A very narrative discussion over Shock & Haemorrhage, Blood Transfusion, Blood Products which is presented in seminers. A concise guideline of a vast chapter.

1. Shock, Hemorrhage,
Blood Transfusion & Products
Topic Discussion by
Dr. Anick Saha Shuvo
MBBS (RpMC)
MS Resident (P-A), Pediatric Surgery, DMCH

2. Shock:
 Def: Shock is a systemic state of low tissue perfusion that is inadequate for
normal cellular respiration.
 Shock is the most common and therefore the most important
cause of death of surgical patients. Death may occur rapidly
due to a profound state of shock, or be delayed due to the
consequences of organ ischaemia and reperfusion injury. It
is important therefore that every surgeon understands the
pathophysiology, diagnosis and priorities in management of
shock and haemorrhage.

3. Classification of Shock
Based on the Initiating Mechanism:
Type of Shock Cause
Hypovolemic Shock Hemorrhage, Vomiting, Diarrhoea, Third Spacing,
Burn, Crush injury, Diuretics
Cardiogenic Shock MI, Cardiac Dysrhythmias, Valvular HD, Blunt
Myocardial Injury, Cardiomyopathy
Obstructive Shock Cardiac Tamponade, Tension Pneumothorax,
Massive Pulmonary Embolism
Distributive Shock Septic Shock, Anaphylaxis, Spinal Cord Injury
Endocrine Shock Adrenal Insufficiency, Hypothyroidism,
Thyrotoxicosis
Based on the Severity:
Type of Shock Subtype
1. Compensated Shock -
2. Decompensated Shock Mild, Moderate, Severe

4. Classification of Shock
 Differences between clinical features of different types of shock:

5. Pathophysiology of Shock
Cellular
1. ↓Tissue Perfusion/↓Tissue O2
▼
Anaerobic Metabolism
▼
Produce Lactic Acid
▼
Systemic Metabolic Acidosis
2. Intracellular Glucose Exhaustion
▼
Na, K Pump failure
▼
Cell lysis starts by Lysosome released
autodigestive enzymes
Microvascular
Hypoxia & Acidosis
▼
↑Oxygen free Radicals & Cytokines
▼
Capillary Endothelial Cell Injury
▼
Damaged Endothelium, looses it’s
integrity and becomes leaky
▼
Tissue Edema
Respiratory
↑RR & Minute Ventilation
▼
Compensatory Resp. Alkalosis

6. Pathophysiology of Shock
Cardiovascular
↓Preload & Afterload
▼
↑Sympathetic Activity
▼
Tachycardia with Systemic
Vasoconstriction
Renal
↓Perfusion in Kidney
▼
↓Urine Output
▼
Stimulates Renin Angiotensin axis
▼
Further Vasoconstriction with Sodium
& Water reabsorption
Endocrine
↑Vasopressin, Adrenalin, Cortisol
▼
Vasoconstriction with Sodium & Water
reabsorption

7. Hypovolemic Shock
 Hypovolaemia is probably the most common form of
shock, and to some degree is a component of all other forms
of shock.
 Hypovolaemic shock is due to a reduced circulating volume. Hypovolaemia may be due
to haemorrhagic or nonhaemorrhagic causes. Nonhaemorrhagic causes include poor
fluid intake (dehydration), excessive fluid loss due to vomiting, diarrhoea, urinary loss
(e.g. diabetes), evaporation, or ‘thirdspacing’
where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in
bowel obstruction or pancreatitis.
 Classification:
Class Percentage of Blood loss
1 <15%
2 <15%-30%
3 <30%-40%
4 >40%

8. Hypovolemic Shock - Pathogenesis
Reversible
Hemorrhage/Fluid Loss
▼
Acute Hypovolemia
▼
↓Central Venous Pressure (CVP)
▼
↓Cardiac Filling (↓EDV)
▼
↓Cardiac Output (CO)
▼
↓Arterial Pressure
Compensatory Autoregulation If uncontrolled
▼ ▼
↑Arterial Pressure Shock passes to
▼ progressive stage
Shock reverse

9. Hypovolemic Shock - Pathogenesis
Irreversible
Chronic Hemorrhage/ Chronic Fluid Loss
▼
Severe Hypovolemia
▼ if untreated
Compensatory mechanism failure
▼
Arteriolar dilatation & Venular Constriction
▼
Sludging of Blood
▼
Hypoperfusion of tissue
Endothelial Injury Impaired Intracellular Aerobic glycolysis
▼ ▼
Coagulation Cascade Triggered Anaerobic Glycolysis
▼ ▼
DIC ↑Lactic Acid/↑PpH
Severe Hypoxia ▼
▼ ↓Vasomotor Response
Damage to Cell & Tissue ▼
▼ Vasodilation
Acute Tubular Necrosis ▼
▼ ↓ BP
Complete Renal Shutdown
▼
Death

10. Hypovolemic Shock – C/F
 Clinical Feature:
1. Cold Clammy skin
2. Rapid Thready Pulse
3. Hypotension
4. Collapsed Vein
5. Rapid Shallow Breathing
6. Oliguria
7. Restlessness
8. Anxiety
9. Mental Confusion

11. Investigation for Shock
 Mostly Clinical by Assessment of Pt. condition:
1. Vitals: BP, HR, RR, Temp.
2. Sate of hydration
3. Urine Output
4. Rate & amount of bleeding if any
5. Proper History taking
 Lab Investigations:
1. CBC
2. Coagulation profile
3. Blood sugar, S. Electrolyte, S. Urea, S. Creatinine
4. Blood Culture
5. Imaging: CXR, USG, CT, MRI

12. Shock - Mx
 Management of shock at a glance:
 Immediate Resuscitation:
1. Maintenance of airway – OP suction
2. Maintenance of breathing – O2 inhalation/Intubation
3. Maintenance of circulation – I/V Fluid (R/L or H/S)
4. Blood transfusion (PCV/WB) or Blood Vol. Expanders
(Hypovolemic Shock)
5. Catheterization
6. Broad Spectrum Antibiotics (Septic Shock)
7. H2 blocker/PPI
8. Tetanus Prophylaxis (TT/Tig) (RTA/Trauma)
 Specific Measures:
1. Vasopressor/Ionotropic Support
2. Prevention of ARF (U/O kept 50ml/hour)
3. Excision of dead tissue or drainage of pus
 Monitoring:

13. Dynamic Fluid Response
 The shock status can be determined dynamically by the Cardiovascular response to
the rapid administration of a fluid bolus.
 Amount of bolus: 250-500 ml over 5-10 mins.
 Route: CV line.
 Parameter Monitored: HR, BP, CVP.
 Classification of Pt.:
a) Responders: Improved and sustained cardiovascular status, not actively loosing
fluid only require filling to normal volume status.
b) Transient Responders: Initially have improvement but gradually over 10-20mins
deteriorates with ongoing fluid loss.
c) Non Responders: No improvement with severe volume depletion and loss.

14. Consequences of Shock
(If unattended)
 Unresuscitatable shock
Patients who are in profound shock for a prolonged period of time become ‘unresuscitatable’. Cell
death follows from cellular ischaemia and the ability of the body to compensate is lost. There is
myocardial depression and loss of responsiveness to fluid or inotropic therapy. The peripheries no
longer respond appropriately to vasopressor agents. Death is the inevitable result. Conversely, when
patients present in this late stage, and have minimal responses to maximal therapy.
 Multiple organ failure
Multiple organ failure is defined as two or more failed organ systems. The result of prolonged
systemic ischaemia and reperfusion injury is endorgan damage and causes multiple organ failure. There is
no specific treatment for multiple organ failure. Management is supporting of organ systems, with
ventilation, cardiovascular support and haemofiltration/dialysis until there is recovery of organ function.
Multiple organ failure currently carries a mortality of 60% .

15. New Concept of End Point Resuscitation
 Traditionally, patients have been resuscitated until they have a normal pulse, blood
pressure and urine output. However, these parameters are monitoring organ
systems whose blood flow is preserved until the late stages of shock .
 According to new concept Resuscitation algorithm for end point are:
1. Base Deficit
2. Lactate
3. Mixed Venous O2 saturation

16. Haemorrhage

17. Haemorrhage
 Def: Escape of blood from the vascular compartment to the exterior.
 Classification:
a) According to source of Haemorrhage/Visibility:
- Arterial
- Venous
- Capillary
b) According to duration:
- Primary Haemorrhage
- Reactionary Haemorrhage
- Secondary Haemorrhage
c) According to site of bleeding:
- External/Revealed
- Internal/Concealed
d) According to mode of onset: e) According to nature of Attention:
- Acute - Surgical Haemorrhage
- Chronic - Non-Surgical Haemorrhage

18. Deference among various Haemorrhage
Traits Primary Hemorrhage Reactionery Hemorrhage Secondary Hemorrhage
Time of
Occurrence
Occurs at any time of
operation or trauma
Occurs within 24 hours of
primary haemorrhage (Usually
4-6 hours)
Occurs after 7-14 days of
primary haemorrhage
Cause Injury to blood vessel
during operation or
trauma
a) Slipping of ligature
b) Dislodgement of clot
c) Cessation of reflex
vasospasm
d) Normalization of BP
a) Infection
b) Sloughing of wall of
blood vessel
c) Pressure Necrosis
d) Maliganancy
Example During any operation Commonly occurs after:
a) Tonsillectomy
b) Thyroidectomy
c) Prostatectomy
d) Haemorrhoidectomy
In any type of surgery
where there is infection or
malignancy.

19. Pathophysiology
 Haemorrhage got worsen by factors mentioned below:
1. Acute traumatic coagulopathy (ATC)
2. Acidosis due to hypoperfusion Called triad of death
3. Hypothermia
4. Dilution of coagulation factor by continuous bleeding
Incidence: Upto 25% of trauma Pt. develop ATC within minutes of injury. It is
associated with four fold increase in Mortality.

20. Diagnosis
 Careful examination of the operation/trauma site Excessive swelling can be present
referring internal bleeding/Hematoma)
 Carefully examination of the drain tube for excessive collection of blood.
 Patient may be severely anemic.
 Increased Pulse rate.
 Decreased BP.
 Temperature may be cold/normal.
 Respiratory rate may be increased.
 Reduced Urine output
 Lab Investigation: HB%, HCT, ESR etc.

21. Management of Haemorrhage
 Identify Haemorrhage:
a) External Haemorrhage: can be seen
b) Concealed Haemorrhage: Any shock should be assumed to be hypovolemic until
proven otherwise.
 Immediate Resuscitative Maneuver:
a) Direct pressure over external haemorrhage site.
b) Airway and breathing should be assessed and controlled.
c) Large bore I/V access.
d) Blood drawn for cross matching.
 Identify the site of Haemorrhage:
 History:
a) Previous episodes
b) Known aneurysm
c) Non-Steroidal therapy/Drug history

22. Management of Haemorrhage
 Examination:
a) Nature of blood (Fresh/Melaena)
b) Abdominal tenderness
c) External signs of injury
 Investigation:
a) CXR, Pelvic x-ray, USG W/A
b) Diagnostic peritoneal aspiration
c) Computed Tomography (CT)
 Haemorrhage Control:
a) Pt. moved rapidly to a place of Haemorrhage control.
b) Surgical intervention may need to be limited to the minimum necessary to stop
bleeding and control sepsis.
c) Definitive repairs can be delayed until Pt. is hemodynamically stable.
d) Once haemorrhage controlled, Pt. should be aggressively resuscitated, warmed and
coagulopathy corrected.

23. Management of Haemorrhage
 Haemorrhage Control:
a) Anticipate & treat acute traumatic coagulopathy
b) Permissive hypotension until haemorrhage control
c) Limit crystalloid & colloid infusion to avoid dilutional coagulopathy
d) Damage control surgery to control haemorrhage and preserve physiology

24. Haemostasis during Surgery
 Endoscopic:
a) Injection
b) Thermal & Photocoagulation
c) Banding
d) Balloon tamponed
 Radiological: Embolization of bleeding vessel
 Surgical:
• Position & rest: Elevation of the limb
• Pressure Packing:
a) Pressure dressing
b) Digital Pressure
c) Roller Bandage
d) Ribbon Bandage
e) Tourniquets (Pneumatic/Rubber)
f) Use of double balloon tamponade to control bleeding
from oesophageal varices

25. Haemostasis during Surgery
• Operative Technique:
a) Pressure by artery forceps/clips
b) Topical application of haemostatic agents (Gelatin sponge) or adrenalin
c) Coagulation with diathermy
d) Ligation with catgut/silk
e) Temporary occlusion of inflow vessels – Pringle maneuver
f) Grafting (Another vessel/Tephlon)
g) Whole or part of bleeding viscous may be excised, eg. Splenectomy

26. Blood Transfusion &
Blood Products

27. Blood Transfusion
 Def: Introduction of blood or blood product in human body is called blood
transfusion.
 The first successful transfusion in 1818. Although there was many incidence of
severe transfusion reactions but now infections or reaction is now very low.

28. Type of Blood Transfusion
 Homologous Blood Transfusion: One person to another
 Autologous: Derived from same individual
o Intra and Postoperative cell storage: Collection of blood shed from intraoperative wound & drain
then process the blood to remove plasma constituents.
Use: Major orthopedic surgery
Cardiovascular Surgery
Hepatic Surgery, e.g. Liver transplantation
Contraindication: Dirty wound, Active Infection, Malignancy
o Normal normovolaemic hemodilution: Anesthetist withdraws several packs of Pt. blood replacing
with Crystalloid or Colloid. Collected blood then reinfused during operation. This is useful when
anticipated blood loss is >1L and Pt’s HCT is relatively high.
o Preoperative autologous deposit (PAD): Predonate Pt’s own blood 3 weeks prior surgery, around
2-4 units are collected. HB% kept >10gm/dl with oral iron supplementation .
Use: Major orthopedic & gynecological surgery
Contraindication: Active infection, Unstable Angina, AS, Severe HTN

29. Blood Products
 Whole Blood
 Blood Components:
a) Packed Red Cell
b) White Cell (Buffy coat)
c) Platelet
 Plasma Component:
a) Fresh Frozen Plasma (FFP)
b) Cryoprecipitate
c) Human Albumin Solution
d) Immunoglobulin
e) Coagulation Factor Concentrate:
 Recombinant Factor VIII, Factor IX
 Recombinant Factor VIIa
 Fibrinogen Concentrate

30. Indication & Storage of Blood Products

31. Indication of Blood Transfusion

32. Complication of Stored Blood
 Hyperkalaemia
 Reduced 2,3 DPG (Lt. shift of O2 dissociation curve)
 Acidosis (pH 6.6-6.8)
 Contain citric anticoagulant – Intoxication
 Ammonia intoxication
Changes Occur in Stored Blood
 Potassium lactate, Ammonia value rises
 Labile clotting factor (V,VIII) diminished
 2,3 DPG level remain adequate for 14 days but virtually absent @21 days
 CPD Preservative gradually decrease the pH upto 6.5 at the end of 2nd week
 Platelet becomes functionally inactivated when it is stored in 4˚C and after 3 days no
platelet remains viable

33. Criteria of Ideal Donor
 Must have good health status
 Unpaid volunteers
 Age: Within18-65 years
 Weight: >45 kg/ 100 lb.
 Body Temperature: <99˚F
 Pulse: 60-100 b/min
 BP: Within normal range
 Medical History:
• No H/O recent fever, tooth extraction within 3wks, Operation within 3months.
• Vaccination within 3 months
• At time of menstruation
• Any H/O heart disease or current pregnancy
 Hematological History:
• Hb%: >12 gm/dl
• No H/O anemia, leukemia, coagulopathy

34. Screening before Transfusion
 Compatibility Test:
a) Blood grouping
b) Cross matching
 Screening Test:
a) Viral: HBsAg, Anti HCV strip test
b) Malaria Parasite
c) VDRL/Syphilis
d) HIV

35. Complication of Blood Transfusion
Complications from a Single Transfusion
 Complications from a single transfusion
include:
● Incompatibility haemolytic transfusion
reaction
● Febrile transfusion reaction
● Allergic reaction
●Infection:
1. Bacterial infection (usually due to faulty
storage)
2. Hepatitis
3. HIV
4. Malaria
5. Air embolism
6. Thrombophlebitis
7. Transfusion related acute lung injury
(usually from FFP)
Complications from a Massive Transfusion
● Coagulopathy
● Hypocalcaemia
● Hyperkalaemia
● Hypokalaemia
● Hypothermia
● Iron overload (In repeated transfusion)

36. Management of Mismatched
Blood Transfusion
Symptoms
Feeling of something wrong
Restlessness
Anxiety
Headache
Pain & Heaviness in chest, lumber region,
Limbs
Pain venipuncture site
Fever
Rigors
Dyspnoea
Acute collapse
Rash, itch
Signs
Pallor
Raised Temperature
Rapid thread pulse
Low BP
Pulmonary Oedema (B/L Basal Creps)
Cervical vein engorgement
Cyanosis
Facial puffiness
Jaundice
Haemoglobunuria
Haemoglobinaemia
Oliguria F/B Uraemia

37. Management of Mismatched
Blood Transfusion
 Immediate measures:
1. Stop blood transfusion immediately
2. Recheck Pt. identity against donor unit
3. Inj. Hydrocortisone Hemisuccinate (2vials I/V Stat)
4. Inj. Anti-Histamine
5. Maintain I/V access with 0.9% NaCl solution
6. Monitoring urine output by catheterization > if U/O is less than 1.5ml/kg/hour will insert
CVP line and give fluid > If CVP adequate and U/O still less than 1.5ml/kg/hour then,
frusemide (80-120mg)
7. If suspicion of bacterial contamination, broad spectrum antibiotic should started.
8. Contact senior Medical personnel for advice and inform transfusion department.
9. Contact blood transfusion laboratory before sending back blood pack and for advice on
blood samples required for further investigation.

38. Management of Mismatched
Blood Transfusion
 Investigation:
1. Blood grouping, cross matching of pt. and transfusion bag (donor)
2. S. Electrolytes
3. Blood Urea, S. Creatinine
4. Coagulation status – BT, CT, Platelet count, FDP, Fibrinogen
5. ECG – to see hyperkalaemia
 Management of Complication:
1. DIC: Fresh blood, clotting factor, Inj. Hydrocortisone
2. Renal Failure: Treatment of renal failure.

39. Blood Substitute
 Def: Are an attractive alternative to costly process of donating, checking, storing
and administrating blood.
 Mechanism: Mimic the standard Oxygen carrying capacity of blood.
 Advantages:
1) Reduce the immunogenic complication
2) Reduce potential infectious complication
 Types:
1) Biomimetic: Haemoglobin based
2) Abiotic: Perfluorocarbon based
Substitute Use
Albumin Severe Hypoalbuminemia
Dextran Hypovolemia, Prevent Thromboembolism
Gelatin Plasma Expander
Hydroxy Ethyl Starches Plasma Expander

40. Stay Safe & Stay Home in this COVID-19 Pandemic