Haemorrhage & Blood Transfusion

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 stateslocal• Vasoconstriction• Platelet aggregation and plug formation• Coagulation leading to Fibrin formation –

Intrinsic & Extrinsic PathsGeneral• 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 TypesClass 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 TypesClass 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

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

Natural control/arrest of haemorrhage

Compensatory Mechanisms

Acute short term Neurohumoral Postural change-fall Vasoconstriction Redistribution of circulation to centerLong 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


ABCDE of Resuscitation


Surgical treatment of haemorrhage

General measures Treat the cause -specific

measures


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


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.


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


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


Specific measures The surgical treatment of organ injuries Splenectomy Resection and repair of Gut Ectopic pregnancy -surgery


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 .


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 transfusionin 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.


• 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 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


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 cascadeIntrinsic• Contact Tissue factor + VIIa• XIa + VIII Common Pathway• Xa + V• IIa• Clot

• 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).(PMID9329304)(PMID2351300)(PMID8912283)(PMID15254304)(PMID7627034)

• 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. (PMID8912283)

• [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)• Maintain • haemoglobin > 90 g/l

• 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.• •

• Note:

• This table is based on the protocol used by the Gastrointestinal Bleeding Unit, Royal Infirmary, Aberdeen. (PMID8912283)

• [Table 11 resources: View large format or download as Word™ document]

• Transfusion management

• 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

Haemorrhage & Blood Transfusion

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