Hemorrhagic shock and resusitation
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Hemorrhagic shock and resusitation

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Lecture By Dr.Essam Salem

Lecture By Dr.Essam Salem
ICU Registrar,Meeqat Hospital,Madina,KSA

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Hemorrhagic shock and resusitation Hemorrhagic shock and resusitation Presentation Transcript

  • points 1. Shock is hypoperfusion not hypotension 2. Rapid identification of HS and initiation of ttt before hypotension occur is essential to minimize morbidity
  • Class I A. Loss of up to 15% of total blood volume (0 to 750 ml in 70 kg person). B. Characterized by normal blood pressure, urine output, slight tachycardia, tachypnea, slight anxiety.
  • Class II A. Loss of 15 % to 30% of total blood volume (750 to 1,500 ml ) B. Characterized by normal blood pressure, tachycardia, mild tachypnea, decrease urine output and mild anxiety.
  • Class III A. Loss of 30% to 40% of total blood volume (1,500 to 2,ooo) B. Characterized by hypotension, tachycardia, tachypnea, decreased urine output , anxiety and confusion.
  • Class IV A. Loss of > 40% of total blood volume (>2,ooo) B. Characterized by severe hypotension and tachycardia, tachypnea, negligible urine output and lethargy
  • Notes that BP is normal until significant blood loss occur. ( class III ) Tachycardia is the earliest reliable sign of shock.
  • 1. Replace three times the volume of blood lost with warm crystalloids. (1L of blood lost should be replaced with 3L of crystalloids) A. The 3-to-1 rule comes from classic experiments B. Mortality for resuscitation with shed blood alone 80% shed blood plus plasma was 70% lactated Ringer`s plus shed blood (in 3:1 ratio) 30%.
  • 1. Replacement of hemorrhage with blood only or less than the required ratio of crystalloid to blood loss results in persistent hypoperfusion and acidosis and increase mortality. 2. Fluid resuscitation of the interstitial space is obligatory in HS. Note The interstitial space volume in 70 –Kg male is approximately 10 L The resultant edema and fluid retention is the expected result not a harmful side effect
  • Rapid response I. Become hemodynamically stable after initial fluid bolus II. Early surgical consultation is necessary
  • Transient response I. Pts respond to initial fluid bolus but again become hemodynamically unstable or shown signs of hypoperfusion. II. Cont` with fluid & blood transfusion maintain normal hemodynamics III. These Pts most often require rapid surgical intervention
  • No response I. Pt who show no response to fluid boluses and blood transfusion have continued hemorrhage and require Immediate surgical intervention to stop bleeding. II. Must keep in mind non hemorrhagic causes of shock . A. Tension pneumothorax. B. Cardiac tamponade. C. Spinal cord injury. D. Cardiogenic shock.. E. Septic shock
  •  The goal of HS resuscitation is restoration of end- organ perfusion  Traditional endpoints (normalization of BP- heart rate- urine output- capillary refill). Tricks BP does not equal cardiac output Increase systemic vascular resistance (SVR) may raise BP Pt with shock but normal BP are referred to as being “compansated shock” despite bleeding and hypoperfusion.
  •  Even experienced practitioners can be fooled by patient in compensated shock.  Normalization of acidosis and oxygen consumption are the best current indicators of adequate resuscitation  Base deficit and lactate level are good indications of tissue perfusion.
  • 1-Albumin  Albumin shown to decrease glomerular filtration and urine output  increase sodium retention  worsen oxygenation  Increase coagulopathy when used in HS
  • 2. Inotropes and vasopressors  Increase SVR and rise BP according to formula BP = CO X SVR  Increase BP not mean PERFUSION  NORMAL tissue perfusion is the GOAL of shock resuscitation.  VASOPRESSORS may have opposite effect of worsening perfusion through vasoconfusion
  • 3. Diuretics  Well resuscitated Pts mobilize 3th space fluid naturally 3 to 5 days after resuscitation  Induced diuresis (eg. Furosemide ) is unnecessary and may be harmful if it reduces intravascular volume and perfusion  Since normal edema resulting from proper shock resuscitation is the result of an inflammatory response (not cardiogenic failure) and is obligatory it is not reversible in the early stages of shock.
  •  Intravascular volume status should be estimated by measurements of  central venous pressure .
  • 4. Bicarbonate  HCO3 combined with hydrogen ion to form water and carbon dioxide  CO2 diffuses into cells and worsens intracellular acidosis  It is not indicated for lactic acidosis from HS  Best treatment of acidosis from HS is restoring perfusion to ischemic tissue.
  • complications
  • MOF Multiple organ failure Coagulopathy
  • Multiple organ failure  pt who survive HS but die in the hospital later usually die of MOF or sepsis  MOF results from systemic inflammatory response  Duration and severity of HS correlate with incidence of MOF  Patients who get > 6 units of packed RBCs in the first 12 hours of HS resusitation have higher risk of MOF
  • Coagulopathy 1-Hypothermia  Most common cause of coagulopathy in HS  Significant coagulopathy begins at 34o c  Undetectable on lab tests of coagulation ,blood warmed to 37 c before testing Note that Treate with warmed fluids and external rewarming
  • 2-Platelet dysfunction and deficiency  Second most common cause  Hypothermia cause plt dysfunction  Thrombocytopenia is common is massive HS  Degree of thrombocytopenia not correlated directly with volume of blood loss  Platelets transfusion