4. Pathophysiology:
Cellular
When perfusion to
the tissue reduces
Glucose within cells are exhausted
↓ O2 delivery to tissue
Anaerobic respiration ceases
Cell Metabolism
Failure of Na/K pump in the cell
(aerobic
membrane & intracellular organelle
anaerobic)
Accumulation of Intracellular lysosome release
lactic acid in blood autodigestive enzymes
Cell lysis
Systemic metabolic
acidosis Intracellular content including K
released into the bloodstream
5. Pathophysiology:
Microvascular
Tissue ischemia Hypoxia & Activate
progresses acidosis complement & prime
neutrophils
Activation Of
Immune Generation of
& Coagulation oxygen free radicals
System & cytokine release
Tissue oedema
Injury of the capillary
ensues →
endothelial cells
exacerbating cell
hypoxia
Fluid leaks out
6. Pathophysiology:
Systemic
Systemic
Cardiovascular: vasoconstriction
↓ Preload Compensatory Catecholamines
& baroreceptor ↑ release into the
Afterload response sympathetic circulation
activity
Tachycardia
Respiratory:
Tachypnea
↑ Compensatory
Metabolic Respiratory
sympathetic
acidosis alkalosis
response
Excretion of
CO2 increased
7. Renal:
↓ Glomerular ↓ urine
filtration output
↓ Kidney
Perfusion
Stimulate ↑ Na & water
Renin-angiotensin- reabsorption
aldosterone
Endocrine:
vasoconstriction
Hypothalamus Vassopressin
Na & water
reabsorption
Adrenal Cortisol
Cortex Sensitizing cell to
catecholamine
11. Severity of Shock
Decompensated
Compensated
Mild Moderate Severe
Consciousness Normal Mild Anxiety Drowsy Comatose
Blood Pressure Normal Normal Mild ↓ Severe ↓
Pulse Rate Mild Increase ↑ ↑ ↑
Resp Rate Normal ↑ ↑ Laboured
Urine Output Normal Normal Reduced Anuric
Lactic Acidosis + ++ ++ +++
Compensated : Compensatory responses reduce flow to non-essential organs to
preserve preload & flow to the lungs & brain.
Decompensated : Further loss body’s compensatory mechanisms, Progressive
renal, respiratory & CVS decompensation; Occurs when there’s 30-40% loss of
Blood Volume.
17. HAEMORRHAGE
Further haemorrhage Hypothermia
↓ Perfusion to the
tissue unable to
generate heat
Coagulopathy Acidosis
Decrease function of coagulation
proteases coagulopathy
Trauma Triad of Death
20. Management:
After control
aggressively
resuscitated,
warmed and
coagulopathy
corrected
21. Transfusion
Definition:
Process of transferring whole blood or blood components from
one person (donor) to another (recipient).
Indications:
Acute blood loss
to replace circulating volume & O2 delivery
Perioperative anemia
To ensure adequate O2 delivery during perioperative phase.
Symptomatic chronic anemia without haemorrhage or impending surgery
Hb < 6 g/dl
22. Perioperative red blood cell transfusion criteria
Source: Bailey & Love’s Short Practice of Surgery 25th ed
23. Blood & Blood Products
Blood component Explanation
Whole blood • Very rarely used
[can be broken down to: RBC, • Carries greater risks of adverse reactions owing
platelets, fresh frozen plasma (FFP)] to the presence of leucocytes.
Packed Red Cell • Each unit is approximately 330 ml and has a
[do not provide viable platelets or haematocrit of 50–70%.
neutrophils] • For use in substantial hemorrhage & anemia,
symptomatic anemia
Platelet • For patients with bleeding due to either
[for the coagulation; also contain thrombocytopenia, platelet dysfunction
plasma (coagulation factors), some • Temporary thrombocytopenia occuring after
red cells and some white cells radio- and chemotherapy,
(leukocytes)] • Bleeding in patients with thrombocytopenia or
functional platelet abnormality,
• After massive transfusion (RBC) and
thrombocytopenia
24. Blood & Blood Products
Blood component Explanation
Fresh frozen Plasma (FFP) • Corrections of known congenital or acquired
[contains all coagulation factors in coagulation factor deficiencies.
normal amounts and is free of red cells, • Treatment of microvascular hemorrhage in the
leukocytes and platelets] presence of prolonged PT, aPTT
Cryoprecipitate • For Hemophilia A, von Willebrand disease, DIC,
[supernatant precipitate of FFP and is Hypofibrinogenemia (<100 mg/dl)
rich in
factor VIII and fibrinogen]
Factor VIII concentrates • Hemophilia A, & low titer factor VIII inhibitors
Factor IX Concentrates • Hemophilia B
25. Complication
Single transfusion Massive transfusion
incompatibility haemolytic • coagulopathy;
transfusion reaction;
• febrile transfusion reaction;
• hypocalcaemia;
• allergic reaction; • hyperkalaemia;
• infection: • hypokalaemia;
– bacterial infection (usually as a
result of faulty storage);
• hypothermia.
– hepatitis; Patients who receive repeated
– HIV; transfusions over long periods of
time (e.g. patients with
– malaria;
thalassaemia) develop iron
• air embolism; overload. (Each transfused unit of
• thrombophlebitis; red blood cells contains
• transfusion-related acute lung approximately 250 mg of
injury (usually from FFP). elemental iron.)
26. Management of coagulopathy
Correction of coagulopathy is not necessary if no active
bleeding/ haemorrhage
However, coagulopathy following during massive
transfusion should be anticipated and managed
aggressively
Standard guidelines:
FFP : if PT or PTT > 1.5 X normal;
Cryoprecipitate : if fibrinogen < 0.8 g/l
Platelet : if platelet count < 50 x 109 ml
hypothyroid : result of disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls because of low inotropy and bradycardia. There may also be an associated cardiomyopathy. Thyrotoxicosis may cause a high-output cardiac failure. Adrenal insufficiency leads to shock as a result of hypovolaemia and a poor response to circulating and exogenous catecholamines. Adrenal insufficiency may result from pre-existing Addison’s disease or it may be a relative insufficiency caused by a pathological disease state such as systemic sepsis.
Anaphylaxis (vasodilatation is caused by histamine release) High spinal cord injury (failure of sympathetic outflow & adequate vascular tone: neurogenic shock) Sepsis (release of endotoxins by bacteria causes vasodilatation