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J Koller-Strametz

Publications and source records attributed to J Koller-Strametz.

26 records · Page 2Linked to original sources
PubMed1995

[Modified surgical technique for reduction of bone marrow spilling in cement-free hip endoprosthesis].

Since 1970 the fat embolism syndrome (FES) has been recognised as a severe complication of cemented total hip arthroplasty (THA). Initially and still today the toxicity of bone cement has been though to be responsible for the cardiorespiratory problems. Meanwhile several reports have confirmed the causal relationship between intramedullary pressure (IMP), bone-marrow release into the circulation and subsequent cardiorespiratory deterioration during cemented THA. In recent publications it has been reported that bone-marrow release due to increased IMP also occurs during cementless THA. The clinical implication of these observations is controversial. For this reason in the first part of this paper two autopsy-proven FES deaths and five further clinically manifest FES cases are presented. In the second part of the study, IMP courses during four different surgical techniques (2 conventional, 2 modified) are compared. The aim of the modified surgical technique developed in our department was to minimize IMP peaks and bone-marrow release during cementless THA. Both modified techniques showed significantly lower IMPs during opening of the medullary canal, preparation with rasps, and implantation of the prosthesis than the conventional techniques. The observed FES cases for the first time strongly confirm the clinical relevance of the FES, also during cementless THA. On the basis of the data presented we recommend the modified surgical technique to reduce bone-marrow release during cementless THA.

Aged↗
PubMed1995

[Modified surgical technique for the reduction of bone marrow spilling in knee endoprosthesis].

In the literature 20 cases of fat embolism syndrome (FES) after total knee replacement (TKR) are reported; 16 cases had cemented hinged TKR and 4 resurfacing TKR. Initially, it was believed that the bone cement was responsible for the FES. Since then, however, Fahmy et al. have published extraordinary data, demonstrating the causal relationship between increased intramedullary pressure (IMP) during the insertion of the intramedullary rod (IR) and cardiorespiratory deterioration. The industry responded by developing a fluted IR, disregarding the overdrilling in the distal femur required by Fahmy. In the first part of this paper clinically manifest FES cases after resurfacing TKR are reported. In the second part of the study the conventional surgical technique is compared with a modified technique, which focuses on a reduction of bone-marrow release into the circulation. In the conventional and the modified group, IRs with and without flutes were compared. It was shown that only the opening of the intramedullary canal and insertion of the IR generated relevant IMP peaks during implantation of resurfacing TKR. When compared with the conventional surgical technique, the modified technique revealed significantly lower IMPs, and in neither group was a difference demonstrated between the IR with or without flutes. In 4 patients (2 conventional, 2 modified) transesophageal echocardiography (TEE) was performed for detection of bone-marrow release into the circulation. In the two patients operated on conventionally, TEE showed a markedly higher bone-marrow release than in the patients with modified operations. In conclusion, we recommend the presented modified surgical technique in order to reduce bone-marrow release into the circulation.

Aged↗
PubMed1995

[Therapeutic approach to the management of fat embolism syndrome].

So far, no clinical or experimental study has demonstrated that any drug has a beneficial effect (heparin, cortisone, dextran, etc.) on the course of fat embolism syndrome (FES). Thus, prevention, early diagnosis, and adequate symptomatic treatment are of paramount importance. Besides surgical measures, such as reduction of intraosseous pressure and bone-marrow release during hip or knee replacement, proper treatment of shock in traumatized patients, recognition of risk factors and maintainance of intraoperative cardiorespiratory stability are cornerstones in the prevention of fat embolism syndrome. It is well documented that bone-marrow release into the circulation and pulmonary embolism occurs during any hip or knee arthroplasty. As a result of improvements in anesthesia management, the clinical appearance of FES has moved into the postoperative period. This calls for mandatory cardiorespiratory monitoring up to 24 h postoperatively. When facing a clinically manifest fat embolism syndrome, monitoring and symptomatic treatment must be adapted to the patient's needs in order to ensure adequate oxygenation and acceptable circulatory conditions to protect organ function.

Catheterization, Swan-Ganz↗
PubMed1995

[Pathophysiology of fat embolisms in orthopedics and traumatology].

It is well known that fat embolisms can occur after long bone fractures, and this has been feared for more than 100 years. Since 1970 fat embolisms have also been recognized in endoprosthetic surgery. The clinical manifestation was described as the fat embolism syndrome (FES) by Gurd in 1974. Based on reports in the literature and our own data, a concise pathophysiological model of the FES is presented in this paper. The increase in intramedullary pressure (IMP) in the long bones is the most decisive pathogenic factor for the development of an FES. Any long bone fracture, stabilization of fractures, or implantation of knee or hip endoprostheses can generate IMP peaks leading to bone marrow release into the circulation. Bone marrow itself is a tremendous stimulus for activation of the clotting system. As a result, hypercoagulation and venous stasis in the draining veins generate mixed macroemboli from the initial bone-marrow microemboli. Bone-marrow embolization of the lung in phase I leads to mechanical obstruction of pulmonary arteries. In phase II, release of local mediators, triggered by a systemic inflammatory response (SIR) of the lungs, causes damage to the pulmonary membranes. Disturbed gas exchange and respiratory insufficiency with possible cardiac and cerebral decompensation are the result. In most cases an FES may not be detected clinically, and any mild cardiorespiratory changes are treated easily with oxygen insufflation and usually disappear within 48 h. Of paramount importance for clinical manifestation of an FES are the quantity and duration of bone-marrow release and co-factors (cardiorespiratory compliance and perioperative stability of the patient). Patients with preexisting cardiorespiratory disease in combination with massive intraoperative bone-marrow release may even face a deadly FES event. Increased IMP causes local obstruction of cortical vessels with bone marrow. In combination with the damaged endosteal blood supply, avascular necrosis of the cortical bone occurs. During endoprosthetic procedures, mechanical-and mediator-triggered damage of the intima of big veins, in combination with venous stasis and hypercoagulation may be responsible for the high incidence of proximal thrombosis of femoral veins. As a delayed result of the disseminated intravascular coagulopathy, petechial bleeding in the trunk and subconjunctiva can be seen. A better understanding and recognition of the FES's pathophysiology may help to use prophylactic, diagnostic and therapeutical measures more effectively.

Blood Coagulation↗
PubMedDate not supplied

Primary hyperparathyroidism and the heart: cardiac abnormalities correlated to clinical and biochemical data.

Comparing patients with primary hyperparathyroidism (PHP) to a normocalcemic control population, those with PHP have a higher incidence of cardiovascular disease and cardiac abnormalities. This study aimed at correlating cardiac findings (valvular and myocardial calcification, myocardial hypertrophy) with clinical data (age, sex, clinical manifestation, nephrolithiasis, nephrocalcinosis, hypertension, skeletal abnormalities, hypercalcemic syndrome) and biochemical data (serum calcium, serum phosphate, serum iPTH level, serum creatinine). A group of 132 consecutive patients with surgically verified PHP (94 women, 38 men; ages 15-86, mean age 57 +/- 16 years) were included in this study. Blood chemistry, clinical presentation, radiography, and echocardiography were carried out in all patients for univariate and multivariate analyses of all parameters. There was no statistical correlation between clinical symptoms, biochemical data, and cardiac calcific alterations. Typical skeletal manifestations (osteolysis/subperiostal resorption) and valvular calcifications were significantly correlated to left ventricular hypertrophy (p = 0.005). Cardiac abnormalities such as calcific myocardial deposits or mitral and aortic valvular calcifications do not correlate with laboratory findings and clinical presentation at the time of diagnosis. There was no biochemical or clinical variable that could predict the frequency or severity of valvular sclerosis or calcific deposits in the myocardium. However, PHP-related skeletal abnormalities and valvular calcification were predicting factors for left ventricular hypertrophy, a reversible cardiac manifestation of PHP. Myocardial hypertrophy is more often found with classic symptomatic PHP with osseous abnormalities.

Adolescent↗
PubMedDate not supplied

Thromboembolism associated with junctional escape rhythm and atrial standstill after orthotopic heart transplantation.

We report on thromboembolism in a heart transplant recipient with mechanical atrial standstill and spontaneous echocardiographic contrast during intermittent periods of sinus arrest and junctional escape rhythm. The temporal relationship between the conversion of atrial flutter to junctional bradycardia and two episodes of thromboembolism strongly suggest a role of the lack of atrial contraction during junctional rhythm for the development of spontaneous echocardiographic contrast and thromboembolism.

Arrhythmias, Cardiac↗