The Lethal Triad A series on triads (Lethal Triad) In this - TopicsExpress



          

The Lethal Triad A series on triads (Lethal Triad) In this series we review some of classic trauma symptoms that exist in groups of three, collectively called Triads. This instalment reviews the dark horses of the trauma room. The silent killers that creep out from nowhere and cause catastrophic deterioration. The Lethal triad is: • Hypothermia • Coagulopathy • Acidosis Hypothermia is a common feature of the trauma patient who is a young child, elderly, burns or spinal. Whilst many mechanisms exist to cause hypothermia in trauma patients, loss of further heat must be avoided in the trauma room. Hypothermia affects coagulation. In a bleeding patient where there is some reliance on the patients ability to stem haemorrhage, a cold patient has impaired ability. Hypothermia interferes with the coagulation cascade which is a complicated chemical reaction in plasma. Think- colt blood wont clot. Hypothermia also causes alteration in oxygen transport. When cold, haemoglobin binds tightly to oxygen (left shift) and becomes reluctant to release oxygen at the cellular end . They appear well saturated (because they are) but hypoxic at cellular level (shock). The old adage of keep them warm with a blanket so they dont go into shock, Is as true today as it ever was. Coagulopathy as spoken about in a previous blog. Is an altered ability to coagulate. Coagulation is not the same as clotting Blood is a suspension of water, proteins and cells. Traveling through pipes that are dynamic. Your blood vessel walls actually secrete substances that keep your blood liquid. Plasma will coagulate unless it is told not to by blood vessels. So what is coagulation? Coagulation is a property whereby a liquid becomes a solid. In blood, it is a series of chemical reactions that convert a protein called prothrombin into thrombin, then fibrinogen into fibrin. the plasma turns to jelly Fibrin forms strands that trap cells floating past. Clumps of platelets get trapped in the mesh of spiderweb like fibrin strands, which forms a stable clot. Clotting is not coagulation, it is a process whereby platelets are stimulated (by vessel walls) to become activated and clump together. Clotting works in synergy with coagulation to effect haemostasis (stop bleeding). In trauma patients who have bled, haemodilution (automatic shock response) and over use of fluid resuscitation agents, contribute to poor coagulation by diluting out the coagulation factors in plasma. Dont over water the patient. 100-200 increments of warm crystalloids- n/saline or Hartmanns to keep SBP between 80-90. In a bleeding trauma patient, the inflammatory cascade is activated, causing a pro-inflammatory chemical to be released by ischaemic tissues. This chemical is thrombomodulin and as its name implies, it modulates (inhibits) an important coagulation protein (thrombin) . Thrombin converts Fibrinogen into fibrin to stabilise clotting blood. If inhibited by Thrombomodulin , bleeding cant stop. Finally Acidosis. Lowering of the pH occurs in shocked patients through three primary mechanisms • Under ventilation leads to CO2 rise, • fluid overloading with Saline causes a hyperchloraemic acidosis • hypo oxygenation which causes lactic acidosis because cellular pyruvate cant enter the kerbs cycle without oxygen. Ventilate the trauma patient with O2, keep them warm to promote cellular oxygenation and much of the problems with acidosis can be averted. Now... This is Free Open Access Medical education #FOAMed If you got any value from this post, please share it on your page.
Posted on: Mon, 20 Jan 2014 06:27:37 +0000

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