Complications of Mechanical Injuries PDF

COMPLICATIONS OF MECHANICAL INJURIES ACUTE RESPIRATORY DISTRESS SYNDROME  It is known as diffuse alveolar damage, shock lung, acute lung injury.  It is characterized by the abrupt onset of significant hypoxemia and diffuse pulmonary infiltrates with increase in pulmonary vascular permeabil...

COMPLICATIONS OF MECHANICAL INJURIES ACUTE RESPIRATORY DISTRESS SYNDROME  It is known as diffuse alveolar damage, shock lung, acute lung injury.  It is characterized by the abrupt onset of significant hypoxemia and diffuse pulmonary infiltrates with increase in pulmonary vascular permeability, and epithelial and endothelial cell death.  Macroscopically: the lungs are heavy, firm, red and having dry-oedema appearance.  Microscopically: shedding of type I pneumocytes, proliferation of type II pneumocytes , interstitial and intra-alveolar edema, alveolar walls lined with waxy hyaline membranes, granulation tissue response in the alveolar walls and in the alveolar spaces, and finally pulmonary fibrosis.  Causes: - Sepsis - Diffuse pulmonary infection - Mechanical trauma, including head injuries - Gastric aspiration - Pulmonary contusions - Fractures with fat embolism - other: radiation, burns, Near-drowning heroin overdose, pancreatitis, organic solvents  SUPRARENAL HEMORRHAGE  Massive adrenal hemorrhage is not common complication (0.3%) and Causes:- not related to direct injury to - Trauma of all types (traffic accident) adrenal gland. - Perinatal, newborn, stillborn infant  It can be bilateral or unilateral. (breech births, fetal anoxia)  The sudden collapse and death - Meningococcal septicemi usually occur few days after trauma (Waterhouse-Friderichsen syndrome) (2-21 days) - Post-operative septicemia  Autopsy: the adrenal glands appear swollen with dark red hemorrhage - Tumor occupying the medulla. - Thrombosis to central vein with adrenal infarction - HTN and chronic renal failure  PULMONARY THROMBOEMBOLISM  It is most underdiagnosed cause of death.  The peak incidence is 2 weeks after trauma. The victims of many forms of trauma are at risk from venous thrombosis and pulmonary embolism because: 1- Tissue trauma increases the coagulability of the blood for several weeks, the peak being between one and two weeks. 2- Injury to the tissues, especially the legs or pelvic region, may cause local venous thrombosis in the contused muscles or around fractured bones. 3- The injury may confine the victim to bed: - This leads to pressure on the calves and immobility causes reduced venous return and stasis. - The common result is thrombosis of the deep veins of the legs, which can extend proximally into the popliteal and femoral vessels.  These thrombi act as dangerous sources of pulmonary thromboemboli.  The effects of pulmonary embolism depend on the size of emboli and the occluded vessels, numbers of emboli, the cardiovascular status of the victim.  Small emboli may break off and impact in more peripheral branches of the pulmonary arteries, sometimes causing pulmonary infarcts.  A massive embolus that impacts in the major lung vessels and causes rapid death.  Saddle embolism : large embolus impacted at the bifurcation of the main pulmonary artery.  Very rare paradoxical embolism may occur by passage of an embolus from the right heart to the left through atrial or ventricular septal defect. V Ante mortum AUTOPSY FINDINGS : 1- The embolism:  large emboli are readily visible and can usually be easily distinguished from post- mortem clot: Postmortem clot:  Dark red, soft and jelly-like, with a shiny, glistening surface. It is often separated into 'chicken-fat' plasma clot and dark red-cell clot by sedimentation after death.  When pulled out of the vessels it forms a cast of the branches. Less evident in peripheral branches.  Does not pour out of cut small vessels. Antemortem clot:  Firm, Brittle, Matt and has a dull striated surface from fibrin lamination.  Older thrombus tends to be greyish-red and varies in color from place to place.  It may appear to be a cast of the large vessel in which is impacted, or often be unraveled to form a long length similar to original leg vein.  Side branches may seen not corresponding to pulmonary artery where they lie.  may be seen in the more peripheral vessels.  Slightly pour out of the surface of cut small vessels  Post-mortem clot may be adherent to the ante-mortem embolus and sometimes forms a sheath around it  Histological confirmation of an ante-mortem origin must be made if there is any doubt. 2- The thrombus:  In almost all cases this will be found in the vessels draining into the femoral veins.  Rarely, the pelvic vessels are involved (pregnancy, abortion).  Extremely rare, the thrombus seen in jugular, axillary or subclavian veins.  Transverse or longitudinal incisions can be made into the calf of the leg to examine the deep veins.  The soleus and gastrocnemius muscles are transected to view their contained veins.  Often the thrombus seen in the interosseous veins between tibia and fibula.  Section of the thrombus should taken with adjacent muscle for histological examination.  DATING OF DEEP VEIN THROMBOSIS AND PULMONARY EMBOLISM: 1- The embolism: It is difficult to use histological  Endothelial buds proliferate into the fibrin mass criteria to date free embolus from the lung as the and break it to compartment from 4th day. thromboendothelial junction in the most useful part in dating.  Fibrin can be seen as purplish strands on the first day, but they aggregate into small masses 2- The thrombus: with a meshwork of thicker strands and sheets by 4 days. After 2 weeks, the fibrin becomes  The junction between thrombus and vein wall more deeply purple stained but begins to be that offers the most information about the absorbed by about the 25days. maturity of the thrombus.  Collagen fibers do not appear for about 5-10 Though accuracy about dating is impossible, the days, often much later. following is a useful scheme to provide at least an approximate idea of the duration :  Fibroblasts may be seen as early as 2 or 3 days, but tend to appear towards the end of the first  Polymorphs may be seen within the first day, but week and reach a maximum at 2-4 weeks. they vanish rapidly, often by the next day when mononuclears take their place.  Hemosiderin, blue granules demonstrated by Perl‘s reaction, may be seen by the end of the  Platelet and RBCs begin to hemolysis between first week and reach a maximum in 3 weeks. 1-2d.  Capillaries begin to appear on the second day,  Endothelial proliferation is most useful in the but do not contain red cells until about 2 first week, as buds begin to arise from the vessel weeks. wall about the second day and proliferate during the first week.  Elastic fibers appear late, not before 28 days, and reach maximum density in about 2m months. Polymorphis First day Platelets and RBCs 1-2 days Endothelial proliferation 4th day - week Fibrin Purple strand = 1st d thicker strands and sheets = 4th d Deep purple = 2w Absorbed = 25d Collagen Fibrers 5-10d Fibroblasts 2-4 d -> 1w -> 2/4w Hemosidrin End of first week and max by week 3 Capillary 2d -> 2w Elastic fibers 28 days -> 2mon  AIR EMBOLISM  It consists of interruption of the circulatory system by bubbles of air (or other gas) that gain access to the circulation.  usually through venous side but can occur in arterial side. Venous air embolism:  Entry of air into the circulation is usually from trauma.  Other causes : Surgical or therapeutic Pressure changes (barotrauma) Criminal abortion homicides (mercy killing)  The air gets sucked towards the right heart through pulmonary trunk and arteries.  The volume of air producing a fatal embolism varying from 10 to 480 ml.  In general, about 100 ml or more has been considered fatal. Arterial air embolism:  Rare complication.  Can occur in laceration of carotid artery, laceration of lung, or some forms of barotaurma.  Death can be result of air locks in the cerebral vessels or of ventricular fibrillation from coronary air embolism.  Peripheral arterial air injection is not harm at all as the gas is absorbed in the tissue. Fat and bone marrow embolism  It is often seen after injury to bone or fatty tissue.  Fat embolism is commonly attributed to fractures of the pelvis and long bones with marrow and fat forced to the circulation via torn blood vessels.  It may also occur in the absence of fractures in which fatty tissues is compressed or lacerated and forced to the blood vessels.  After entering the venous system, the fat globules usually embolise to the lungs.  After appearing in the pulmonary capillaries and may leak to the systemic circulation and impact in the brain, heart or kidneys.  The emboli travel usually at the time of trauma but the symptoms get delayed probably because of time required for hydrolysis of fat to release fatty acids which damage the endothelium and activate blood coagulatory process.  This so called lucid interval and may be confused with extradural or subdural hemorrhages in cases where cerebral fat embolism is suspected. - Pulmonary fat embolism:  Lehman and Moore showed that half the death of non-trauma has histological evidence of fat in the lung.  Mason found fat in the lungs of 20% of his non-trauma death but emphasized that quantitatively the amount was small as compared to that found in cases of fatal trauma. - systemic fat embolism:  Fat embolism can appear in any organ or structure as petechial-like lesion.  brain, heart or kidneys are most vulnerable target, the brainstem is one most likely to lead to death.  He used a simple scale for assessing the histological severity of embolism as seen in Oil red –O frozen sections of the lung: Mason's criteria : Grade 0 : no emboli seen. Grade 1 : found after some searching. Grade 2 : easily seen. Grade 3 :present in large number. Grade 4 : present in potentially fatal number. - Autopsy finding:  Petechial hemorrhages are typical lesion, caused by impaction of fat droplets in small venules and may be seen in skin of any part of body especially on the front of chest , face and eyelids.  they are widespread but are typically seen in the white matter of the brain, both cerebral and cerebellar hemispheres.  In the heart, the fat can seen in interfiber capillaries.  In kidney, the glomeruli may be stuffed with fat. CRUSHING SYNDROME  This is a common sequel to extensive muscle damage or to extensive burns , as well as from certain poisons as mercuric salts or carbon tetrachloride.  Crushed muscles sequesters many liters of fluid, reducing the effective intravascular volume , which result in renal vasoconstriction and ischemia of the kidneys.  Myoglobin ( from crushed muscles ) gets concentrated in the tubules and forms brown casts which block the tubules and cause destruction of the renal tubular epithelium and distal tubular necrosis.