Haemorrhage short note
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I now have sufficient material from the textbooks to write a comprehensive short note on Haemorrhage. Let me compile this.
Haemorrhage
Definition
Haemorrhage (from Greek haima = blood, rhegnynai = to burst) is the escape of blood from the vascular system — i.e., bleeding from damaged blood vessels into surrounding tissues, body cavities, or the external environment.
Classification
1. By Source of Vessel
| Type | Source | Features |
|---|---|---|
| Arterial | Artery | Bright red, spurts with pulse, profuse, life-threatening |
| Venous | Vein | Dark red, flows steadily; can be controlled by firm pressure even at high venous pressures (e.g., dialysis patients) |
| Capillary | Capillaries | Slow ooze; usually self-limiting |
2. By Location
- External — blood escapes to outside the body (wound, epistaxis, haematemesis)
- Internal — blood collects within body cavities or tissues:
- Intracavitary: haemothorax, haemoperitoneum, haemopericardium
- Interstitial: haematoma (a localised collection)
3. By Time of Onset (Surgical Classification)
| Type | Timing | Mechanism |
|---|---|---|
| Primary | At time of injury/surgery | Direct vessel damage |
| Reactionary | Within 24 hours (usually 4–6 h) | Slipping of ligature; vasodilation as BP recovers |
| Secondary | 7–14 days post-injury | Vessel wall erosion by infection/sepsis |
4. By Size of Skin/Mucosal Lesion
- Petechiae — pinpoint haemorrhagic macules (< 2 mm); capillary bleeds
- Purpura — larger non-blanching red/purple macules or patches (do not blanch on pressure, as blood has extravasated)
- Ecchymosis — purpuric patch/bruise; may turn yellow-green as haemoglobin degrades
- Haematoma — dermal or subdermal collection of blood forming a palpable swelling
Causes
- Trauma — penetrating or blunt injury (most common)
- Vascular disease — atherosclerotic aneurysm rupture, aortic dissection
- Coagulation disorders — thrombocytopenia, haemophilia, DIC, anticoagulant therapy
- Hypertension — intracerebral haemorrhage
- Infection/Sepsis — vessel wall erosion causing secondary haemorrhage
- Erosion by tumour — invasion of vessel walls
- Iatrogenic — inadvertent arterial puncture during central venous access, surgical complications
Effects & Consequences
Local Effects
- Haematoma formation: clot retraction increases haematocrit and local pressure
- Compression of adjacent structures (e.g., cerebral herniation from intracranial haematoma, cardiac tamponade)
- Ischaemia/necrosis of downstream tissue
Systemic Effects — Haemorrhagic Shock
Blood loss triggers a cascade of compensatory responses:
Compensatory mechanisms (dominant: sympathetic reflex):
- Arteriolar vasoconstriction → ↑ peripheral vascular resistance
- Venoconstriction → ↑ venous return
- ↑ Heart rate and myocardial contractility
Sympathetic reflexes can compensate until 30–40% blood volume is lost; without them (e.g., spinal anaesthesia), only 15–20% loss may be fatal. — Roberts and Hedges' Clinical Procedures in Emergency Medicine
ATLS Classification of Haemorrhagic Shock
| Class | Blood Loss (mL) | Blood Loss (%) | HR | BP | RR | GCS |
|---|---|---|---|---|---|---|
| I | < 750 | < 15% | < 100 | Normal | 14–20 | Normal |
| II | 750–1500 | 15–30% | 100–120 | Normal | 20–30 | Anxious |
| III | 1500–2000 | 30–40% | > 120 | ↓ | 30–40 | Confused |
| IV | > 2000 | > 40% | > 140 | ↓↓ | > 35 | Lethargy/coma |
Clinical signs of shock: pallor, cool clammy skin, tachycardia, hypotension, altered sensorium.
Imaging of Haemorrhage (CT/MRI)
Unenhanced CT:
- Acute haemorrhage appears hyperdense (40–100 HU) relative to brain parenchyma due to clot retraction and high haematocrit in the fibrin-haemoglobin meshwork
- Density decreases by ~1 HU/day as haematoma evolves
MRI (intracranial haematoma stages):
| Stage | Hb State | Signal |
|---|---|---|
| Hyperacute | Oxyhaemoglobin (Fe²⁺, diamagnetic) | T1 iso, T2 bright |
| Acute | Deoxyhaemoglobin (4 unpaired e⁻, paramagnetic) | T1 iso, T2 dark |
| Subacute early | Intracellular methaemoglobin (Fe³⁺) | T1 bright, T2 dark |
| Subacute late | Extracellular methaemoglobin | T1 bright, T2 bright |
| Chronic | Haemosiderin (paramagnetic) | T1/T2 dark rim |
— Grainger & Allison's Diagnostic Radiology
Management Principles
Haemostasis
- Direct pressure — most effective first-line measure for venous bleeding
- Ligature/suture — surgical vessel control
- Thrombin injection into tunnel tracts (for uncontrollable tunnel tract bleeding post-catheter placement)
- Correct coagulopathy — stop anticoagulants, correct platelet count
Resuscitation of Haemorrhagic Shock
- Two large-bore IV lines; send blood for type & crossmatch
- Damage Control Resuscitation:
- Balanced blood products: packed RBCs : FFP : platelets in 1:1:1 ratio
- Permissive hypotension (target SBP 70 mmHg or palpable radial pulse) until definitive haemorrhage control — reduces mortality vs aggressive crystalloid resuscitation
- Tranexamic acid (TXA) — given within 3 hours of injury; reduces mortality from trauma bleeding
- Avoid aggressive crystalloid (causes dilutional coagulopathy, hypothermia, acidosis — the "lethal triad")
- Resuscitation is an adjunct to haemorrhage control, not a substitute — Current Surgical Therapy 14e
Summary
Haemorrhage is a fundamental pathological process with local (compression, ischaemia) and systemic (hypovolaemic shock) consequences. Its severity depends on the rate and volume of blood loss, the vessel involved, and the patient's compensatory reserve. Management requires simultaneous haemorrhage control and goal-directed resuscitation, guided by the ATLS framework.
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