CHEST TRAUMA

CHEST TRAUMA

Causes and introduction of chest trauma

Chest injuries may be blunt or penetrating blast injuries frequently involve a combination of these

Fewer than 15% of chest injuries require surgery tube thoracostomy ,blood or fluid replacement oxygen therapy and analgesia are the mainstay of treatment in most patients hypoxia is the final common pathway of most chest injuries and all patient should receive oxygen at an FIO2 of at least 0 .85 -

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BLADDER OUTFLOW OBSTRCUTION

BLADDER OUTFLOW OBSTRCUTION

the pathology may be neuropathic due to the failure of the sphincters to relax in harmony with detrusor contraction or due to obstruction from bladder neck hypertrophy being prostate hyperplasia (BPH)urethral stricture urethral calculus meatal stenosis or a tight phimosis 1- urethral stricture once a urethral stricture always a urethral stricture this adage still holds good pharaohs even took dilators with them to their burial chambers for the after life the causes are numerous as 1- catheter urethral site penoscrotal mechanism by pressure necrosis and paraurethral gland sepsis 2- perineal injury urethral site bulbar mechanism by crush injury 3- pelvic fracture urethral site membranous mechanism by prostatic displacement shear injury 4- infection throughout urethra by gonorrhoea and chlamydia 5- BXO urethral site meatal mechanism by fibrosis 6- chemotherapy throughout the urethra by causing chemical urethritis 7- instruments throughout urethra either iatrogenic or masturbation 2- presentation depending on the degree and length of narrowing and

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The deep venous thrombosis

 The deep venous thrombosis

the significance of deep vein thrombosis(DVT) lies in its potential to cause pulmonary embolism and post-thrombotic calf pump failure .virtually all venous thrombi arise in the deep veins of the legs or pelvis .the incidence of DVT in the general population is approximately .5% where no preventative measures are employed .the incidence of DVT in general surgical patients over 40 years undergoing to major surgery is 30%and 60-80% in patients undergoing hip or knee replacement or surgery for hip fracture in patients recovering from myocardial infarction or cerebro vascular accident the incidence is 20-60% 1- aetiology VIRCHOW,S TRAID hypercoagulability antithrombin 111 deficiency ,protein c deficiency ,protein s deficiency factor v leiden ,antiphospholipid syndrome heparin co factor alpha 11 macroglobulin alpha 1 antitrypsin fibrinolytic impairment oral contraceptive .stasis as in surgery and bed rest. vein wall damage as in surgical injury trauma and radiotherapy risk factor include age sex race operation anaesthetic pregnancy trauma immobilization bed rest malignancy previous thrombosis obesity cardiac failure contraceptive pill congenital venous abnormalities .pathology thrombosis is frequently initiated in the vein valve sinuses of the soleal plexuses platelets adhere to the venous endothelium initially and fibrin and red cells are deposited between the layers of platelets giving rise to laminated thrombus this propagates to extend up th vein being free or loosely attached to the wall initially thrombus then become firmly adherent to the endothelium organizes retracts and recanalizes to varying degrees destroying the endothelium and valves as it resolve clinical features limb swelling pain tenderness erythema and dilated superficial veins are the classic signs but are frequently absent even in a major thrombosis a swollen white leg (phegmasia alba dolens)or blue leg(phlegmasia cerulea dolens

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Head injury

 Head injury

Pathology of head injury The Monreo-Kelly  doctrine confirms that the skull cannot easily accommodate an increase in volume of its contents without a significant rise in intracranial pressure (ICP) .cerebral perfusion pressure (CPP)equals the systemic arterial pressure(SAP)minus the ICP this relationship is fundamental and explains the pathophysiology of brain injury .brain injury causes swelling .this volume increase causes a rise in ICP and thus a fall inCPP resulting in brain ishaemia . deterioration in cerebral function causes respiratory failure resulting in reduced PaO2 and rise in PaCO2 , which both

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