1. HAEMORRHAGE & BLOOD TRANSFUSION
By;
Col Abrar Hussain Zaidi

2. SEQUENCE INTRODUCTION importance physiology/homeostasis
integrity of circulatory system
TYPES/CAUSES
CONTROLE METHODS
BLOOD TRANSFUSION

3. INTRODUCTION

4. INTRODUCTION Definitions
Haemorrhage--bleeding
Escape of blood from a blood-vessel
Exsanguination- total loss of blood
Desanguination- major loss of blood
[Encyclopedia Britannica]

5. INTRODUCTION Subject’s importance
Haemorrhage is one of the basic problems and considerations in surgery
From-trivial trauma or major abdominal organ injuries-to- congenital and acquired coagulation disorders
A wide spectrum of problems involves haemorrhage
Transfusion of blood is the main remedy

6. INTRODUCTION Clinical Situation
Trauma /accidents
General operatiove interventions
Gynaecological procedures
Congenital coagulation disorders
Acquired coagulation disorders
Dic
Anticoagulants
Fulminent sepsis
Mof
Common surgical conditions pres w bleed
Intracranial haemorrhages/cva
Upper git bleed/haemetemesis and melena
Bleeding haeorrhoids
Chronic wounds
Anal fissures
Aneurysms

7. INTRODUCTION Physiology
BODY’S SYSTEM OF HOMEOSTSIS
INTEGRITY OF EVERY SYSTEM
ANATOMICAL
FUNCTIONAL

8. INTRODUCTION Claude Bernard’s concepts
French physiologist Claude Bernard ( ), the founder of experimental physiology and experimental pharmacology.
Bernard believed that the body has mechanisms by which it seeks to maintain a stable internal environment despite changes in the external environment- Homeostasis
[ 1851]

9. INTRODUCTION What Prevents Haemorrhage
NATURAL BARRIERS AGAINST HAEMORRHAGE
Integrity of vascular wall
Coagulation system

10. INTRODUCTION Body’s response to haemorrhage/injury
Attempts to repair the loss & restore normality
There are several interrelated stages
Local response / Gen response
Aims at:
wall repair
Restoration of volume loss

11. INTRODUCTION Body’s response to haemorrhage/injury
Virchow 1856 famous triad:
1. Stasis
2. Endothelial damage
3. Hypercoaguable states
local
Vasoconstriction
• Platelet aggregation and plug formation
• Coagulation leading to Fibrin formation –Intrinsic & Extrinsic Paths
General
Compartmental Volume movement

12. PATHOLOGICAL BASIS OF HAEMORRHAGE
BLEEDING CAN RESULT DUE TO:
LOSS OF INTEGRITY OF WALL
TRAUMA/OERATIONS
COAGULATION DEFECTS
CONGENITAL - H.PH
AQUIRED DIC

13. ETIOLOGY OF HAEMORRHAGE CAUSES OF HAEMORRHAGE
INJURY /TRAUMA [+ operations]-It commonly results in
tearing or cutting of a blood-vessel-integrity of
wall breached Trivial OR Major
DISEASES that alter coagulation
Congenital –platelet defects
Coagulation factor defects
Acquired
scurvy
Sepsis
DIC

14. TYPES OF HAEMORRHAGE AMOUNT OF LOSS --MINOR/MAJOR ACUTE/CHRONIC
ARTERIAL/VENOUS/CAPILLARY/MIXED
LOCALIZED/DIFFUSE
EXTERNAL/ INTERNAL
OVERT/OCCULT

15. TYPES OF HAEMORRHAGE
Bleeding from an artery is of a bright red colour, and escapes from the end of the vessel nearest the heart in jets synchronous with the heart's beat
Bleeding from a vein is of a darker colour; the flow is steady, the bleeding is from the distal end of the vessel .
Capillary bleeding is a general oozing from a raw surface .

16. TYPES OF HAEMORRHAGE SPECIFIC TYPES Bruise or ecchymosis .
Extravasation of blood /pouring out of blood
into the areolar tissues, which become boggy
Haematemesis and melena
Haemoptysis .
Haematuria
Epistaxis

17. TYPES OF HAEMORRHAGE CLASSIFICATION OF SURGICAL HAEMORRHAGE
Haemorrhage has been classified as—
1-Primary, occurring at the time of the injury
2-Reactionary, or within twenty-four hours of the accident, during the stage of reaction
3-Secondary, occurring at a later period and caused by faulty application of a ligature or septic condition of the wound . In severe haemorrhage, as from the division of a large artery, the patient may collapse and death ensue from syncope .

18. Hemorrhage -four classes American College of Surgeons' Advanced Trauma Life Support (ATLS)
Class I Hemorrhage involves up to 15% of blood volume. There is typically no change in vital signs and fluid resuscitation is not usually necessary.
Class II Hemorrhage involves 15-30% of total blood volume. A patient is often tachycardic (rapid heart beat) with a narrowing of the difference between the systolic and diastolic blood pressures. The body attempts to compensate with peripheral vasoconstriction. Skin may start to look pale and be cool to the touch. The patient may exhibit slight changes in behavior. Volume resuscitation with crystalloids (Saline solution or Lactated Ringer's solution) is all that is typically required. Blood transfusion is not typically required.

19. Hemorrhage -four classes American College of Surgeons' Advanced Trauma Life Support (ATLS
Class III Hemorrhage
involves loss of 30-40% of circulating blood volume.
blood pressure drops, the heart rate increases, peripheral perfusion (shock), such as capillary refill worsens, and the mental status worsens. Fluid resuscitation with crystalloid and blood transfusion are usually necessary.
Class IV Hemorrhage involves loss of >40% of circulating blood volume. The limit of the body's compensation is reached and aggressive resuscitation is required to prevent death.

20. NB
Fit Individuals may have more effective compensatory mechanisms before experiencing cardiovascular collapse.
These patients may look deceptively stable, with minimal derangements in vital signs, while having poor peripheral perfusion.
Elderly patients or those with chronic medical conditions may have less tolerance to blood loss, less ability to compensate, and may take medications such as betablockers that can potentially blunt the cardiovascular response. Care must be taken in the assessment of these patients.

21. EFFECTS OF HAEMORRHAGE
Depend upon following:
Acute loss vs Chronic loss
The amount of loss
The compensatory mechanisms
General state of health

22. EFFECTS OF HAEMORRHAGE
Depends upon the amount of blood loss
Stages of Hypovolemia
Stage 1
Up to 15% blood volume loss (750mls)
Compensated by constriction of vascular bed
Blood pressure maintained
Normal respiratory rate
Pallor of the skin
Slight anxiety

23. EFFECTS OF HAEMORRHAGE
Stage 2
15-30% blood volume loss ( mls)
Cardiac output cannot be maintained by arterial constriction
Tachycardia >100bpm
Increased respiratory rate
Blood pressure maintained
Increased diastolic pressure
Narrow pulse pressure
Sweating from sympathetic stimulation
Mildly anxious/Restless

24. EFFECTS OF HAEMORRHAGE
Stage 3
30-40% blood volume loss ( mls)
Systolic BP falls to 100mmHg or less
Classic signs of hypovolemic shock
Marked tachycardia >120 bpm
Marked tachypnoea >30 bpm
Decreased systolic pressure
Alteration in mental status (Anxiety, Agitation)
Sweating with cool, pale skin

25. EFFECTS OF HAEMORRHAGE
Stage Shock
Loss greater than 40% (>2000mls)
Extreme tachycardia with weak pulse
Pronounced tachypnoea
Significantly decreased systolic blood pressure of 70 mmHg or less
Decreased level of consciousness
Skin is sweaty, cool, and extremely pale (moribund)

26. MANAGEMENT OF HAEMORRHAGE
Prevention
Precautions during surgery
Operative method of control of
haemorrhage
Blood Transfusion

27. SURGICAL HAEMOSTASIS
NATURAL OR ARTIFICIAL
Natural CONTROLE/arrest of haemorrhage arises from ;
(1) the coagulation of the blood itself,
(2) the diminution of the heart's action as in fainting,
(3) changes taking place in the cut vessel causing its retraction and contraction .

28. SURGICAL HAEMOSTASIS EXTERNAL HAEMORRHAGE /WOUNDS
The surgical procedure for the treatment of an open wound is-
(1) arrest of haemorrhage;
(2) cleansing of the wound and removal of any foreign bodies;
(3) careful apposition of its edges and surfaces— sutures of aseptic silk or catgut, the surfaces by carefully applied pressure;
(4) free drainage, if necessary, to prevent accumulation either of blood or serous effusion;
(S) avoidance of sepsis;
(6) perfect rest of the part .

29. SURGICAL HAEMOSTASIS Surgical treatment of haemorrhage
minor means of arresting bleeding are:
cold, which is most valuable in general oozing and local extravasations;
very hot water, 130° to 16o F., a powerful haemostatic; position, such as elevation of the limb, valuable in bleeding from the extremities;
styptics or astringents, applied locally, as perchloride of iron, tannic acid and others, the most valuable being suprarenal extract .

30. SURGICAL HAEMOSTASIS Surgical treatment of haemorrhage DIRECT PRESSURE
In small blood-vessels pressure will be sufficient to arrest. haemorrhage permanently .
LIGATURE
In large vessels with a reef-knot
main artery of the limb exposed by dissection at the most accessible point .

31. SURGICAL HAEMOSTASIS Diathermy Sutures Harmonic devices
Surgical treatment of haemorrhage
Diathermy
Sutures
Harmonic devices

32. TRANSFUSION MANAGEMENT
Early recognition of significant blood loss
it is commoner to see patients who have been under-transfused than over-transfused. I
t is essential to pay attention to and act on recordings of pulse rate and blood pressure.
In a fit patient without cardiac disease, persistent tachycardia − even if blood pressure is maintained − is likely to indicate continuing blood loss.

33. SURGICAL HAEMOSTASIS INTERNAL HAEMORRHAGE /WOUNDS
Causes
Penetrating wounds
chest,abdomen,neck,limbs
Upper GI haemorrhage
BleedingUlcers
Lower GI haemorrhage
Diverticulosis
Haemorrhoids
Carcinomas

34. SURGICAL HAEMOSTASIS INTERNAL HAEMORRHAGE /WOUNDS
Principles of management
Teat the primary cause
Avoid irrevercible shock
Flid electrolytes
Blood and blood produvts

35. Types of bleeding
A subconjunctival hemorrhage is a common and relatively minor post-LASIK complication.
The endoscopic image of linitis plastica, a type of stomach cancer leading to a leather bottle-like appearance with blood coming out of it.

36. RESPONSE IN INJURY
Vasoconstriction is mediated through intrinsic mechanisms and various vasoactive agents (thromboxane A2 and serotonin) released during platelet aggregation.
COAGULATION SYSTEM
Virchow in 1856 described the famous triad:
1. Stasis
2. Endothelial damage
3. Hypercoaguable states
The coagulation system is based on the coagulation cascade. The end points of this cascade include the formation of thrombin and fibrin.
Throughout this system there can be defects in the multiple enzymes or extrinsic factors contributing to its dysfunction.
Fibrinolysis
There is a delicate balance between formation and lysis of clot.
Lysis of fibrindeposits is mediated by antithrombin III, protein C and S and plasmin. Antithrombin II as the name suggests blocks thrombin. When combined with heparin it also blocks factors XII, XI, IX and X (intrinsic pathway).
Tests used to measure fibrinolysis include fibrin degradation products (FDB),fibrinogen, d-dimer
In DIC –the FDP’s are raised
I Fibrinogen
II Prothrombin
III Tissue thromboplastin
IV Calcium
V Proaccelerin VI
VII Proconnectin
VIII Antihemophilic factor
IX Christmas factor
X Stuart-Prower factor
XI Plasma thromboplastin
XII Hageman factor
XIII Fibrin stabilizing factor

37. Transfusion management
All patients require large-bore intravenous cannulas. Central venous pressure monitoring is valuable in major haemorrhage or if there is cardio-respiratory disease.
Haemoglobin concentration − interpretation
The haemoglobin can underestimate the extent of blood loss in cases of acute haemorrhage before haemodilution has occurred, or can overestimate it if the patient is already anaemic from chronic blood loss.

38. Table 3.2. Coagulation cascade
Intrinsic
Contact Tissue factor + VIIa
XIa + VIII
Common Pathway
Xa + V
IIa
Clot

39. Gastrointestinal haemorrhage: haematemesis and melaena
Haematemesis: vomiting fresh red blood.
Coffee-ground vomiting: vomiting of altered black blood.
Melaena: the passage of black tarry stools.
Bleeding may be from oesophageal varices or from other sites (non-variceal bleeding).
Acute upper gastrointestinal (GI) bleeding affects 50 to 150 per 100,000 of the population each year and accounts for a substantial proportion of all blood used in UK hospitals. In the UK in 1995, mortality was reported to be 11% in patients admitted to hospital because of bleeding and 33% in those who developed gastrointestinal bleeding while hospitalised for other reasons. In the west of Scotland in 1997, the corresponding figures were 8.2% and 43%. Most deaths are in elderly patients with significant co-morbidity. Mortality is reported to be lower in specialist units where there is close medical/surgical/endoscopic cooperation and adherence to management protocols. This section is intended only to give an overview of transfusion, which is just one part of the overall management of patients with GI haemorrhage (Tables 10 and 11).(PMID )(PMID )(PMID )(PMID )(PMID )
Table 10 Use of fluids and transfusion in GI bleeding in chronic liver disease (with variceal bleeding)
Features
Transfusion management
End points
Bleeding is often but not always from oesophageal varices and is often severe. Other causes such as peptic ulcer are not uncommon and must be excluded.
Bleeding from varices usually recurs if there is no intervention to control the varices or to reduce portal pressure. The prognosis depends on the severity of the liver disease.
Hepatic failure may follow variceal bleeding, but usually recovers if bleeding can be stopped and recurrence prevented.¹
Insert one or two large bore cannulas. A central line may be indicated.
Ensure red cells are available quickly; use local emergency transfusion protocol: order 4−6 units.
Crystalloids should be used carefully. Saline should be avoided as sodium retention is usual and leads to ascites.
Systolic pressure
> 100 mmHg
Urine output > 40 ml/hr
CVP 0−5 mmHg
(not higher)
Haemoglobin up to 90 g/l
Thrombocytopenia is usual. Provided the platelet count is above 50 x 109/l, bleeding is unlikely to be controlled or prevented by platelet transfusion.
Normal (i.e. pre-bleed) systolic blood pressure is often lower than in non-cirrhotic patients.
Platelet transfusion is rarely needed. If there is continued bleeding with a platelet count below 50 x 109/l, platelet transfusion may be considered in an effort to control variceal bleeding.
Platelet count may show little increment following platelet transfusion in patients with splenomegaly.
Deficiency of coagulation factors is frequent (except fibrinogen and factor VIII).
Coagulation factor concentrates may be indicated. Seek expert advice as some of the products have a risk of thrombogenicity, especially in patients with liver disease.
Fresh frozen plasma is indicated only if there is documented coagulopathy, e.g. INR >2.0.
Keep INR < 2.0 if possible. Complete correction is rarely possible with FFP due to the large volume needed.
Giving red cells to try to raise Hb towards normal values may raise portal venous pressure, since blood volume is often increased. Over-transfusion may contribute to rebleeding.
Provided blood volume is replaced and cardio-respiratory function was previously adequate, haemoglobin of 90 g/l appears to be adequate.
Transfuse red cells to approach but not exceed end point of 90 g/l.
Note:
This table is based on the protocol used by the Gastrointestinal Bleeding Unit, Royal Infirmary, Aberdeen. (PMID )
[Table 10 resources: View large format or download as Word™ document]
Table 11 Use of fluids and blood components in acute non-variceal gastrointestinal bleeding
Severity
Clinical features
IV infusion
End point
Severe
History of collapse
and/or shock
− systolic BP < 100 mmHg
− pulse > 100/min
Replace fluid rapidly
Ensure red cells are available quickly; use local emergency transfusion protocol
Transfuse red cells according to clinical assessment and Hb/Hct
Maintain
urine output > 40 ml/hour
systolic BP > 100 mmHg
haemoglobin > 90 g/l
Significant
Resting pulse > 100/min
and/or
haemoglobin < 100 g/l
Replacement fluid
Order compatible red cells (four units)
Trivial
Pulse and haemoglobin normal
Maintain intravenous access until diagnosis is clear
Send patient sample for red cell group and antibody screen
Recheck haemoglobin at 24 hours to reassess blood loss
No evidence of bleeding
May have 'coffee
grounds' or altered blood in vomitus. Faecal occult blood negative.
[Table 11 resources: View large format or download as Word™ document]
Early recognition of significant blood loss is important. In clinical practice, it is commoner to see patients who have been under-transfused than over-transfused. It is essential to pay attention to and act on recordings of pulse rate and blood pressure. In a fit patient without cardiac disease, persistent tachycardia − even if blood pressure is maintained − is likely to indicate continuing blood loss.
All patients require large-bore intravenous cannulas. Central venous pressure monitoring is valuable in major haemorrhage or if there is cardio-respiratory disease.
Haemoglobin concentration − interpretation
The haemoglobin can underestimate the extent of blood loss in cases of acute haemorrhage before haemodilution has occurred, or can overestimate it if the patient is already anaemic from chronic blood loss.
If liver disease is suspected (e.g. oesophageal varices)
The platelet count and prothrombin time should be checked and correction with blood components may be indicated. It is not necessary to check clotting screen routinely in every case of GI haemorrhage.
Guidelines for management can be found at the BSG website:
Management of upper GI bleeding and
Management of bleeding in patients with oesophageal varices