Squish head between fingers9/4/2023 ![]() ![]() Rehabilitation should be not only physical but also psychiatric and is a long term process. Recognition of crush syndrome and treatment involves a close link amongst trauma surgeons, physicians, biochemists and radiologists. Paramedical personnel should be taught to suspect this condition and treat aggressively with fluid therapy. Clear history is not always available in combat, and the syndrome may appear insidiously in patients who initially appear well. Casualties are often in shock, and may lose litres of extracellular fluid into the injured extremity. Resuscitation should ideally commence at the site of injury. Noriaki et al have attempted a predictive model for estimating risk of crush syndrome. Apart from the usual modes of combat care principles, some workers advocate use of potassium binders like oral polystyrene sulfonate before transportation to avoid renal damage. Rescue should be a highly coordinated effort, and patient be transported to a higher level of care with dialysis facilities. In scenario of crush injuries, we are dealing with rescue, resuscitation, recognition of the syndrome, treatment and rehabilitation. Doppler studies are done to look for limb ischaemia, and the body weight is recorded. Intracompartmental pressure monitoring is useful as it is generally accepted that levels greater than 30 mm Hg point towards the need for a fasciotomy. Blood gas analysis, haemogram and ECG are also helpful. Urine RE may show presence of myoglobin products. Hypocalcaemia and stress related hyperglycaemia may be seen. Normal range is 25-175 U/l, usually rises 2 to 12 hrs after a crush, peaks in 1 to 3 days and declines after 3 to 5 days.Īmong the other investigations, serum aldolase may be of some help serum myoglobin and myoglobin degradation products are highly sensitive tests serum lactic acid, AST, ALT and LDH show a steady rise serum uric acid -moderate rise may be noticed serum urea and creatinine – steep rise is seen especially after a prolonged crush serum potassium levels show an early rise and is a predictor for dialysis. Serum creatinine kinase (CKMM) levels greater than 1000 IU/l with associated clinical features is generally taken as an indicator of crush syndrome. ![]() However studies show that upto 10% chest trauma is associated with crush injuries. So most of such patients are conscious at rescue and the chest injuries are relatively trivial. It is a ripe setting for ARDS.Ĭrush injuries are not common after head and chest injuries because the prolonged pressure necessary to cause this syndrome often results in death. Ultimately, patients go into shock affecting respiratory gas exchange due to lung edema. The released potassium in the circulation causes alteration in cardiac rhythm. Kidneys also tend to be edematous and show an increase in volume. The muscles are grossly swollen, hard, cold, insensitive and necrotic. The appearance, duration and gravity of oliguria and kidney damage are not related to the severity of muscle damage. It has also been noticed that an element of vasoconstriction of the afferent arterioles induced by myoglobin degradation products adds to this setting of tubular destruction.Įlevated lactic acid levels are well coordinated with muscle ischaemia time, but it is generally accepted that serum creatinine phosphokinase is the most important index of muscle damage. Myoglobin is filtered out of the glomerulus, but once the renal threshold is exceeded, it precipitates in the distal convoluted tubules causing obstruction. In turn, this releases myoglobin degradation products, lactic acid, uric acid and muscle enzymes like creatinine phosphokinase and aldolase, besides ions like calcium, potassium and phosphate into the circulation. Ĭasualties deteriorate only after being rescued out of the debris of collapse or entrapment, because once the tissue tension is released, reperfusion to the ischaemic damaged muscles disrupts sodium-potassium-ATPase mechanism. Nitric oxide system is activated and this further contributes to muscle vasodilatation and aggravation of hypotension. Regional ischemia caused by occlusion of micro and macrocirculation to muscles following crush, releases sodium, calcium and fluids leading to raised muscle volume and tension. Though essential for cell function, they are toxic when released into the circulation in large amounts. Muscles also contain potassium, magnesium, phosphate, acids, enzymes like creatine phosphokinase (CKMM) and lactate dehydrogenase (LDH). Our whole focus has to be centered on tackling this 10%, which has severe and extensive metabolic disturbances.Ĭrush and rupture of muscle cells releases myoglobin, which gets converted to methmyoglobin and finally acid haematin, which is released into the circulation. ![]() Of the 20% that reach hospital, 10% make an uneventful recovery. It is recorded that upto 80% of crush injury patients die due to severe head injuries or asphyxiation. ![]()
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