01 Haemorrhage and shock

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01 Haemorrhage and shock

  1. 1. Haemorrhage and shock ByDr. Abdel-Motaleb Effat M.D. Lecturer of Pediatric Surgery. Tanta University.
  2. 2. Haemorrhage Haemorrhage means escape ofblood outside its containing vessel.Acute haemorrhage causes loss ofboth circulating blood volume and oxygen carrying capacity.
  3. 3. Classification:According to:Site: External (revealed). Internal(concealed).Type of disrupted blood vessel: Arterial. Venous. Capillary.
  4. 4. Timing in relation to trauma: Primary. Reactionary. Secondary.Aetiology: Traumatic (accidental, surgicaland intervetional procedures). Pathological (atherosclerotic, inflammatory and neoplastic). Bleeding diathesis.
  5. 5. Physiological response to haemorrhage:The Physiological response tohaemorrhage has two aims: 1. Stopping the bleeding 2. Maintaining effective circulatory volume and perfusion of critical tissues which is achieved by neural and endocrinal factors.
  6. 6. Neural factors. A sympathoadrenal responsewhich will cause: (constriction of theveins, constriction of arterioles raisingthe peripheral resistance andincreased rate and contractility of theheart).Endocrine factors.Transcapillary refill.
  7. 7. Clinical picture:The manifestations depend upon: Amount of haemorrhage. Rate of haemorrhage. Cardiovascular reserve.Symptoms: Weakness and fainting especially when standing. The patient feels cold and thirst.
  8. 8. Signs:*Pulse : small and rapid. Later on itbecomes imperceptiple.*B.P. : low, later on it is seriously lowered.*Respiration : rapid and shallow.(over 35/minute is serious)*Lethegic mind till the end.*Pallor and light cyanosis.*Cold skin and clammy sweat.*Urine flow : oliguria (normal 30-60ml./h).*collapsed veins indicate severe oliguria.
  9. 9. Estimating blood loss:Normal blood volume is estimated as70 ml/kg in adults and 80ml/kg inchildren.Clinical data.Four classes of haemorrhage arerecognized based on clinical changesin haemodynamic parameters andindices of tissue perfusion.Type of injury.Blood loss at operation.
  10. 10. ManagementStop of haemorrhage: First aid treatment by packing, pressure, position, andtourniquets.Restore blood volume: by lactated ringer solution, and blood transfusion to correctdeficit according to the class ofhaemorrhage.
  11. 11. Management(Cont.):Optimize oxygen delivery: by oxygen and inotropes.Monitoring: pulse, blood pressure,temperature, urine output,conscious level, C.V.P., bloodgases and blood lactate.
  12. 12. SHOCKDefinition: Shock is a state of peripheralcirculatory failure characterized byhypotension, inadequate tissueperfusion and disordered cellularmetabolism.
  13. 13. Types:1.Primary (neurogenic) shock.2. Secondary (oligaemic orhypovolaemic) shock.3. Cardiogenic shock.4. Septic shock.5. Anaphylactic shock.6. Endocrinal shock.7. Obstructive Shock.
  14. 14. Primary (neurogenic) shockVasovagal syncope resulting from painfulstimuli or emotional disturbance.Clinical picture:*Patient collapses and fall to the ground. Feeble pulse.*Slow and shallow respiration.*Low BP.*Subnormal temperature.*Normal CVP (5 cm water).*Warm skin.
  15. 15. Treatment: Transient condition responding to:Rest and warmth.Remove the pain or distressing factor.Stimulants as coffee.Adrenaline IM. If delayed recovery, suspectassociated secondary shock.
  16. 16. Secondary (oligaemic or hypovolaemic) shock.Hypovolaemia due to:Blood loss (haemorrrhage).Plasma loss (burn).Water loss (vomiting anddiarrhea).
  17. 17. Pathophysiology:I.Cardiovascular responses: Hypotension stimulates V.C.C. andstimulation of C.N.S.with catecholaminesrelease causing :1.Increased peripheral resistance due to arteriolar vasoconstriction.2.Increased heart rate and contractility and cardiac output.3.Increased vasomotor tone squeezingblood to the central circulation.
  18. 18. Pathophysiology(Cont.):II.Endocrine response:*A.D.H. is released by baroreceptors stimulation*Increased aldosterone.*Stimulation of rennin angiotensinmechanism. All of these cause salt and waterretention.
  19. 19. Pathophysiology(Cont.):III. Blood viscosity is increased due to haemoconcentration resulting in sludging and Rouleaux formation.IV. Microcirculatory changes.V. Cellular derangement.VI. Acid-base impalance.VII. Individual organs (heart, GIT, liver, kidneys and lungs).
  20. 20. If these mechanisms succeed inmaintaining a good tissue perfusionthis is known as compensated shock.Irreversible shock ; occurs when shock persists leading to:1. Vasodilatation of capillaries with pooling of blood and severehypotension.2. Progressive tissue anoxia affecting the heart, kidneys, liver and brain leading to death in few hours.
  21. 21. Clinical picture:1. The cause of shock may be evident.2. Signs: Pulse : small and rapid. Later on itbecomes imperceptiple. B.P. : low, later on it is seriouslylowered. Respiration : rapid and shallow.(over 35/minute is serious)
  22. 22. Clinical picture(Cont.): Lethegic mind till the end. Pallor and light cyanosis. Cold skin clammy sweat. Urine flow : oliguria (normal 30-60ml./hour). collapsed veins indicatesevere oliguria. C.V.P. markedly reduced.
  23. 23. Measurements:*Urine output.*C.V.P.*Arterial blood gases.*Haematocrit.*Arterial blood lactate.*Cardiac output.
  24. 24. Prophylaxis:
  25. 25. Traumatic shock: by Proper first aid measures.1. Control external bleeding.2. Ensure adequate pulmonary perfusion.3. Deal with the injured part by dressing,splintage, firm bandage and elevation.4. Raise the foot end of the bed.5. Morphia I.V.(not given I.M. nor S.C.).6. Start I.V. therapy by Ringer solution tillblood is available.7. Conserve body heat by blankets.8. Transport the patient to hospital.
  26. 26. Operative shock:1. Preoperative measures: avoid purgationand starvation and give proper sedation.2. Operative precautions: avoid cold andexposure of the viscera, fine bloodlesstechnique, ensure adequate anaesthesiawithout anoxia or hypercapnoea andmaintain the blood pressure by transfusionand suitable infusions.3. Postoperative measures: put in recoveryroom for 24-48 hours.
  27. 27. Treatment: The aim should be to restore normaltissue perfusion by correcting the twomajor components in shock which are:1. The hypotension which stimulates thesympatho-adrenal response and2. The disturbance in the microcirculationwhich leads to tissue hypoxia. These measures should be adopted assoon as possible to abort the onset ofirreversible or septic shock.
  28. 28. Treatment(Cont.):1. Control external bleeding.2. Ensure adequate pulmonary perfusion.3. Deal with the injured part by dressing,splintage, firm bandage and elevation.4. Raise the foot end of the bed.5. Morphia I.V. (not to be given I.M. norS.C.).6. Start I.V. therapy by Ringer solution tillblood is available.7. Conserve body heat by blankets.8. Hydrocortisone I.V. injection.
  29. 29. Septic shockAetiology: *Causative organisms. *Common sources of infection. *Predisposing factors.
  30. 30. Pathophysiology: *Mediators cascade. *Microcirculation. *Cellular derangement. *Acid-base impalance. *Individual systems and organs(heart, lungs, brain, kidneys, liverand GIT).
  31. 31. Clinical features: Occurs in two stages1. Hyperdynamic (warm) septic shock. The patient has:*Restlessness and confusion.*Fever above 38 and chills.*Mild reduction in BP.*Tachypnoea.*Tachycardia.*Flushed with warm and dry extremities.*Oliguria.*The cardiac output is elevated.
  32. 32. Clinical features(Cont.):2.Hypodynamic (cold) septic shock. If the previous stage is nottreated efficiently, the patient willdevelop a picture similar tohypovolaemic shock with reducedcardiac output. Multiple organfailure starts at this stage.
  33. 33. Diagnosis:Is helped by: *Polymorphonuclear leucocytosis. *High lactate level. *Looking for source of sepsis. *Repeated blood culture at thepeak of fever or from any septic focus.
  34. 34. Treatment:*Support different systems(cardiovascular, respiratory andrenal support).*Fighting infection.*Control of blood sugar.*Prophylaxis against DVT and stress ulceration.*Monitoring as in hypovolaemic shock.
  35. 35. Prognosis:Mortality ranges from 25 to 90%.
  36. 36. Thank you

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