Surgery chapters
Haemorrhage, blood transfusion and its complications
Types and classes of haemorrhage, the lethal triad and damage control, blood products with their storage and uses, transfusion triggers, cross-matching, and the complications of single and massive transfusion.
- Blood volume is about 70 mL/kg (5 L in an adult); ATLS classes I–IV are <15%, 15–30%, 31–40% and >40% loss, and systolic BP reliably falls from class III.
- Stop the bleeding; avoid the lethal triad (coagulopathy, acidosis, hypothermia) with damage control resuscitation: permissive hypotension, little crystalloid, 1:1:1 products, tranexamic acid within 3 h.
- Know product storage (red cells 2–6°C, platelets 20–24°C for 5 days, FFP frozen), the Hb trigger (below 6–8 g/dL), and complications such as ABO haemolysis, TRALI and hypocalcaemia, hyperkalaemia, hypothermia after massive transfusion.
On this page
Overview
Haemorrhage is the acute loss of circulating blood and the commonest cause of shock after injury. It is treated by stopping the bleeding, not by fluid or blood alone. Fluids and blood keep organs perfused until control is achieved; trying to resuscitate a patient who keeps bleeding leads to the lethal triad and death.
Blood transfusion saves lives but carries immunological, infective and metabolic risks, and supplies are limited, so it must be used for a clear clinical need. The shock chapter covers fluid challenge, monitoring and end points.
Types of haemorrhage
Revealed and concealed
- Revealed: visible external bleeding (open arterial wound, haematemesis).
- Concealed: inside the body, must be actively looked for: chest, abdomen, pelvis, retroperitoneum, long-bone fractures ("blood on the floor and four more"); also ruptured aortic aneurysm, occult GI bleeding.
Timing
| Type | When | Cause |
|---|---|---|
| Primary | At the time of injury or operation | Direct vessel damage |
| Reactionary | Within 24 hours | Clot dislodged as BP rises and vessels dilate after resuscitation; slipped ligature |
| Secondary | 7–14 days | Sloughing of the vessel wall from infection, pressure necrosis (e.g. from a drain) or malignancy |
Surgical and non-surgical
- Surgical: from a specific injured vessel; controlled by operation, ligation or angioembolisation.
- Non-surgical: generalised ooze from coagulopathy; needs correction of clotting (packing may help).
Reactionary = Recent (first day); Secondary = Sepsis (second week).
Estimating blood loss
- Adult blood volume is about 7% of body weight (70 mL/kg), about 5 litres in a 70 kg adult; children 80 mL/kg (ATLS gives 70–80 mL/kg).
- Visual estimation usually underestimates loss; in theatre, measure suction and weigh swabs.
- Haemoglobin is a poor early guide: whole blood is lost, so the concentration is initially normal and falls only as fluid shifts into vessels.
ATLS classes of haemorrhage
| Feature | Class I | Class II | Class III | Class IV |
|---|---|---|---|---|
| Severity label | - | Mild | Moderate | Severe |
| Approximate % of volume lost | <15% | 15–30% | 31–40% | >40% |
| Pulse | Normal | Normal/raised | Raised | Raised/greatly raised |
| Blood pressure | Normal | Normal | Normal/falls | Low |
| Pulse pressure | Normal | Reduced | Reduced | Reduced |
| Respiratory rate | Normal | Normal | Normal/raised | Raised |
| Urine output | Normal | Normal | Reduced | Very low |
| GCS | Normal | Normal | Reduced | Reduced |
| Base deficit (mEq/L) | 0 to −2 | −2 to −6 | −6 to −10 | −10 or worse |
| Blood products | Monitor | Possibly | Yes | Massive transfusion protocol |
- Class I: like donating a unit of blood; refills itself within 24 hours.
- Class II: tachycardia, tachypnoea, narrow pulse pressure (diastolic rises from catecholamines), anxiety; urine about 20–30 mL/h; most settle with crystalloid.
- Class III: the least loss that consistently lowers systolic BP; needs blood and haemorrhage control.
- Class IV: pre-terminal; very narrow or unrecordable diastolic, cold pale skin, negligible urine; immediate transfusion and surgery.
In class II the pulse pressure narrows before systolic BP falls. Of all the signs of haemorrhagic shock, falling blood pressure appears last.
70 kg adult: blood volume = 70 × 70 = 4,900 mL (about 5 L)
Estimated loss 1,750 mL → 1,750 ÷ 4,900 = 0.357 → about 36%
36% lies in 31–40% → Class III: expect a fall in systolic BP; give blood
The lethal triad and acute traumatic coagulopathy
- Tissue injury plus shock causes acute traumatic coagulopathy within minutes in up to about a quarter of trauma patients, with roughly fourfold mortality.
- Dilution of clotting factors by fluids and red cells worsens it.
- Acidosis impairs clotting enzymes.
- Hypothermia: underperfused muscle makes less heat; cold fluids and open cavities add to it; cold blood clots poorly.
- These feed each other: coagulopathy–acidosis–hypothermia spiral to death.
0.9% saline is itself acidic (pH about 6.7) and large volumes add to acidosis. Warm all fluids (ATLS: crystalloid warmed to 39°C); use blood warmers.
Management of haemorrhage
- Direct pressure on external bleeding (scalp wounds bleed briskly: firm pressure, then suture full thickness).
- Airway and breathing; two large-bore cannulas; send blood for cross-match; request emergency blood if needed.
- Find the site: rapid bedside tests (chest and pelvic X-ray, FAST ultrasound) in unstable patients; CT only if stable.
- Move rapidly to haemorrhage control: theatre, angiography (embolisation) or endoscopy. Avoid unnecessary tests or prolonged resuscitation before control.
- Initial fluid (ATLS): warmed isotonic crystalloid, 1 litre in adults, 20 mL/kg in children under 40 kg, then judge the response. More than about 1.5 L of crystalloid has been linked with higher mortality.
Damage control resuscitation (DCR)
| Strategy | Detail |
|---|---|
| Treat coagulopathy early | Balanced products, tranexamic acid |
| Permissive (hypotensive) resuscitation | Accept a lower BP until bleeding is controlled (not in traumatic brain injury, where hypotension must be avoided) |
| Limit crystalloid and colloid | Prevent dilutional coagulopathy |
| Damage control surgery | Stop bleeding and contamination only; definitive repair later once warm, not acidotic and not coagulopathic |
Damage control surgery does four things: stop bleeding, control contamination, protect from further injury, nothing else.
Massive transfusion
- Defined (ATLS) as over 10 units of red cells in the first 24 hours, or over 4 units within an hour.
- Massive transfusion protocol: red cells, FFP and platelets in a 1:1:1 ratio.
- Monitor clotting with laboratory tests or point-of-care thromboelastography (TEG/ROTEM).
- Tranexamic acid (antifibrinolytic): most benefit if given within 3 hours of injury; 1 g over 10 minutes then 1 g over 8 hours.
Blood and blood products
Donated blood (up to 450 mL) is tested for hepatitis B, hepatitis C, HIV-1/2 and syphilis, ABO and RhD typed and screened for irregular antibodies; in the UK it is leukodepleted (reducing vCJD risk and febrile reactions).
| Product | Storage | Shelf life | Main use |
|---|---|---|---|
| Whole blood | 2–6°C | Weeks | Rarely used in civilian practice; rich in clotting factors when fresh |
| Packed red cells (about 330 mL, haematocrit 50–70%) | 2–6°C in SAG-M | 5 weeks (CPD: 2–3 weeks) | Anaemia, blood loss |
| Fresh frozen plasma | −40 to −50°C | 2 years | Coagulopathic bleeding; all clotting factors |
| Cryoprecipitate | −30°C | 2 years | Fibrinogen and factor VIII (low fibrinogen, DIC, haemophilia A) |
| Platelets (pooled) | 20–24°C on an agitator | 5 days | Thrombocytopenia or platelet dysfunction with bleeding or surgery |
| Prothrombin complex concentrate | Pooled plasma concentrate | - | Factors II, IX, X (± VII): emergency warfarin reversal |
Platelets are the only component kept at room temperature; this is why they carry the highest risk of bacterial contamination.
- Patients on clopidogrel may need repeated platelet transfusion during major surgery; aspirin rarely causes a problem. DDAVP has been tried.
- Autologous blood: pre-donation up to 3 weeks before elective surgery, or intra-operative cell saver (washes and returns red cells; avoid in contaminated or malignant fields).
Indications and transfusion trigger
- Acute blood loss; perioperative anaemia; symptomatic chronic anaemia.
| Haemoglobin (g/dL) | Guidance |
|---|---|
| Below 6 | Probably benefits from transfusion |
| 6–8 | Unlikely to benefit unless bleeding or surgery is imminent |
| Above 8 | No indication without other risk factors |
Old targets of Hb above 10 g/dL increased complications and are no longer used.
ABO incompatibility is the most dangerous acute reaction and is almost always due to a wrong-patient or wrong-unit error, so careful bedside identity checks are the main prevention.
Blood groups and cross-matching
| Group | Red cell antigen | Plasma antibodies |
|---|---|---|
| O | None (A and B absent) | Anti-A and anti-B |
| A | A | Anti-B |
| B | B | Anti-A |
| AB | A and B | None |
- Group O = universal red cell donor; AB = universal recipient.
- RhD is present in about 85% of the UK population; anti-D is not naturally present but forms after Rh-positive transfusion or pregnancy and can cause haemolytic disease of the fetus and newborn (hydrops fetalis).
- Full cross-match: up to 45 minutes. Type-specific (ABO/Rh matched only): 10–15 minutes. Emergency group O: immediately (O negative for females of childbearing age, O positive acceptable for males). Switch to type-specific blood as soon as possible.
- Two staff check patient identity, prescription, label and unit number at the bedside.
Complications of transfusion
From a single transfusion
| Complication | Key points |
|---|---|
| Acute haemolytic (ABO incompatibility) | Complement-mediated intravascular haemolysis: fever, loin pain, hypotension, haemoglobinuria, DIC, renal failure. Usually from wrong patient/wrong unit errors. Stop at once, keep line open with saline, supportive care |
| Febrile non-haemolytic | Donor white cell antibodies; fever and rigors; stop the transfusion; rarer with leukodepleted blood |
| Allergic/anaphylactic | Urticaria to anaphylaxis (plasma proteins; IgA-deficient recipients) |
| TRALI (transfusion-related acute lung injury) | Acute non-cardiogenic pulmonary oedema within hours, usually from FFP (plasma-rich products) |
| Circulatory overload (TACO) | Elderly and cardiac patients; raised venous pressure; slow rate and diuretic |
| Infection | Bacterial (faulty storage, platelets), hepatitis B and C, HIV, malaria, syphilis |
| Others | Air embolism, thrombophlebitis, delayed haemolysis, graft-versus-host disease (prevented by irradiated products in the immunocompromised) |
From massive transfusion
| Complication | Why |
|---|---|
| Coagulopathy | Stored red cells lack clotting factors and platelets (dilution) |
| Hypocalcaemia | Citrate anticoagulant binds calcium → perioral tingling, carpopedal spasm, Chvostek sign, arrhythmia. Treat with IV calcium guided by ionised calcium |
| Hyperkalaemia | K+ leaks from stored red cells |
| Hypokalaemia | Later, as cells take K+ back up and citrate is metabolised to bicarbonate |
| Hypothermia | Cold blood (use warmers) |
| Acid–base change, reduced 2,3-DPG | Stored blood releases oxygen less readily |
Repeated transfusion over years (e.g. thalassaemia) causes iron overload: each red cell unit carries about 250 mg iron.
In a patient bleeding from wounds and drains after many units of blood, think of dilutional coagulopathy and platelet deficiency (and hypothermia) before a surgical bleed; give FFP, platelets and cryoprecipitate guided by tests.
Blood substitutes
Haemoglobin-based (human, bovine, recombinant) and perfluorocarbon-based oxygen carriers remain experimental.
Expect: ATLS haemorrhage classes and which sign fails first or last; primary, reactionary and secondary haemorrhage with timing; the lethal triad and damage control resuscitation; massive transfusion definition and 1:1:1 ratio; tranexamic acid timing; storage temperature and shelf life of each product; uses of cryoprecipitate, FFP and prothrombin complex; Hb transfusion trigger; universal donor and emergency O negative blood; cross-match times; ABO haemolytic reaction from clerical error; TRALI with FFP; and citrate hypocalcaemia, hyperkalaemia and hypothermia after massive transfusion.
Quick revision
- Blood volume 70 mL/kg; classes I–IV: <15, 15–30, 31–40, >40%.
- Narrow pulse pressure in class II; BP falls from class III.
- Reactionary within 24 h; secondary at 7–14 days from infection.
- Lethal triad: coagulopathy, acidosis, hypothermia → damage control.
- Permissive hypotension (not in head injury), limit crystalloid, 1:1:1, TXA within 3 h.
- Red cells 2–6°C for 5 weeks; platelets 20–24°C for 5 days; FFP and cryo frozen for 2 years.
- Cryo = fibrinogen and factor VIII; PCC = warfarin reversal.
- Transfuse below Hb 6–8 g/dL depending on bleeding and risk.
- ABO haemolysis = clerical error; TRALI = FFP; tetany after massive transfusion = citrate → IV calcium.
Written by The House Job from standard references (Bailey & Love's Short Practice of Surgery, 27th edition; ATLS Student Course Manual, 10th edition).
FAQ
What is reactionary haemorrhage?
Bleeding within the first 24 hours after injury or surgery, usually as blood pressure recovers and dislodges a clot or a ligature slips.
Why are platelets not kept in a fridge?
Cold damages platelet function, so they are stored at 20–24°C with constant agitation, which limits their shelf life to 5 days and raises bacterial risk.
Which blood should be given when there is no time to cross-match?
Group O red cells, O negative for girls and women of childbearing age, switching to type-specific blood as soon as it is ready.
Why does tetany occur after massive transfusion?
Citrate in stored blood binds ionised calcium, and the resulting hypocalcaemia is treated with intravenous calcium.
Is haemoglobin a good guide to acute blood loss?
No; it stays near normal at first because whole blood is lost, and falls only after fluid shifts or crystalloid dilute the blood.