FEATURE ANAESTHESIOLOGY
«There are a wide variety of procures where FES has been reported, but the most common is total hip replacement»
in the patients at risk for FES is visible aft during urine collection. Clearly, fat has entered the circulation, but there is not direct predictive value for FES. There is a higher probability of fat embolism with primary or metastatic malignancy of long bones since the venous sinuses are enlarged and may have more access to the circulation due to the effect of the tumor. There have been cases reported of FES associated with treatment of pathologic fracture caused by multiple myeloma or pathological fracture of long bones from metastatic malignancy. Another independent predictive variable of FES is age, with more in teens and young adults.
wide variety of procures where FES has been reported, but the most common is total hip replacement. The causative event is either reaming of the femoral canal or pressurized insertion of methyl methacrylate. What all of these potential causative events have in common is tissue trauma, exposure of cancelleous medullary bone, and disruption of blood vessels. While the fulminant FES is relatively uncommon, in the most likely inciting events (trauma, endomedullary reaming), clinically evident fat embolism may be more common that realized. With acute hip fracture, some of the confusion, hypoxemia and increased A-a gradient may be related to fat embolic events. Sudden confusion or brief hemodynamic deterioration during the reaming of the femur for total hip replacement may be sub-acute FES. If evidence of FES is actively sought during high risk procedures with trans esophageal echocardiography, fat can be see passing through the right side of the heart in as many as 50% of patients, although only a fraction are clinically apparent. Another universal observation
PATHOPHYSIOLOGY OF THE FAT EMBOLISM SYNDROME The most likely cause for the fat embolism syndrome is mechanical, with injury to adipose tissue and blood vessels and hydrostatic events that force fat into the circulation. The fulminant FES has cutaneous, central nervous system, pulmonary and hemodynamic consequences that are obvious and less
clinically evident effects on other organs based on the embolic events. Each of these consequences can be explained by the impact of the deposition of fat particles in these tissues.
The cutaneous manifestations are
a result of accumulation of fat in the subcutaneous tissue, causing activity of anti-cellular enzymes. This causes capillary damage, leakage, and edema. Gross leakage of red cells across capillary membranes causes petechiae over the chest, neck, trunk and back. Accumulation of fat and fat metabolism in the eye leads to capillary leakage, causing retinal exudates, seen by fundiscopic exam as ‘cotton-wool’ spots. If there is renal biopsy or at autopsy, there can be evidence of renal accumulation of fat, although the incidence of renal injury with even severe FES is uncommon. When renal failure does occur, tubular necrosis from clogging is the mechanism. The central nervous system signs of fat embolism are caused by the passage of venous fat particles through the lung and into the systemic side, where accumulation produces CNS symptoms. A patent foramen ovale or intra-pulmonary arterio- venous shunts bypasses the pulmonary filtration system allowing macroscopic fat particles direct access to the systemic side. Subsequent enzyme activation, particularly lipases, causes cell damage with release various active substances, including prostaglandins and amines, with direct neurotoxicity. If a CNS injury is the cause of mortality during a fat
Arab Health Show Issue
2012 157
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80 |
Page 81 |
Page 82 |
Page 83 |
Page 84 |
Page 85 |
Page 86 |
Page 87 |
Page 88 |
Page 89 |
Page 90 |
Page 91 |
Page 92 |
Page 93 |
Page 94 |
Page 95 |
Page 96 |
Page 97 |
Page 98 |
Page 99 |
Page 100 |
Page 101 |
Page 102 |
Page 103 |
Page 104 |
Page 105 |
Page 106 |
Page 107 |
Page 108 |
Page 109 |
Page 110 |
Page 111 |
Page 112 |
Page 113 |
Page 114 |
Page 115 |
Page 116 |
Page 117 |
Page 118 |
Page 119 |
Page 120 |
Page 121 |
Page 122 |
Page 123 |
Page 124 |
Page 125 |
Page 126 |
Page 127 |
Page 128 |
Page 129 |
Page 130 |
Page 131 |
Page 132 |
Page 133 |
Page 134 |
Page 135 |
Page 136 |
Page 137 |
Page 138 |
Page 139 |
Page 140 |
Page 141 |
Page 142 |
Page 143 |
Page 144 |
Page 145 |
Page 146 |
Page 147 |
Page 148 |
Page 149 |
Page 150 |
Page 151 |
Page 152 |
Page 153 |
Page 154 |
Page 155 |
Page 156 |
Page 157 |
Page 158 |
Page 159 |
Page 160 |
Page 161 |
Page 162 |
Page 163 |
Page 164 |
Page 165 |
Page 166 |
Page 167 |
Page 168 |
Page 169 |
Page 170 |
Page 171 |
Page 172 |
Page 173 |
Page 174 |
Page 175 |
Page 176 |
Page 177 |
Page 178 |
Page 179 |
Page 180 |
Page 181 |
Page 182 |
Page 183 |
Page 184 |
Page 185 |
Page 186 |
Page 187 |
Page 188 |
Page 189 |
Page 190 |
Page 191 |
Page 192 |
Page 193 |
Page 194 |
Page 195 |
Page 196