Pharmacology — Fluids, Electrolytes and Transfusion, NMC MBBS licence examination syllabus (Nepal Medical Council).
Fluids, electrolytes and transfusion
The most commonly prescribed drug in a hospital, and the one prescribed with least thought.
Intravenous fluid is prescribed more often than almost anything else, frequently by the most junior member of the team, and frequently without a clear reason. It is worth treating as a drug: it has indications, a dose, a duration, contraindications, and the capacity to cause serious harm. Patients are injured by too much fluid as reliably as by too little — pulmonary oedema, tissue oedema that impairs wound healing, and prolonged ileus are all consequences of an unreviewed drip.
The same applies to blood. Transfusion saves lives and carries real risks, and the commonest fatal transfusion error is not immunological at all — it is giving the right blood to the wrong patient.
🩺 Where this lives: The most dangerous transfusion error is clerical. ABO-incompatible transfusion, which can kill within minutes, almost always results from a failure of identification — a mislabelled sample, a form filled in away from the bedside, or a unit checked against the wrong patient. That is why the bedside identity check is not a bureaucratic formality but the single point at which the error can still be caught. In busy or under-staffed settings, where blood may be collected and administered in a hurry, this is precisely where the system is most likely to fail.
💡 A note on numbers. This chapter gives no doses, bolus volumes, maintenance rates, electrolyte reference ranges, sodium correction limits or transfusion thresholds. These are weight-based, age-specific and protocol-specific, and several of them — sodium correction rate and potassium administration above all — can kill if wrong. Learn the direction and the mechanism here; take every figure from your local protocol. Acid-base interpretation is in its own chapter, DKA fluids in the DKA chapter, childhood dehydration in the Sick Child chapter, and fluid caution in severe malnutrition in the Nutrition chapter.
Three questions before prescribing
The three purposes are genuinely different and are routinely conflated. Resuscitation means rapidly restoring circulating volume in a shocked patient. Replacement means matching ongoing losses — vomit, diarrhoea, drain output, fever. Maintenance means supplying daily water and electrolyte requirements for someone who cannot drink. Prescribing a maintenance regimen to a shocked patient, or continuing resuscitation-rate fluid into a stable one, are both common and both harmful.
Which fluid
WHY 5% DEXTROSE WILL NOT RESUSCITATE ANYONE
Give a litre of 5% dextrose and the glucose is metabolised
within minutes. What remains is a litre of FREE WATER,
which distributes across the total body water — most of
which is intracellular.
Only a small fraction stays in the circulation. It is
therefore useless for restoring circulating volume, and
giving large volumes to a shocked patient wastes time
while causing hyponatraemia.
BALANCED CRYSTALLOIDS AND NORMAL SALINE remain largely in
the extracellular compartment, so a much greater
proportion supports the circulation. These are the
resuscitation and replacement fluids.
A NOTE ON NORMAL SALINE: it contains considerably more
chloride than plasma, so large volumes produce a
HYPERCHLORAEMIC METABOLIC ACIDOSIS — which can then be
misread as worsening illness. Balanced solutions are
closer to plasma and avoid this.
MATCH THE FLUID TO THE LOSS. A patient losing litres of
gastrointestinal fluid is losing salt and water together,
and needs salt and water back. A patient who simply cannot
drink needs maintenance water with appropriate electrolytes.
AND ALWAYS ACCOUNT FOR WHAT IS ALREADY GOING IN — drug
infusions and flushes are fluid too, and are frequently
omitted from the daily total.
Potassium
💡 Exam angle: hyperkalaemia demands an immediate ECG, and the progression is examinable — tall tented T waves, then flattening of the P wave, then QRS widening, then a sine wave pattern and arrest. The management framework is equally examinable as three steps in order: protect the myocardium, shift potassium into cells, then remove it from the body. Note that shifting is temporary — the potassium comes back unless removal is addressed.
TWO POTASSIUM TRAPS
1. HYPOKALAEMIA THAT WILL NOT CORRECT
If potassium refuses to rise despite replacement, CHECK
THE MAGNESIUM. Magnesium depletion causes renal
potassium wasting, and until it is corrected the
potassium will keep falling. This is a classic
examination point and a genuine clinical problem.
Remember also that hypokalaemia POTENTIATES DIGOXIN —
see the cardiovascular drugs chapter, where a new
diuretic causes toxicity at an unchanged digoxin dose.
2. INTRAVENOUS POTASSIUM
NEVER give it undiluted or by rapid push. Concentrated
potassium given as a bolus causes cardiac arrest, and
this has happened in hospitals repeatedly — which is why
concentrated ampoules are stored separately and why
pre-diluted preparations exist.
Infusion rates and concentrations come from your local
protocol, and peripheral infusion is painful and
rate-limited.
DRUG CAUSES OF HYPERKALAEMIA worth remembering: ACE
inhibitors and ARBs, aldosterone antagonists, potassium
supplements, and NSAIDs — all covered in the
cardiovascular and prescribing safety chapters.
Sodium
The most important idea about sodium is that the rate of change matters more than the absolute value. A patient whose sodium has fallen slowly over weeks may be almost asymptomatic at a level that would cause seizures if reached acutely — because the brain adapts. That same adaptation is why correcting a chronic hyponatraemia too quickly causes osmotic demyelination: irreversible brain injury appearing days later in a patient who appeared to be improving. Correction rate limits exist for exactly this reason and must come from your protocol.
Transfusion
TRANSFUSION SAFETY
THE BEDSIDE CHECK IS THE LAST DEFENCE
Positively identify the patient — ask them to state their
name and date of birth where they are able — and check
against the unit and the compatibility label at the
bedside, not at the desk. Most fatal ABO reactions are
identification failures, not laboratory ones.
ACUTE HAEMOLYTIC REACTION
Fever, rigors, loin or back pain, dark urine, hypotension,
often within minutes of starting.
STOP THE TRANSFUSION IMMEDIATELY, keep intravenous access
with a new fluid, resuscitate, recheck the identity of
patient and unit, and inform the blood bank urgently.
Complications include acute kidney injury and
disseminated intravascular coagulation.
OTHER REACTIONS TO RECOGNISE
FEBRILE non-haemolytic — common, usually benign, but a
fever during transfusion is treated as haemolysis or
bacterial contamination until excluded
ALLERGIC — from mild urticaria to anaphylaxis
TACO — circulatory OVERLOAD, particularly in the elderly,
the small and those with cardiac or renal impairment
TRALI — acute lung injury within hours of transfusion
BACTERIAL contamination — rapid onset of fever and shock
DELAYED haemolysis, days later
Transfusion-transmitted infection — reduced but not
eliminated by donor screening
MASSIVE TRANSFUSION brings its own problems: HYPOTHERMIA
from cold products, HYPOCALCAEMIA from citrate,
hyperkalaemia, and dilutional COAGULOPATHY — which links
back to the lethal triad in the trauma chapter.
THE PRESCRIBING PRINCIPLE: transfuse for a defined reason,
ONE UNIT AT A TIME in a stable patient, and reassess
between units. In stable anaemia, treat the cause —
iron deficiency needs iron and investigation, not blood.
Thresholds come from current guidance.
Clinical reasoning: four presentations
🔍 Case 1 — dextrose for shock
PresentationA hypotensive, tachycardic patient with profuse diarrhoea is given several litres of 5% dextrose. He remains shocked, and his sodium has fallen.
ErrorUsing a fluid that does not stay in the circulation.
ReasoningOnce the glucose is metabolised, 5% dextrose is free water distributing across total body water. Very little supports circulating volume, and the free water load lowers the sodium.
AnswerResuscitate with a balanced crystalloid or normal saline per protocol, replace ongoing losses matched to what is being lost, and reassess frequently. Match the fluid to the loss.
🔍 Case 2 — potassium that will not rise
PresentationA patient on long-term diuretics has persistent hypokalaemia despite repeated potassium replacement over several days. Each result is low again the next morning.
Missing testMagnesium.
ReasoningMagnesium depletion causes renal potassium wasting, so replacement is lost as fast as it is given. Until the magnesium is corrected, the potassium will not stay up.
AnswerCheck and correct magnesium alongside potassium. Also review the diuretic, and remember that hypokalaemia potentiates digoxin if the patient is taking it.
🔍 Case 3 — better, then worse days later
PresentationA woman with chronic hyponatraemia of several weeks' duration is corrected rapidly overnight. She improves initially, then several days later develops progressive weakness, dysarthria and reduced consciousness.
What happenedOsmotic demyelination.
ReasoningThe brain adapts to chronic hyponatraemia. Rapid correction reverses the osmotic gradient faster than the brain can readjust, causing demyelination that appears days later and is largely irreversible.
AnswerThis is preventable, not treatable — correct chronic hyponatraemia slowly within the rate limits in your protocol, monitoring sodium frequently during correction.
🔍 Case 4 — fever ten minutes into the unit
PresentationTen minutes into a transfusion a patient develops fever, rigors, back pain and hypotension, and passes dark urine. The nurse slows the infusion and gives paracetamol.
ErrorSlowing rather than stopping.
ReasoningThis is an acute haemolytic reaction, most often from ABO incompatibility caused by an identification failure. Every further millilitre worsens it.
AnswerSTOP the transfusion immediately, keep the line open with a new fluid, resuscitate, recheck the identity of patient and unit, inform the blood bank urgently, and monitor for acute kidney injury and coagulopathy.
Commonly confused
Confusion
The distinction
Why it matters
Resuscitation vs maintenance
Three different purposes
The wrong regimen harms in both directions.
Dextrose vs crystalloid
Dextrose becomes free water
It will not correct shock.
Saline vs balanced solution
Chloride load causes acidosis
Can be misread as worsening illness.
Shifting vs removing potassium
Shifting is temporary
It returns unless removal is addressed.
Hypokalaemia vs hypomagnesaemia
Low magnesium wastes potassium
Replacement fails until magnesium is corrected.
Sodium value vs rate of change
Chronic falls are better tolerated
And are more dangerous to correct fast.
Slowing vs stopping a transfusion
Stop it entirely
Every further millilitre worsens haemolysis.
Anaemia vs need for transfusion
Treat the cause where stable
Iron deficiency needs iron and investigation.
Rapid revision
MUST-KNOW FACTS
1. FLUID IS A DRUG — indication, dose, duration, review.
2. Ask: does the patient need it, what for, and when will I reassess?
3. Three purposes: RESUSCITATION, REPLACEMENT, MAINTENANCE.
4. Too much fluid causes real harm — oedema, poor healing, respiratory failure.
5. Balanced crystalloid and saline stay largely EXTRACELLULAR.
6. 5% DEXTROSE BECOMES FREE WATER — it will NOT resuscitate.
7. Large volumes of saline cause HYPERCHLORAEMIC ACIDOSIS.
8. MATCH THE FLUID TO THE LOSS.
9. Count drug infusions and flushes in the daily fluid total.
10. HYPERKALAEMIA: get an ECG IMMEDIATELY.
11. ECG progression: TALL TENTED T WAVES → flat P → wide QRS → sine wave → arrest.
12. Management: PROTECT the myocardium, SHIFT into cells, REMOVE from the body.
13. Shifting is TEMPORARY — potassium returns unless removed.
14. Drug causes: ACE inhibitors, ARBs, spironolactone, NSAIDs, supplements.
15. HYPOKALAEMIA that will not correct — CHECK THE MAGNESIUM.
16. Magnesium depletion causes renal potassium wasting.
17. Hypokalaemia POTENTIATES DIGOXIN.
18. NEVER give undiluted intravenous potassium — it causes arrest.
19. HYPONATRAEMIA: assess the VOLUME STATE first.
20. Symptoms are NEUROLOGICAL and depend on the RATE of fall.
21. Chronic hyponatraemia may be nearly asymptomatic at a low value.
22. CORRECTING TOO FAST CAUSES OSMOTIC DEMYELINATION.
23. It appears DAYS later, in a patient who seemed to be improving.
24. It is preventable, not treatable — follow protocol rate limits.
25. The commonest FATAL transfusion error is CLERICAL.
26. ABO incompatibility is an IDENTIFICATION failure.
27. Check identity AT THE BEDSIDE against the unit and label.
28. ACUTE HAEMOLYSIS: fever, rigors, loin pain, dark urine, hypotension.
29. STOP THE TRANSFUSION IMMEDIATELY — do not merely slow it.
30. Keep the line, resuscitate, recheck identity, inform the blood bank.
31. Other reactions: febrile, allergic, TACO, TRALI, bacterial contamination.
32. A fever during transfusion is haemolysis or contamination until excluded.
33. MASSIVE TRANSFUSION: hypothermia, low calcium, coagulopathy.
34. Transfuse ONE UNIT AT A TIME in a stable patient and reassess.
35. In stable iron deficiency, give IRON and investigate — not blood.
36. Take all volumes, rates and thresholds from local protocol.
💡 Exam angle: four reliable threads — dextrose does not resuscitate, hypokalaemia that will not correct means check the magnesium, correcting sodium too fast causes demyelination days later, and a transfusion reaction means stop rather than slow.
Syllabus points
Fluid as a drug: the three questions
Resuscitation, replacement and maintenance
Why 5% dextrose becomes free water
Hyperchloraemic acidosis from saline
Matching the fluid to the loss
Hyperkalaemia and the ECG progression
Protect, shift and remove
Hypokalaemia and magnesium
Why undiluted potassium is fatal
Hyponatraemia and the volume state
Why rate of change matters more than value
Osmotic demyelination
Transfusion safety and the bedside check
Recognising an acute haemolytic reaction
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