Case: Haemorrhage

Haemorrhage — the loss of blood from the vascular compartment — is a life-threatening emergency. When a patient is vomiting blood, this is clinically serious for two reasons: it indicates internal bleeding somewhere along the gastrointestinal tract, and if erosion is sufficient to damage a major vessel, bleeding is difficult to control. Furthermore, significant fluid and blood loss collapses peripheral veins, making intravenous access difficult.

Understanding where body fluids are distributed is essential for managing haemorrhage. Total body water (TBW) is estimated as 0.6 × weight (kg) in males and 0.55 × weight (kg) in females. For a 70 kg male: TBW = 42 L. Two-thirds of TBW (28 L) is intracellular fluid (ICF). One-third (14 L) is extracellular fluid (ECF). Of the ECF, one-fifth is plasma (2.8 L) and four-fifths is interstitial fluid (11.2 L). It is the plasma compartment that is directly lost in haemorrhage.

Fluid movement between the vascular and interstitial compartments is governed by Starling's Equilibrium. At the arterial end of capillaries, hydrostatic pressure (HP) exceeds colloid osmotic pressure (COP), so fluid moves out. At the venous end, COP exceeds HP, so fluid moves back in. The difference drains into the lymphatic system. Albumin is the main protein contributing to COP.

Under normal conditions, these forces are balanced. After blood loss, arterial hydrostatic pressure falls significantly. The net effect is that HP at the venous end may now be less than COP across the capillary, promoting reabsorption of interstitial fluid into the bloodstream — this is autotransfusion. Clinically, this manifests as shrunken tissues: sunken eyes, dry tongue, reduced skin elasticity.

In heart failure, venous hydrostatic pressure rises (from increased venous backpressure), pushing fluid into the interstitium at both ends of capillaries → oedema. In malnutrition (reduced COP), HP exceeds COP even at the venous end → oedema.

The long-term response to haemorrhage involves RAAS activation: decreased renal perfusion triggers renin release, ultimately increasing sodium reabsorption in the kidney and retaining water with it. Combined with ADH, this expands plasma volume over hours to days.