Elevation of prostate-specific markers after cardiopulmonary resuscitation.

BACKGROUND-Prostate-specific antigen (PSA), acid phosphatase (AP), and prostatic acid phosphatase (PAP) are serum markers for adenocarcinoma of the prostate gland. Previous studies indicated that prostatic ischemia may also produce elevations of PSA. Cardiopulmonary resuscitation (CPR) is frequently associated with profound tissue hypoperfusion. The present study investigated whether PSA, AP, and PAP are influenced by prolonged CPR. METHODS AND RESULTS-PSA, AP, and PAP were assessed immediately, 12 hours, 24 hours, 2 days, 3 days, 5 days, and 7 days after prolonged CPR (>5 minutes) in 14 male and 5 female patients. No changes were noted in women. In men, serum levels increased significantly after CPR and gradually decreased to near baseline values after 7 days. PSA, AP, and PAP values above the normal range were observed in 63%, 71%, and 64% of all patients, respectively. Compared with survivors, nonsurvivors exhibited higher peak serum levels of PSA (98.6+/-14.3 versus 1.1+/-2.2 mcg/L; P<0.03), AP (57.0+/-71 versus 8.6+/-8.8 U/L; P<0.05), and PAP (47.0+/-62 versus 5.7+/-8.0 U/L; P=NS). Patients with poor neurological outcome exhibited higher peak serum levels of PSA (86.4+/-135.5 versus 12.0+/-23.8 mcg/L; P<0.05), AP (50.9+/-68.1 versus 8.7+/-9.6 U/L; P=NS), and PAP (41.6+/-59.5 versus 5.8+/-8.8 U/L; P=NS) than patients with good neurological outcome. CONCLUSIONS-Prolonged CPR is frequently associated with increases of PSA, AP, and PAP serum levels. Therefore, PSA cannot be used for diagnosis of adenocarcinoma of the prostate during the first weeks after CPR. Further evaluation of these parameters as additional prognostic markers after CPR is warranted.

Prognostic impact of big endothelin-1 plasma concentrations compared with invasive hemodynamic evaluation in severe heart failure.

OBJECTIVES: This study sought to test the hypothesis that big endothelin-1 plasma levels in advanced heart failure are related to survival. BACKGROUND: In heart failure, production of the potent vasoconstrictor endothelin-1 is increased. Because elevation of immunoreactive endothelin-1 in severe heart failure is primarily related to the precursor "big" endothelin-1, increased big endothelin-1 levels may be associated with a poor prognosis. METHODS: Plasma big endothelin-1 concentrations, in addition to 16 clinical, hemodynamic and neurohumoral variables, were obtained from 113 patients (mean age -=/[SEM] 53 +/- 1 years) with left ventricular ejection fraction <20% and were related to 1-year mortality by a stepwise Cox regression multivariate analysis. RESULTS: Plasma big endothelin-1 concentrations were significantly higher in patients with moderate and severe heart failure than in those with mild heart failure (4.5 +/- 0.4 and 6.0 +/- 0.1 vs. 2.7 +/- 0.1 fmol/ml, p = 0.0001, respectively) and lower in 58 one-year survivors than in 29 nonsurvivors (2.6 +/- 0.1 vs. 5.9 +/- .04 fmol/ml, p = 0.0001) and 26 heart transplant recipients. By univariate analysis, big endothelin-1 plasma concentrations (p < 0.0001), functional class, daily furosemide dose, left ventricular ejection fraction, most hemodynamic variables and plasma atrial natriuretic peptide, sodium renin activity and aldosterone levels were all related to mortality, but only functional class provided additional prognostic information when big endothelin-1 plasma levels were entered into the multivariate model. CONCLUSIONS: In advanced heart failure, plasma big endothelin-1 is strongly related to survival and appears to predict 1-year mortality better than hemodynamic variables and levels of atrial natriuretic peptide, an established neurohumoral prognostic marker in chronic heart failure.

Effects of physical training on heart rate variability in diabetic patients with various degrees of cardiovascular autonomic neuropathy.

OBJECTIVE: To investigate the effects of regularly performed endurance training on heart rate variability in diabetic patients with different degrees of cardiovascular autonomic neuropathy (CAN). METHODS: Bicycle ergometer training (12 weeks, 2 x 30 min/week, with 65% of maximal performance) was performed by 22 insulin-requiring diabetic patients (age 49.5 +/- 8.7 years; diabetes duration 18.6 +/- 10.6 years; BMI 25.1 +/- 3.4 kg/m2): i.e., by 8 subjects with no CAN, 8 with early CAN and by 6 patients with definite/severe CAN. A standard battery of cardiovascular reflex tests was used for grading of CAN, a short-term spectral analysis of heart rate variability for follow-up monitoring of training-induced effects. RESULTS: While the training-free interval induced no changes in spectral indices, the 12-week training period increased the cumulative spectral power of the total frequency band (P = 0.04) but to a different extent (P = 0.039) in different degrees of neuropathy. In patients with no CAN the spectral power in the high-frequency (HF) band (0.15-0.50 Hz) increased from 6.2 +/- 0.3 to 6.6 +/- 0.4 In [ms2]; P = 0.016, and in the low-frequency (LF) band (0.06-0.13 Hz) from 7.1 +/- 0.1 to 7.6 +/- 0.3 in [ms2]; P = 0.08 which resulted in an increase of total spectral power (0.06-0.50 Hz) from 7.5 +/- 0.1 to 8.0 +/- 0.3 in [ms2] (P = 0.05). Patients with the early form of CAN showed an increase of spectral power in HF (5.1 +/- 0.2 to 5.8 +/- 0.1 in [ms2], P = 0.05) and LF bands (5.6 +/- 0.1 to 6.3 +/- 0.1 in [ms2], P = 0.008), resulting in an increase of total power from 6.1 +/- 0.1 to 6.6 +/- 0.1 in [ms2] (P = 0.04), whereas those with definite/severe CAN showed no changes after the training period. Training improved fitness in the whole patient cohort. The increased autonomic tone as assessed by spectral indices disappeared after a training withdrawal period of 6 weeks. CONCLUSIONS: In diabetic patients with no or early CAN, regularly performed endurance training increased heart rate variability due to improved sympathetic and parasympathetic supply, whereas in subjects with definite/severe CAN no effect on heart rate variability could be demonstrated after this kind of training.

Cardiac abnormalities in patients with primary hyperparathyroidism: implications for follow-up.

Patients with primary hyperparathyroidism (PHPT) show a high incidence of left ventricular hypertrophy, cardiac calcific deposits in the myocardium, and/or aortic and mitral valve calcification and thus may carry an increased risk of death from circulatory diseases. This prospective study was designed to assess an effect of parathyroidectomy on cardiac abnormalities of patients with PHPT. Echocardiography was used to evaluate the mechanical performance of the heart muscle, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications within 12 and 41 months after parathyroidectomy. In a blinded fashion, aortic and mitral value calcifications were determined in 46% and 39% of patients with PHPT. Calcific deposits in the myocardium were found in 74% of patients. Follow-up studies after parathyroidectomy disclosed no evidence of progression of these calcifications. Before operation left ventricular hypertrophy was detected in 82%. After parathyroidectomy and 41 months of normocalcemia and normal PTH concentrations, a regression of hypertrophy of the interventricular septum and the posterior wall by -6% and -19% (P < 0.05) was observed. Subgroup analysis disclosed the most impressive long-term reduction of left ventricular hypertrophy in patients without a history of hypertension (-11% and -21%; P < 0.05 and P < 0.005); no changes were determined in 9 patients who developed secondary hyperparathyroidism after operation. The present data show a high incidence of left ventricular hypertrophy and aortic and/or mitral valve calcifications in patients with PHPT. Follow-up at 1 year and at 41 months after successful parathyroidectomy disclose regression of hypertrophy. Our results give evidence that parathyroid hormone per se plays an important role in the maintainance of myocardial hypertrophy. Post-surgical restoration of normocalcemia and normalization of parathyroid hormone valvular sclerosis persists without evidence of progression. We further conclude that patients with PHPT and parathyroidectomy are at low risk for the development of severe aortic and mitral valve stenosis within this period of time.

Fibrinolytic response to venous occlusion compared to physical stress test in young patients with coronary artery disease.

INTRODUCTION: Venous occlusion (VO) and exercise stress (ES) are stimulators of the fibrinolytic system. Aim of this study was to answer which of both stimulation tests is more useful in patients with symptom-limited coronary artery disease (CAD) to evaluate possible defects in the fibrinolytic system. METHODS AND RESULTS: We investigated 20 patients (M/F = 15/5; mean age = 36.7 years) with angiographically proven CAD for their plasma levels of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-type-1 (PAI-1) at basal conditions as well as after VO and at maximal ES (standardised bicycle stress test) and compared the data to those obtained from 12 sex- and age-matched healthy controls (M/F = 9/3; mean age = 40.4 years). At basal conditions mean t-PA activity and t-PA antigen plasma levels were within the normal range and comparable between the two study groups. After both VO and maximal ES, mean t-PA activity and t-PA antigen levels increased significantly more in the control group as compared to the CAD group. Mean PAI-1 activity plasma levels were significantly higher in the CAD group at basal conditions before VO (patients 7.0 +/- 3.1; controls 3.9 +/- 3.9; IU/ml; p = 0.025) as well as before ES (patients 8.1 +/- 3.5; controls 4.3 +/- 3.8; IU/ml; p = 0.009). PAI-1 activity plasma levels showed a significant decrease for patients and controls only after VO, while PAI-1 activity was not significantly decreased in both study groups at maximal ES. DISCUSSION: The significantly higher increase in mean plasma levels of t-PA activity and t-PA antigen after VO compared to ES in both groups might be explained by the fact that CAD induced symptoms in the patients during ES thus permitting only 80% of their age, sex, and body mass index related optimal work load. CONCLUSION: VO and ES are applicable triggers of the endogenous fibrinolytic system in healthy subjects and patients who are not limited in their physical exercise. Standardised VO appears to be superior to ES as stimulation test of the endogenous fibrinolytic system in patients with symptomatic CAD.

Decrease in pacemaker incidence after orthotopic heart transplantation.

A decrease in sinus node dysfunction and pacemaker requirement after orthotopic heart transplantation was observed over a 6.5-year period, probably indicating the effect of a learning curve. Indirect evidence suggests a traumatic genesis of sinus node dysfunction after cardiac transplantation.

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.

Circulating tumor necrosis factor-alpha levels in chronic heart failure: relation to its soluble receptor II, interleukin-6, and neurohumoral variables.

The cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are increased in the circulation of patients with chronic heart failure. However, their correlation with left ventricular dysfunction has not yet been thoroughly evaluated, and their interrelation with other neurohumoral systems, such as the adrenergic system and endothelin, is unclear. Therefore TNF-alpha, its soluble receptor II, IL-6, big endothelin, and noradrenaline levels were simultaneously measured in venous blood from 65 patients with heart failure in New York Heart Association (NYHA) class II to IV during therapy with digitalis, furosemide, and enalapril. TNF-alpha plasma levels were 3.2+/-0.2 SEM pg/ml in 38 patients in NYHA function class II, 4.0+/-0.3 SEM pg/ml in 16 patients in NYHA function class III, and 5.3+/-0.9 SEM pg/ml in 11 patients in NYHA function class IV (p < 0.001 vs NYHA function class II). IL-6 plasma levels were 3.1+/-0.6 SEM pg/ml in 38 patients in NYHA function class II, 5.2+/-0.8 SEM pg/ml in 16 patients in NYHA function class III, and 13.3+/-3.9 SEM pg/ml in 11 patients in NYHA function class IV (p < 0.0001 vs NYHA function class II andp < 0.0001 vs NYHA class III). Thus both cytokines increased with increasing severity of heart failure, but only IL-6 plasma levels were different in patients in the more severe function classes. TNF-alpha correlated closely with TNF soluble receptor II (r = 0.8, p < 0.0001) and modestly with serum creatinine (r = 0.6, p < 0.0001), whereas IL-6 plasma levels were not statistically related to kidney function. Significant modest correlations were also found among TNF-alpha and IL-6 (r = 0.3, p < 0.01), big endothelin (r = 0.3, p < 0.01), and noradrenaline levels (r = 0.4, <0.001). This study supports the hypothesis that in heart failure both cytokines, TNF-alpha, and IL-6, as well as neurohumoral factors, play a role in the clinical progression of the disease. Thereby levels of TNF-alpha but not IL-6 seem to be related to concomitant kidney dysfunction.

Time course of regression of left ventricular hypertrophy after successful parathyroidectomy.

BACKGROUND: We have shown that primary hyperparathyroidism may induce myocardial hypertrophy that is reversible after successful parathyroidectomy. The present study was designed to assess the time course of regression of left ventricular hypertrophy without further effects of drug treatment or disease states. METHODS: We performed echocardiographic studies in 16 patients with primary hyperparathyroidism and normal resting blood pressure, normal systolic left ventricular function, no evidence of valvular disease, and without any current medication before parathyroidectomy, as well as during intermediate and long-term follow-up after successful parathyroidectomy. RESULTS: Eleven patients (69%) had end-diastolic wall thickness of the interventicular septum and/or posterior wall greater than 11 mm on baseline echocardiogram. After surgical removal of the inciting disease and an average of 12.5 and 45.7 months of follow-up with normocalcemia and normal parathyroid hormone levels a prolonged regression of left ventricular hypertrophy was observed (interventricular septum, -0.68 mm at 12.5 months and -1.69 mm at 45.7 months; p = 0.02; posterior wall, -0.46 mm at 12.5 months and -2.24 mm at 45.7 months; p = 0.02). CONCLUSIONS: We conclude that the removal of the cause of myocardial hypertrophy by successful parathyroidectomy leads to a prolonged reversal of hypertrophy. The progressive reduction of left ventricular wall thickness is not completed within 12 months.

Role of nitric oxide in exercise-induced vasodilation in man.

Nitric oxide (NO) is a potent endothelium-derived vasodilator, which is known to play an important role in the regulation of resting vascular tone in animals and humans. However, the degree to which NO is involved in exercise-induced vasodilation in the skeletal muscle remains unclear. We studied the effect of N-monomethyl-L-arginine (L-NMMA) in a randomized, double-blind, placebo controlled cross over study in 16 young, healthy volunteers ( 8 male, 8 female) at rest and during bicycle exercise stress test. L-NMMA was given as a bolus of 3 mg/kg over 5 minutes followed by a continuous i.v. infusion of 50 microg/kg/min over 75 minutes. Subjects underwent a symptom-limited graded bicycle stress test with a 25 Watt increase in workload every 5 minutes. Skin and muscle blood flow were measured by laser Doppler flowmetry. L-NMMA slightly increased mean arterial blood pressure and decreased NO exhalation, but had no effect on pulse rate, oxygen consumption (VO2), skin or muscle blood flow at rest. Moreover, L-NMMA exerted no effect on exercise-induced changes in hemodynamics. Our results suggest that submaximal inhibition of NO-synthase with L-NMMA at doses that induce moderate hemodynamic changes does not affect exercise induced vasodilation.

Effects of atenolol as add-on therapy to fosinopril in heart failure.

Several trials have demonstrated functional benefit with beta-blockers in patients with chronic heart failure. The aim of this observational study was to investigate if additional beneficial effects can be obtained from beta-blockade in a heart failure population that is already receiving high-dose ACE-inhibitor therapy. Atenolol is a long-acting cardioselective beta-blocking agent and is devoid of additional vasodilatory properties. Twenty-five male patients with class II or III heart failure and background therapy of digitalis, furosemide and 20 mg fosinopril per day were treated with 40 mg fosinopril per day and additional 75 mg atenolol per day (beta-blocker group) or with 40 mg fosinopril per day alone (control group). At the end of one year, changes in left ventricular function, exercise parameters and plasma neurohumoral variables reflecting vasoconstriction (noradrenaline, big endothelin) were measured and compared in the two treatment groups. Nineteen patients completed the study. Drop-outs were due to death (4 patients) and non-compliance (2 patients) with no significant difference between the groups. There was a beta-blocker related improvement in left ventricular ejection fraction (p < 0.05 between groups) and an increase in peak oxygen consumption in the control group only (p < 0.05 between groups). Thus, in a heart failure population receiving high-dose ACE inhibitor background therapy beta-blockade with atenolol produced additional benefit by reversing left ventricular dysfunction.

Milrinone therapy in catecholamine-dependent critically ill patients with heart failure.

BACKGROUND: Treatment with the PDE-III inhibitor milrinone improves hemodynamics in patients with heart failure. We examined whether therapy with milrinone is safe and effective in critically ill patients with catecholamine-dependent heart failure and whether treatment with milrinone facilitates weaning from prolonged catecholamine therapy. METHODS: Twenty adult patients with reduced left ventricular function and prolonged (7+/-4 days) catecholamine therapy in whom attempts at catecholamine weaning had failed were examined. Patients were prospectively randomised either to group A (addition of a fixed dose of 0.5 microg x kg(-1) x min(-1) milrinone to catecholamine therapy) or to group B (continued catecholamine therapy without milrinone). Dobutamine and norepinephrine treatment and fluid intake were titrated according to predefined hemodynamic goals. Hemodynamic parameters, fluid requirements and catecholamine dose were monitored. RESULTS: After 24 h of study treatment goup A showed a significant increase in cardiac index (2.2+/-0.4 1 min(-1) x m(-2) to 2.7+/-0.51 min(-1) x m(-2); P<0.005), a decrease in systemic vascular resistance (1,427+/-609 dyn x s x cm(-5) to 951+/-184 dyn x s x cm(-5); P<0.005), required lower doses of dobutamine (5.9+/-4.2 microg x kg(-1) x min(-1) to 2.2+/-3.3 microg x kg(-1) x min(-1); P<0.02), but showed a tendency for higher vasoconstrictor (0.14+/-0.16 microg x kg(-1) x min(-1) to 0.29+/-0.43 microg x kg(-1) x min(-1); P=n.s.) and fluid requirements (+1,404+/-2,257 ml/24 h to +2,508+/-1,873 ml/ 24 h; P=n.s.). No significant changes occurred in group B. Weaning from catecholamine therapy was more often achieved in group A and more milrinone treated patients were discharged alive from the ICU (80% vs. 30%; P<0.05). CONCLUSIONS: Milrinone improves central hemodynamics and may facilitate weaning from prolonged catecholamine support in critically ill patients with heart failure. Its administration in this subset of critically ill patients is safe, but eventually is associated with additional vasoconstrictor and fluid requirements.

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.

[Modified surgical technique for reduction of bone marrow spilling in cement-free hip endoprosthesis]. / Modifizierte Operationstechniken zur Reduzierung der Knochenmarkausschüttung in der zementfreien Hüftendoprothetik.

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.

[Monitoring of bone marrow spilling and cardiopulmonary changes in fat embolism syndrome]. / Monitoring der Knochenmarkausschüttung sowie der kardiopulmonalen Veränderungen beim Fettemboliesyndrom.

After long bone fractures, as well as hip or knee total arthroplasty, the increase in intramedullary pressure induces bone marrow release into the circulation in more than 90% of patients. Three to four percent of the patients reveal fat embolism syndrome with pulmonary and cerebral involvement and a petechial rash. In about 20% of these patients a fulminant and fatal course is possible. Although fat embolism syndrome was described more than a century ago, there is still no sufficient therapeutic strategy. Because of these facts we try to prevent fat embolism syndrome and monitor patients at risk perioperatively. We have evaluated different diagnostic methods and monitoring facilities and recommend pulse oximetry, capnography, ECG, blood pressure controls and, if indicated, blood gas analyses for perioperative monitoring. Patients at risk and patients who are suffering from fat embolism syndrome require more intensive monitoring, such as transesophageal echocardiography and a pulmonary artery catheter to obtain more detailed information about the hemodynamic and oximetric variables. Furthermore, these patients must be admitted to an intensive care unit.

[Modified surgical technique for the reduction of bone marrow spilling in knee endoprosthesis]. / Modifizierte Operationstechniken zur Reduzierung der Knochenmarkausschüttung in der Knieendoprothetik.

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.

[Therapeutic approach to the management of fat embolism syndrome]. / Therapeutische Ansätze zur Behandlung des Fettemboliesyndroms.

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.