while vessels are partly and sometimes completely occluded by fat droplets of different size. The vascular walls are markedly swollen. Fluid escape from smaller vessels results in an edematous swelling of varying degree in the perivascular space combined with fibrin uptake and partly or totally destroyed cell structures. The type I epithelial cells of the lung tissue are swollen and show poor cellular structures. There is in increase of the type II epithelial cells in the shock lung with their lamellary corpuscles partly transferred into the alveolar lumen. The pathomechanisms leading to these changes are discussed. We would like to point out that fibrin was never found intravascularly but was always seen in regions. These findings could indicate increased fibrinolytic activity in shock. Platelet aggregations in smaller vessels are of secondary significance in the material we examined while fat globules, however, play an important part due to their large surface extension. Our electronmicroscopic investigations prove that the lung biopsy method is of great importance for further information on the pathologenesis of early damages in the shock lung not easily discovered by light microscopy.

Biopsy, Needle↗