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Lecture on Haemorrhage
This document discusses haemorrhage or bleeding from blood vessels. It defines haemorrhage and describes the pathophysiology where bleeding leads to hypovolaemic shock and complications like acidosis. It then classifies haemorrhage based on anatomical source, timing, visibility, duration and amount of blood loss. Clinical features and investigations for haemorrhage are provided. Management of haemorrhage focuses on arresting bleeding through pressure, packing and procedures before restoring blood volume.
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Lecture on Haemorrhage
- 1. HAEMORRHAGE DR MD SWHERAJULISLAM FCPS(SURGERY), FACS(USA) ASSISTANT PROFESSOR(SURGERY) SHEIKH SAYERA KHATUN MEDICAL COLLEGE
- 2. HAEMORRHAGE Haem means Blood Rhegmyniameans to burst forth(rush out)
- 3. HAEMORRHAGE Extravasation of bloodfrom close cardiovascular system (Don’t use the term escape of Blood)
- 4. Pathophysiology Haemorrhage leads toa state of hypovolaemic shock.
- 5. Pathophysiology Bleeding ↓↓ ↓↓ ↓ Hypovolaemia ↓↓↓↓ ↓ Low cardiac output ↓↓ ↓↓ ↓ Tachycardia and shunting of blood from splanchnic vessels by venoconstriction to maintain perfusion of vital organs like brain, heart, lungs, kidneys
- 6. Pathophysiology ↓↓ ↓↓ ↓ Hypoxia ↓↓↓↓ ↓ Activation of cardiac depressants ↓↓ ↓↓ ↓ Anaerobic metabolism and altered cell membrane function causing influx of more sodium and calcium inside the cell and potassium comes out of the cell
- 7. Pathophysiology ↓↓ ↓↓ ↓ Hyponatraemic,hyperkalaemic, hypocalcaemic metabolic acidosis ↓↓ ↓↓ ↓ Lysosomes of cell get lysed releasing powerful enzymes which is lethal to cell itself ↓↓ ↓↓ ↓ SICK CELL SYNDROME
- 8. Pathophysiology Platelets and coagulantsare activated leading to formation of small clots DIC and further bleeding. ↓↓ ↓↓ ↓ Progressive haemodilution leading to total circulatory failure Initially there is compensatory hypovolaemic shock and later there is decompensatory hypovolaemic shock which will lead to MODS and death. DIC, acidosis and hypothermia are the major factors in worsening the situation in haemorrhage
- 9. Physiological exhaustion ( Thetriad of death) Hypothermia Coagulopathy Acidosis
- 10. Classification According to 1. Anatomicalsource 2. Timing 3. According to Visibility 4. Duration 5. According to amount of blood loss 6. Cause 7. Amount of blood loss (Degree)
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- 13. According to Timing Primary haemorrhage -- occurring immediately as a result of an injury (or surgery) Reactionary haemorrhage is delayed haemorrhage (within 24 hours) caused by Dislodgement of clot by resuscitation Normalization of blood pressure Vasodilatation Slippage of a ligature
- 14. According to Timing Secondaryhaemorrhage usually occurs 7–14 days after injury caused by sloughing of the wall of a vessel precipitated by infection, pressure necrosis (such as from a drain) or malignancy.
- 15. According to Visibility *Revealedhaemorrhage obvious external haemorrhage, such as exsanguination from an open arterial wound *Concealed haemorrhage contained within the body cavity In trauma within the chest, abdomen, pelvis or retroperitoneum or in the limbs, with contained vascular injury or associated with long-bone fractures non-traumatic concealed haemorrhage include occult gastrointestinal bleeding or ruptured aortic aneurysm.
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- 18. Initially concealed butlater revealed Any bleeding from natural orifices Haemoptysis Haematemesis Epistaxis Haematuria Haematocazia Melaena P/V bleeding Bleeding through Ear
- 19. According to Duration Acute haemorrhage (exsanguinous haemorrhage: The most extreme form of hemorrhage, with an initial blood loss of > 40% and ongoing bleeding which, if not surgically controlled, will lead to death) chronic haemorrhage Acute on chronic haemorrhage
- 20. According to amountof blood loss Mild-----< 500 ml blood loss Moderate…..500-1000 ml blood loss Severe……>1000 ml blood loss.
- 21. According to Cause Surgicalhaemorrhage Non-surgical haemorrhage
- 22. According to Cause Surgical haemorrhage is the result of a direct injury and is amenable to surgical control (or other techniques such as angioembolization) Non-surgical haemorrhage is the general ooze from all raw surfaces due to coagulopathy; it cannot be stopped by surgical means (except packing) but requires correction of the coagulation abnormalities
- 23. According to Amountof blood loss (Degree) Degree of haemorrhage is classified in to four classes Class1: Blood volume lost as percentage of < 15% Class 2 :Blood volume lost as percentage of 15–30% Class 3 :Blood volume lost as percentage of 30–40% Class 4: Blood volume lost as percentage of > 40%
- 26. Clinical Features of Haemorrhage •Pallor, thirsty • Cyanosis • Tachycardia • Tachypnoea • Air hunger. • Cold clammy skin due to vasoconstriction • Dry face, dry mouth and goose skin appearance (due to contraction of arrector pilorum)
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- 28. Clinical Features of Haemorrhage •Rapid thready pulse • Oliguria • Features related to specific causes • Hypotension
- 29. Signs of significantblood loss Pulse > 100/minute Systolic BP< 100 mmHg Diastolic BP drop on sitting or standing > 10 mmHg Pallor/ sweating Shock index (ratio of pulse rate to blood pressure) > 1
- 30. Measurement of BloodLoss Clot size of a clenched fist is 500 ml Blood loss in a closed tibial fracture is 500-1500 ml; in a fracture femur is 500-2000 ml Weighing the swab before and after use is an important method of on-table assessment of blood loss
- 31. Measurement of BloodLoss Hb% and PCV estimation. Blood volume estimation using radioiodine technique or micro hematocrit method. Measurement of CVP or PCWP Investigations specific for cause: U/S abdomen, Doppler and often angiogram in vascular injury, chest X-ray in haemothorax, CT scan in major injuries, CT scan head in head injuries
- 32. Rains Factor Total amountor of Blood loss = Total difference in swab weight × 1.5 Or Total difference in swab weight × 2 (For larger wounds and larger operations)
- 33. Effects of haemorrhage Acute renal shut down Liver cell dysfunction Cardiac depression • Hypoxic effect • Metabolic acidosis • GIT mucosal ischaemia • Sepsis • Interstitial oedema, AV shunting in lung- ARDS • Hypovolaemic shock- MODS
- 36. Management Identify haemorrhage Immediate resuscitativemanoeuvres Identify the site of haemorrhage Haemorrhage control Arrest of bleeding Restoration of blood volume
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- 38. Arrest of bleeding 1.Pressure and Packing 2. Position and Rest 3. Operative procedure -Ligation -Diathermy coagulation -Suturing -Pressure by ‘peanut’ of gauze -Topical application for oozing biological gauze or sponge (Oxycel or gelatin sponge), gauze soaked in adrenalin -Patches of vein or Dacron mesh -Excision of whole or part of viscus
- 39. Haemostasis Haemostasis is thehuman body's response to blood vessel injury and bleeding It involves a coordinated effort between platelets and numerous blood clotting proteins (or factors), resulting in the formation of a blood clot and subsequent stopping of the bleeding.
- 42. Local haemostatic agents: •Gelatin sponge (Gel foam) • Oxidised cellulose (Surgicel) • Collagen sponge (Helistat) • Cyano acrylic Glue(vietnum war) • Microfibrillar collagen (Avitene) • Topical thrombin • Bone wax (derived from bees wax + almond oil) • Gelatin matrices (Floseal) • Topical cryoprecipitate