HAEMORRHAGE

&
BLOOD TRANSFUSION

By;
Col Abrar Hussain Zaidi
 Definitions

Haemorrhage--bleeding
Escape of blood from a blood-vessel

Exsanguination- total loss of blood

Desanguination- major loss of blood

[Encyclopedia Britannica]
 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

 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 [ External vs
Internal]
Intracranial haemorrhages/cva
Upper GIT bleed / haematemesis and melena
Lower GIT Bleeding haemorrhoid/cancers
Chronic wounds
Anal fissures
Aneurysms
 Physiology

• Body’s system of homeostasis

• Integrity of every system
Anatomical
Functional
 Claude Bernard’s
concepts
French physiologist Claude Bernard (1813-
1878), 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]
 What Prevents
Haemorrhage
NATURAL BARRIERS AGAINST
HAEMORRHAGE

• Integrity of vascular wall

• Coagulation system
 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
 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
 Pathological aspects of
Haemorrhage
Bleeding can result due to:
Loss of integrity of wall

trauma/operations
Coagulation defects
Platelet defects or disorders of coagulation factors
Congenital - H.Ph
Aquired - DIC
- Autoimmune disorders
 Etiology Of Haemorrhage-
causes
• 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
 Haemorrhage Types
• MINOR/MAJOR
• ACUTE/CHRONIC
• ARTERIAL/VENOUS/CAPILLARY/MIXED
• LOCALIZED/DIFFUSE
 Haemorrhage Types

Arterial haemorrhage-- bright red colour, escapes

from the end of the vessel nearest the heart in jets
synchronous with the heart's beat

Venous haemorrhage- darker colour - flow is steady,

the bleeding is from the distal end of the vessel .

Capillary haemorrhage - a general oozing from a raw

surface .
 Haemorrhage Types
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
• Subconjunctival hemorrhage .
 Haemorrhage Types
Amount of blood loss

Four classes [American College of Surgeons' Advanced Trauma

Life Support (ATLS)]

Class I Hemorrhage
up to 15% of blood volume. [750mls]
no change in vital signs
fluid resuscitation is not usually necessary.
 Haemorrhage Types
Class II Hemorrhage
15-30% of total blood volume. (750 - 1500mls)
Tachycardic
narrowing 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.
slight changes in behavior.
Volume resuscitation with crystalloids typically required
Saline solution or
Lactated Ringer's solution.
Blood transfusion is not typically required.
 Haemorrhage Types
Class III Hemorrhage
loss of 30-40 (1500 - 2000mls) % of circulating
blood volume.
The patient's blood pressure drops
the heart rate increases,
peripheral perfusion such as capillary refill
worsens, and the mental status worsens.
STATE OF SHOCK
Fluid resuscitation with crystalloid
Blood transfusion are usually necessary.
 Haemorrhage Types
Class IV Hemorrhage

loss of >40% (>2000mls)of circulating blood volume.

The limit of the body's compensation is reached
aggressive resuscitation is required to prevent death.

• Individuals in good physical and cardiovascular shape 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.
 Haemorrhage Types

Haemorrhage has also been classified as—

(1) Primary, occurring at the time of the injury/surgery

(2) Reactionary, or within twenty-four hours of the
accident/operation, 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 .
Effects Of Haemorrhage
Depend upon following:
• The amount of loss
• Acute loss vs Chronic loss
• The compensatory mechanisms
• General state of health
Natural control/arrest of
haemorrhage
Body makes efforts;
To save vital organs on one hand
And tries to minimize the loss +restores the
circulating volume

(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

(4) Compensatory machanisms

 Compensatory
Mechanisms
Acute short term
Neurohumoral
Postural change-fall
Vasoconstriction
Redistribution of circulation to center
Long term
ADH, Aldosteron, Renal mach
Fluid and salt retention
 Management of
haemorrhage
• Prevention
• Emergency measures in trauma
• Precautions during surgery
• Operative method of control of
haemorrhage

• Blood Transfusion
 Management of
haemorrhage

ABCDE of Resuscitation
 Management of
haemorrhage
Surgical treatment of
haemorrhage

General measures
Treat the cause -specific
measures
 Management of
haemorrhage
Think, listen, see, feel, act
• Anticipate a problem
Blunt chest /abdominal injury
A major limb fracture
• Assess expected volume of loss
Haemorrhage has already occurred- injury
Significant haemorrhage is expected-major surgery
 Management of
haemorrhage
General measures

• Early recognition of significant blood loss

• It is commoner to see patients who have been under-

transfused than over-transfused.

• 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.
 Management of
haemorrhage
General measures
• Position
• large-bore intravenous cannulas. Central
venous pressure monitoring is valuable in major
haemorrhage or if there is cardio-respiratory
disease.
• Crystalloids
• 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.
 Management of
haemorrhage
General measures
Transfusion of blood
• Directly from the vein of a healthy person
• Autotransfusion
• Uncross mached o-ve blood
• Grouped blood-Standard practice
In a congenital condition known as haemophylia
it is difficult to stop the flow of blood –Factor viii
In platelet disorders –give platelet concentrates
 Management of
haemorrhage
Specific measures
The surgical treatment of an open wounds

(1) arrest of haemorrhage;

(2) cleansing of the wound and removal of any
foreign bodies;
(3) careful apposition of its edges and surfaces—the
edges being best brought in contact by 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;
(5) avoidance of sepsis;
(6) perfect rest of the part .

Treatment require to be modified for wounds in

special situations
Provide against septic conditions
 Management of
haemorrhage
Specific measures
The surgical treatment of organ injuries

Splenectomy
Resection and repair of Gut
Ectopic pregnancy -surgery
 Management of
haemorrhage
surgical methods of haemorrhage control
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;
Vasoconstrictors, applied locally, Adrenaline
perchloride of iron, tannic acid and others, the most valuable
being suprarenal extract .
Direct Pressure and dressings
must be accurately applied . If the bleeding point cannot be
reached, the
pressure should be applied to the main artery between the
bleeding point and the heart . In small blood-vessels
pressure
will be sufficient to arrest. haemorrhage permanently .
 Management of
haemorrhage
surgical methods of haemorrhage control

Ligature
In large vessels it is usual to pass it round the vessel and
tie it with a reef-knot . Apply the ligature, if possible, at
the bleeding point, tying both ends of the cut vessel . If
this cannot be done, the main artery of the limb must be
exposed by dissection at the most accessible point
between the wound and the heart, and there ligatured .
Sutures
Diathermy
Fibrin glue
 Part 2
Blood transfusion
• Indications
• Blood products
• Grouping and cross match
• Screening
• General technique and Precautions
during transfusion
• Complications of transfusion
Indications for blood transfusion
in surgical practice

• Major Trauma
• Major operative procedures
Pre-op
Per op
Post-op
• Coagulation disorders
 Blood products
Whole blood
can provide improved O2-carrying capacity,
volume expansion, and replacement of clotting
factors and was previously recommended for rapid
massive blood loss
RBCs: Packed RBCs are ordinarily the component of
choice with which to increase Hb. Indications
depend on the patient. O2-carrying capacity may
be adequate with Hb levels as low as 7 g/L in
healthy patients, but transfusion may be indicated
with higher Hb levels in patients with decreased
cardiopulmonary reserve or ongoing bleeding. One
unit of RBCs increases an average adult's Hb by
about 1 g/dL
 Blood products
Fresh frozen plasma:
• Fresh frozen plasma (FFP) is an
unconcentrated source of all clotting
factors without platelets. Indications
include correction of bleeding
secondary to factor deficiencies for
which specific factor replacements are
unavailable, multifactor deficiency
states (eg, massive transfusion,
disseminated intravascular coagulation
[DIC], liver failure), and urgent warfarin
 Blood products
• Cryoprecipitate: Cryoprecipitate is
a concentrate prepared from FFP.
Each concentrate usually contains
about 80 units each of factor VIII
and von Willebrand factor and
about 250 mg of fibrinogen.
 Blood products
WBCs:
• Granulocytes may be transfused
when sepsis occurs in a patient
with profound persistent
neutropenia (WBCs < 500/μL) who
is unresponsive to antibiotics.
 Blood products
Immune globulins:
• Rh immune globulin (RhIg), given IM or
IV, prevents development of maternal
Rh antibodies that can result from
fetomaternal hemorrhage.
• Other immune globulins prophylaxis for patients
exposed to a number of infectious diseases, including
cytomegalovirus, hepatitis A and B, measles, rabies,
respiratory syncytial virus, rubella, tetanus, smallpox,
and varicella (for usage, see under specific disease).
 Blood products
Platelet concentrates:
• Platelet concentrates are used to prevent
bleeding in asymptomatic severe
thrombocytopenia (platelet count <
10,000/μL), for bleeding patients with less
severe thrombocytopenia (platelet count <
50,000/μL), for bleeding patients with platelet
dysfunction due to antiplatelet drugs but with
normal platelet count, for patients receiving
massive transfusion that causes dilutional
thrombocytopenia, and sometimes before
invasive surgery, particularly with
extracorporeal circulation for > 2 h (which
often makes platelets dysfunctional).
 Blood substitutes

Being developed that use inert

chemicals or hemoglobin solutions to
carry and deliver O2 to tissues.
Perfluorocarbons are chemically
and biologically inactive and are
capable of dissolving O2 and CO2
under pressure.
 Grouping and screening

• ABO
• Rh
• Hepatitis
• HIV
 Technique of Transfusion
•
• Caution: Before transfusion is started, the patient's wristband,
blood unit label, and compatibility test report must be checked at the
bedside to ensure that the blood component is the one intended for the
recipient.
• Use of an 18-gauge (or larger) needle A standard filter should
always be used for infusion of any blood component. Only 0.9%
saline IV should be allowed into the blood bag or in the same tubing
with blood.
• Transfusion of 1 unit of blood or blood component should be
completed by 4 h; If transfusion must be given slowly because of
heart failure or hypervolemia,o
• Close observation is important, particularly during the first 15 min,
and includes recording temperature, BP, pulse, and respiratory rate.
Periodic observation continues throughout and after the transfusion,
during which fluid status is assessed. The patient is kept covered and
warm to prevent chills, which may be interpreted as a transfusion
reaction. Elective transfusions at night are discouraged.
Technique of Transfusion

Observe Strict asepsis

 Complications of Transfusion

The most common complications

febrile nonhemolytic and chill-rigor
reactions.
The most serious complications
acute hemolytic reaction due to ABO
incompatible transfusion and transfusion-
related acute lung injury, which have very
high mortality rates.
 Complications of
Transfusion
• Acute hemolytic transfusion reaction
(AHTR )
• Delayed hemolytic transfusion reaction
• Febrile nonhemolytic transfusion reaction
• Allergic reactions
• Graft-vs-host disease (GVHD):
Transfusion-associated GVHD in Transplantation:
usually caused by transfusion of products
containing immunocompetent lymphocytes to an
immunocompromised host.
 Complications of
Transfusion
Complications of massive transfusion
dilutional thrombocytopenia is the most
likely complication. Platelets in stored
whole blood are not functional. Clotting
factors (except factor VIII) usually remain
sufficient. Microvascular bleeding
(abnormal oozing and continued bleeding
from raw and cut surfaces) may result.
Acute lung injury
Hypothermia
Citrate and K toxicities
 Complications of
Transfusion
Infectious complications
Bacterial
Viral
Hepatitis
Cytomegalovirus (CMV)
Parasitic - Malaria
• Stages of Hypovolemic Shock
• 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

• Stage 2
• 15-30% blood volume loss (750 - 1500mls)
• 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

• Stage 3
• 30-40% blood volume loss (1500 - 2000mls)
• 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

• Stage 4
• 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)
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
• Table 3.2. Coagulation cascade
Intrinsic
• Contact Tissue factor + VIIa
• XIa + VIII
Common Pathway
• Xa + V
• IIa
• Clot