2020B Question 12
Outline the effects of intravenously administering 500mL of 20% mannitol. Outline the potential problems associated with its use.
Examiner Report
The expected domains in the answer were:
- Mechanism of action of mannitol as an osmotic agent (this explanation could have been incorporated within the other domains below, or included under a separate heading)
- Cerebral effects
- Circulatory effects
- Renal effects
- Problems associated with its use (especially cerebral, circulatory and renal)
The intended effects, and associated problems, needed to be addressed appropriately to achieve a pass.
Similar to previous examination reports, confusion appears to have occurred with the phasic nature of the cardiovascular changes, and the mechanism of the diuretic effect. The misconceptions about the mechanism of reducing intracranial pressure were of concern (with many candidates suggesting this was secondary to decreased blood volume). Candidates are reminded to be specific in the description of intracellular, extracellular, intravascular and interstitial fluid in a discussion of osmotic effects. Few candidates described the effects on blood viscosity, and how this might affect cerebral blood flow.
Model Answer
Structure:
- Introduction: Mannitol
- Cerebral
- Circulatory
- Renal
Introduction
| Term | Detail |
|---|---|
| Summary | - Large (182g.mol-1) and polar hence does not cross cell membranes including blood-brain barrier - Substance derived from mannose, a monosaccharide - Uses: Emergency reduction in ICP, osmotic diuresis |
| Numbers | - 20% Mannitol → 200mg/mL –> 1100mOsmol/L (cf. plasma 290mOsmol/L) - 20% 500mL = 550moSmoles |
| Fluid shifts | - Volume expansion phase (VE): ↑ 500mL plasma volume, ↑ plasma osmolality → Contraction of ICF - Volume contraction phase (VC): Osmotic diuresis, ↓ plasma volume |
Renal
| Variable | Detail |
|---|---|
| VE | Direct: - Mannitol freely filtered, not reabsorbed, not secreted - ↑ Tonicity of glomerular filtrate → Impairment of proximal tubular reabsorption (most important effect) - ↑ Renal plasma flow rate, washout of medullary interstitium - ↑ Urine flow rate (osmotic drag) Compensation: - ↑ Na+/K+ exchange in distal nephron due to high flow rate |
| VC | Direct: - ↓ GFR if MAP ≤70 (failed autoregulation) Compensation: - ↑ Na+/K+ exchange in distal nephron: Due to aldosterone |
Circulatory
| Variable | Detail |
|---|---|
| VE | Direct: - ↑ Preload → Risk of APO Compensation: - ANP: ↑ RA stretch → ↑ Release → Diuresis, natriuresis |
| VC | Direct: - ↓ Preload → ↓ CO, ↓ MAP, ↓ Organ perfusion → Lactic acidosis if severe - Vascular irritation Compensation: - RAAS: ↓ MAP → ↑ Renin/angiotensin 2/aldosterone → ↑ Na+ and H2O reabsorption, vasoconstriction - ADH: ↓ Blood volume (if 10%) → ↑ Release → ↑ H2O reabsorption - SNS: ↓ Blood vol → ↑ Release → Vasoconstriction, ↑ CO |
Cerebral
| Variable | Detail |
|---|---|
| VE | - Osmotic dehydration - Hence ↓ brain volume, ↓ ICP |
| VC | - Production of idiogenic osmoles (glycine, glutamine, taurine, inositol etc.) - Hence risk of rebound cerebral oedema |