Acute Haemorrhage

Goals of management

Find the bleeding, stop the bleeding. Restore circulating volume while preserving functional blood composition — haemostasis, oxygen-carrying capacity, oncotic pressure, biochemistry.

Critical bleeding is major, life-threatening haemorrhage that may need massive transfusion. Shock here is inadequate perfusion of tissues due to the imbalance between oxygen demand of tissues and the body’s ability to supply it.

Where the blood is

Blunt or penetrating trauma is the most common cause, followed by upper and lower gastrointestinal sources. Obstetric, vascular, iatrogenic and urological sources are all described.

Six regions can account for major blood loss — think SCALPeR:

• Scalp / external sources (especially small children)
• Chest
• Abdomen
• Long bones (especially femurs) — the thigh itself can hold up to 1 L to 2 L of blood
• Pelvis
• Retroperitoneum

Be systematic, and don’t settle for the first bleeding site found (search satisficing).

Recognition

Recognition is the first step, and ideally happens before hypotension develops. Tachycardia is typically the first abnormal vital sign of haemorrhagic shock. Cool extremities and delayed capillary refill signal peripheral vasoconstriction.

Physiology is unreliable as the sole test. Beta blockers blunt the tachycardic response, and a patient with baseline hypertension may be functionally shocked at a systolic of 110mmHg. Haemoglobin is also a poor early marker — it does not fall immediately with acute blood loss.

FAST scanning helps localise bleeding where available, but a negative ultrasound does not rule out intra-abdominal pathology.

Pulse palpation as a rough guide

Traditional ATLS teaching: carotid pulse palpable only means SBP 60–70mmHg; carotid plus femoral means SBP 70–80mmHg; a palpable radial pulse means SBP above 80mmHg.

Classification of haemorrhagic shock

The ATLS classification links the amount of blood loss to expected physiologic responses in a healthy 70kg patient, whose total circulating blood volume is about 5L — roughly 7% of body weight.

	Class 1	Class 2	Class 3	Class 4
Blood loss	≤750mL (≤15%)	750–1500mL (15–30%)	1500–2000mL (30–40%)	over 2000mL (over 40%)
Heart rate	Normal or minimally raised	100–120/min	above 120/min	above 120/min, pronounced
Blood pressure	Normal	Unchanged to slightly decreased	Significant drop	Hypotension
Pulse pressure	Normal	Narrowing	Narrowed	Narrow, under 25mmHg
Respiratory rate	Normal	20–24/min	Significantly raised	Significantly raised
Urine output	over 30mL/h	20–30mL/h	Declining	Minimal or absent
CNS	Slightly anxious	Mildly anxious	Altered mental state	Increasingly altered

Controlling the bleeding

Whenever you think control haemorrhage, also think correct coagulopathy.

• Get help early — surgeon, interventional radiology, anaesthetics, ICU, retrieval.
• Initial measures: direct pressure and elevation; adrenaline-soaked gauze or haemostatic dressings; reduce and splint long bone and pelvic fractures; tourniquets.
• Invasive measures: sutures; tamponade (packing, or a Foley catheter with the balloon inflated); vessel ligation; cautery; interventional radiology; damage control surgery.
• Correct coagulopathy in parallel, not afterwards.

Damage control resuscitation is to occur in conjunction with prompt intervention to control the source of bleeding, and strategies differ with distance from definitive care — relevant to every rural transfer decision.

The lethal triad

Hypothermia, coagulopathy and acidosis both cause and result from acute coagulopathy of trauma. Each worsens the others, so bleeding begets more bleeding.

Coagulopathy is not purely dilutional. A degree of coagulopathy begins in 25% to 56% of patients before initiation of the resuscitation. The activity of coagulation factors, fibrinogen depletion, and platelet quantity are all adversely affected by acidosis. Hypothermia below 34°C compounds coagulopathy by impairing coagulation and is an independent risk factor for death in haemorrhagic shock.

Preventing hypothermia: warmed fluids and blood (rapid infusers with warmers); active warming blankets; minimise exposure; raise ambient temperature; continuous temperature monitoring.

Damage control resuscitation

Three components, run alongside prompt source control:

1. Permissive hypotension — restrict fluid until haemorrhage is controlled, accepting a short period of suboptimal end-organ perfusion rather than inducing re-bleeding from freshly clotted vessels. Not for the patient with head trauma.
2. Haemostatic resuscitation — early blood products in ratios resembling whole blood, instead of large-volume crystalloid.
3. Damage control surgery — limited procedures to stop bleeding and limit contamination, deferring definitive surgery until the triad is corrected.

Resuscitation targets

• MAP 60–65mmHg, or systolic 80–90mmHg, in penetrating trauma.
• MAP above 85mmHg, or systolic above 120mmHg, in blunt trauma with suspected brain or spinal cord injury.
• Fibrinogen 1.5–2 g/L; platelets above 50 × 10⁹/L.
• pH 7.35–7.45; core temperature above 35°C.
• Urine output above 0.5mL/kg/h; lactate under 2mmol/L.

Crystalloid — the older approach, now de-emphasised

Traditional teaching started with 1–2L of crystalloid. For crystalloid resuscitation, normal saline and lactated ringers are the most commonly used fluids. Large volumes cause harm:

• Dilutional coagulopathy.
• Dilutional anaemia and impaired oxygen delivery.
• Hypothermia.
• Hyperchloraemic non-anion-gap acidosis with normal saline.
• Clot dislodgement as blood pressure rises.

Massive transfusion

Classically the administration of 10 units or more of whole blood or packed red blood cells within 24 hours. That figure is arbitrary and delays recognition. Dynamic triggers are more useful: more than 3 to 4 units within 1 hour with ongoing bleeding, or replacing more than 50% of blood volume within 3 hours.

ABC score — one point each for heart rate above 120/min, systolic below 90mmHg, positive FAST, and penetrating torso injury. A score of 2 or more should prompt protocol activation. Other American College of Surgeons activation criteria are persistent haemodynamic instability, active bleeding requiring surgery or angioembolisation, and transfusion given in the trauma bay.

Practical points where the blood bank is off site:

• Notify the blood bank the moment the protocol is activated — early warning is what lets products arrive before they are needed.
• Type O RhD-negative blood is the universal donor. Reserve it for patients of childbearing potential and use O-positive for others if supply is tight.
• Give red cells with plasma and platelets rather than red cells alone. A 1:1:1 ratio of red cells, plasma and platelets is the usual default.
• Warming blood products helps prevent hypothermia.
• Tranexamic acid, particularly when administered within 3 hours of trauma, improves survival.
• One unit of red cells raises haemoglobin by about 10g/L and haematocrit by about 3%.
• Cryoprecipitate is the fibrinogen source — roughly 250mg of fibrinogen per unit, plus factor VIII and von Willebrand factor.
• Recheck FBC with platelets, PT, APTT and fibrinogen after 5 units of red cells, and gases, electrolytes, glucose and lactate every 30 to 60 minutes.

Complications to watch for

• Coagulopathy — from the injury, consumption, dilution and the triad together.
• Hypocalcaemia — citrate in stored products binds ionised calcium, causing paraesthesiae and cardiac dysrhythmias and worsening coagulopathy. Treat symptomatic patients; routine calcium for everyone has no demonstrated benefit.
• Hyperkalaemia — stored red cells leak potassium, and rapid infusion of older units can precipitate arrhythmia.
• Metabolic alkalosis from citrate metabolism, or acidosis from ongoing hypoperfusion.
• Hypothermia — many patients with acute blood loss are susceptible to hypothermia, which can lead to coagulopathy. Cold stored blood held at 4°C lowers core temperature directly.
• TRALI — non-cardiogenic pulmonary oedema, typically within 1 to 2 hours of the transfusion but sometimes delayed up to 6 hours.

Non-fatal complications are observed in over 50% of patients when transfusing more than 5 units of blood products.

Differential in the shocked trauma patient

Haemorrhage is the most common cause of shock in the trauma patient, but other causes of shock remain on the differential.

• Obstructive — tension pneumothorax, cardiac tamponade.
• Neurogenic — head or neck injury, suggested by an inappropriately low heart rate in the setting of hypotension.
• Cardiogenic — cardiac contusion or infarction.
• Non-traumatic — septic and toxic causes in the undifferentiated patient.