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L.f. Sherdukalova - One of the best experts on this subject based on the ideXlab platform.
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Classification and treatment in protracted Crush Syndrome
Khirurgiia, 1999Co-Authors: L.f. Sherdukalova, R A Ovanesian, V O GalikianAbstract:Based on the analysis of clinical and laboratory findings in 223 patients with protracted Crush Syndrome and results of their combined treatment pathogenetic classification of protracted Crush-Syndrome is proposed. The applied modern methods of detoxication combined with surgical correction of organic damages contributed to substantial reduction of lethality (14.3%) in comparison with existing literature data.
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Pathogenetic aspects of Crush Syndrome
Pathophysiology, 1998Co-Authors: R.a. Hovanessian, L.f. SherdukalovaAbstract:This research IS based on the exammatlon of the state of microcirculation of bulbar conjunctlva, blood cell aggregation, and transcapillary metabohsm at 273 patients with Crush Syndrome Exammatlons had been made during acute period and on different stages of mtenslve therapy The results of self-research made to propose the followmg scheme of Crush Syndrome pathogenesrs The first pathologic phenomena of mrcrocnculatton, developmg In response to pam shock, are spasm of arterioles and precapillaries, venulectasia and decaprllaropathy of tissues This causes the deceleration of cnculatron rate and appearance of mtravascular agregatton of erythrocytes Quick rise of capillary permeabthty leads to massrve exudation of plasma and erythrocytes into interstitial space After decompresston rhabdomyolysrs products mtenstfy and generalize existing mtcrocirculation disturbance Increasmg mrcrocirculatton drsturbances lead to acute hypoxta and tschemta of different ttssues and organs, and cause polyorgan msufftcrency whrle Crush Syndrome In the end acute cardiovascular insuffrcrency IS bemg developed. leading to death
Akira Asada - One of the best experts on this subject based on the ideXlab platform.
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Crush Syndrome sustained in the 1995 kobe japan earthquake treatment and outcome
Annals of Emergency Medicine, 1997Co-Authors: Yutaka Oda, M Shindoh, Hidekazu Yukioka, S Nishi, Mitsugu Fujimori, Akira AsadaAbstract:Abstract Study objective: To assess the treatment and outcome of patients with Crush Syndrome sustained in an earthquake disaster. Methods: We conducted a retrospective analysis of eight patients with Crush Syndrome and subsequent acute kidney failure who were treated in the ICU of a university hospital. All eight patients had been extricated from buildings that collapsed in the 1995 Kobe, Japan, earthquake. Crush injury involved the upper extremities in one patient and the lower extremities in seven. Each patient received intravenous fluid infusion and diuretic drugs and underwent hemodialysis. Emergency fasciotomy was performed in some patients, 17 to 100 hours after extrication. Results: All patients were conscious and lucid on admission, and blood pressure and heart rate were normal. All the patients demonstrated kidney failure with increased concentrations of serum creatinine (1.9 to 9.6 mg/dL [169 to 852 μmol/L]). Six patients were oliguric. Hyperkalemia (5.6 to 8.8 mEq/L) was present in six patients. We found close correlations between the serum potassium and creatine kinase concentrations, between the serum myoglobin and potassium concentrations, and between the serum myoglobin and creatine kinase concentrations. All the patients were weaned from hemodialysis. The serum creatinine concentration decreased to a normal level within 20 to 52 days of admission in all patients. No patients underwent amputation. Muscle weakness and sensory deficits persisted in all patients 6 months after the earthquake. Conclusion: Our findings support current therapeutic strategies for Crush Syndrome, despite the long delay to initiation of intensive therapy. All the patients recovered kidney function and were weaned from hemodialysis; none required amputation. [Oda Y, Shindoh M, Yukioka H, Nishi S, Fujimori M, Asada A: Crush Syndrome sustained in the 1995 Kobe, Japan, earthquake: Treatment and outcome. Ann Emerg Med October 1997;30:507-512.]
R.a. Hovanessian - One of the best experts on this subject based on the ideXlab platform.
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Pathogenetic aspects of Crush Syndrome
Pathophysiology, 1998Co-Authors: R.a. Hovanessian, L.f. SherdukalovaAbstract:This research IS based on the exammatlon of the state of microcirculation of bulbar conjunctlva, blood cell aggregation, and transcapillary metabohsm at 273 patients with Crush Syndrome Exammatlons had been made during acute period and on different stages of mtenslve therapy The results of self-research made to propose the followmg scheme of Crush Syndrome pathogenesrs The first pathologic phenomena of mrcrocnculatton, developmg In response to pam shock, are spasm of arterioles and precapillaries, venulectasia and decaprllaropathy of tissues This causes the deceleration of cnculatron rate and appearance of mtravascular agregatton of erythrocytes Quick rise of capillary permeabthty leads to massrve exudation of plasma and erythrocytes into interstitial space After decompresston rhabdomyolysrs products mtenstfy and generalize existing mtcrocirculation disturbance Increasmg mrcrocirculatton drsturbances lead to acute hypoxta and tschemta of different ttssues and organs, and cause polyorgan msufftcrency whrle Crush Syndrome In the end acute cardiovascular insuffrcrency IS bemg developed. leading to death
Nina Sulen - One of the best experts on this subject based on the ideXlab platform.
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Crush Syndrome in severe trauma
Lijecnicki vjesnik, 2007Co-Authors: Marija Rakarić Poznanović, Nina SulenAbstract:Crush injury or traumatic rhabdomyolysis is caused by Crushing of large muscule mass, usually of the femoral and gluteal compartment. Crush Syndrome is general manifestation of Crush injury with renal failure (ARF). ARF is caused by deposition of myoglobin in distal tubules. The concentration of serum creatin phosphokinase is an indicator of the extent of injured muscule. The serum concentration of myoglobin is an indicator of the extent of injured muscule and the main cause of development of Crush Syndrome. In a prospective study the concentration of myoglobin and CPK was measured in 81 patients with injuries of lower extremities and pelvis as a part of severe trauma. The increase of CPK concentration above 1000 U/L was measured in all patients. The increase of CPK concentration above 2000 U/L was measured in 78 (96.3%) patients. The increase of myoglobin concentration of >700 mcg/L was measured in 19 (23.5%) patients. In the group of 19 patients with CPK concentration of >2000 U/L and myoglobin concentration of >700 mcg/L Crush Syndrome developed in 6 (7.4%) patients with oliguria (urin output
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Crush Syndrome in severe trauma
Lijec̆nic̆ki vjesnik, 2007Co-Authors: Marija Rakaric Poznanovic, Nina SulenAbstract:: Crush injury or traumatic rhabdomyolysis is caused by Crushing of large muscule mass, usually of the femoral and gluteal compartment. Crush Syndrome is general manifestation of Crush injury with renal failure (ARF). ARF is caused by deposition of myoglobin in distal tubules. The concentration of serum creatin phosphokinase is an indicator of the extent of injured muscule. The serum concentration of myoglobin is an indicator of the extent of injured muscule and the main cause of development of Crush Syndrome. In a prospective study the concentration of myoglobin and CPK was measured in 81 patients with injuries of lower extremities and pelvis as a part of severe trauma. The increase of CPK concentration above 1000 U/L was measured in all patients. The increase of CPK concentration above 2000 U/L was measured in 78 (96.3%) patients. The increase of myoglobin concentration of >700 mcg/L was measured in 19 (23.5%) patients. In the group of 19 patients with CPK concentration of >2000 U/L and myoglobin concentration of >700 mcg/L Crush Syndrome developed in 6 (7.4%) patients with oliguria (urin output <50 ml/h) and the increase of serum potassium, phosphate and creatinine concentrations. The decrease of CPK and myoglobin concentrations was achieved in 5 patients during 10-12 days and 1 patient with associated craniocrebral injury died.
Sacit Turanli - One of the best experts on this subject based on the ideXlab platform.
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response to delayed fluid therapy in Crush Syndrome
Nephron, 2002Co-Authors: Cuneyt Ensari, Omac Tufekcioglu, Deniz Ayli, Tulin Gumus, Seval Izdes, Sacit TuranliAbstract:Background: Although early treatment is valuable in the prognosis of Crush Syndrome, the diagnosis and treatment of many victims are inevitably delayed in major disasters. Patients and Methods: Among the 38 victims of the Marmara earthquake with Crush injury, 27 were diagnosed as Crush Syndrome on the basis of findings of acute renal failure. Intensive intravenous fluid treatment was started in all patients on admission. Of these 27 patients, 10 required dialysis treatment while 17 did not. The laboratory data on admission were evaluated and compared between the two groups. Results: The mean admission time of 27 patients was 46.5 ± (SE) 3.08 h. There was no significant difference between the dialysis and the nondialysis groups with regard to patient’s age, trapped time or admission time. A significantly higher number of patients had Crush injury in more than one extremity in the dialysis group. The dialysis group had significantly lower systolic blood pressure, central venous pressure but a higher heart rate together with higher levels of serum urea nitrogen, creatinine, creatinine kinase, C-reactive protein, fibrinogen on admission compared to the nondialysis group. Conclusion: Our results suggest that even delayed application of aggressive specific fluid treatment under close monitoring may prevent the development of established acute renal failure.