SHOCK & BLOOD TRANSFUSIONBY: R. NANDINII

GROUP K1

Overview:

• SHOCK

-Definition

-Pathophysiology

-Classification

-Severity

-Management

-Monitoring

• HAEMORRHAGE

-Definition

-Classification

-Management

• BLOOD TRANSFUSION

-Definition

-Indication

-Blood products

-Complication

SHOCK

Pathophysiology:Cellular

When perfusion to the tissue reduces

↓ O2 delivery to tissue

Cell Metabolism (aerobic anaerobic)

Accumulation of lactic acid in blood

Systemic metabolic acidosis

Glucose within cells are exhausted

Anaerobic respiration ceases

Failure of Na/K pump in the cell membrane & intracellular

organelle

Intracellular lysosome release autodigestive enzymes

Cell lysis

Intracellular content including K released into the bloodstream

Pathophysiology:Microvascular

Tissue ischemia progresses

Activation Of Immune

& Coagulation System

Hypoxia & acidosis

Activate complement &

prime neutrophils

Tissue oedema ensues →

exacerbating cell hypoxia

Generation of oxygen free radicals & cytokine release

Injury of the capillary

endothelial cells

Fluid leaks out

Cardiovascular:

Respiratory:

Pathophysiology:Systemic

Compensatory baroreceptor

response

↑ sympathetic

activity

Catecholamines release into the

circulation

Systemic vasoconstriction

Tachycardia

↓ Preload & Afterload

Metabolic acidosis

Tachypnea

Compensatory Respiratory

alkalosis

↑ sympathetic

responseExcretion of

CO2 increased

Renal:

Endocrine:

↓ Glomerular filtration

↓ urine output

↓ Kidney Perfusion

Stimulate Renin-angiotensin-

aldosterone

↑ Na & water

reabsorption

Hypothalamus

Adrenal Cortex

Vassopressin

Cortisol

vasoconstriction

Na & water reabsorption

Sensitizing cell to

catecholamine

Classification of shock:

Classification of shock:

Classification of shock:

Severity of Shock

Compensated

Decompensated

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.

ResuscitationA. Conduct of resuscitation:

ResuscitationB. Fluid therapy:

SHOCK STATUS:

ResuscitationC. Vasopressor & Inotrope Support:

MONITORING

HAEMORRHAGE

Further haemorrhage ↓ Perfusion to the tissue unable to

generate heat

Trauma Triad of Death

Coagulopathy

Hypothermia

Acidosis

Decrease function of coagulation proteases coagulopathy

Definitions:

Degree & Classification

Management:

After control aggressively resuscitated, warmed and coagulopathy corrected

TransfusionDefinition:

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

Perioperative red blood cell transfusion criteria

Source: Bailey & Love’s Short Practice of Surgery 25th ed

Blood & Blood Products

Blood component Explanation

Whole blood[can be broken down to: RBC, platelets, fresh frozen plasma (FFP)]

• Very rarely used• Carries greater risks of adverse reactions

owing to the presence of leucocytes.

Packed Red Cell[do not provide viable platelets or neutrophils]

• Each unit is approximately 330 ml and has a haematocrit of 50–70%.

• For use in substantial hemorrhage & anemia, symptomatic anemia

Platelet[for the coagulation; also contain plasma (coagulation factors), some red cells and some white cells (leukocytes)]

• For patients with bleeding due to either thrombocytopenia, platelet dysfunction

• Temporary thrombocytopenia occuring after radio- and chemotherapy,

• Bleeding in patients with thrombocytopenia or functional platelet abnormality,

• After massive transfusion (RBC) and thrombocytopenia

Blood & Blood Products

Blood component Explanation

Fresh frozen Plasma (FFP)[contains all coagulation factors in normal amounts and is free of red cells, leukocytes and platelets]

• Corrections of known congenital or acquired coagulation factor deficiencies.

• Treatment of microvascular hemorrhage in the presence of prolonged PT, aPTT

Cryoprecipitate[supernatant precipitate of FFP and is rich infactor VIII and fibrinogen]

• For Hemophilia A, von Willebrand disease, DIC, Hypofibrinogenemia (<100 mg/dl)

Factor VIII concentrates • Hemophilia A, & low titer factor VIII inhibitors

Factor IX Concentrates • Hemophilia B

ComplicationSingle transfusion incompatibility haemolytic

transfusion reaction; • febrile transfusion reaction; • allergic reaction; • infection: – bacterial infection (usually as a

result of faulty storage); – hepatitis; – HIV; – malaria; • air embolism; • thrombophlebitis; • transfusion-related acute lung

injury (usually from FFP).

Massive transfusion • coagulopathy;

• hypocalcaemia;

• hyperkalaemia;

• hypokalaemia;

• hypothermia.

Patients who receive repeated transfusions over long periods of time (e.g. patients with thalassaemia) develop iron overload. (Each transfused unit of red blood cells contains approximately 250 mg of elemental iron.)

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

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