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Classification & Assessment in Psychiatry · Paper A

Eating disorder: physical complications

The idea

Starvation and purging damage the body in predictable ways, and these physical complications can be fatal. This concept is about recognising them and the special danger of refeeding too quickly, e.g. a severely malnourished patient started on full-calorie feeding too fast who then develops a dangerously low phosphate level. In practice, that specific danger is exactly why refeeding must start cautiously.

How it works

Anorexia nervosa produces starvation physiology: a slow heart rate (bradycardia), low blood pressure, low body temperature, a shrunken heart, switched-off sex hormones (causing loss of periods), thin bones (osteoporosis), low blood counts and raised liver enzymes. The ECGElectrocardiogram, a recording of the heart's electrical activity.Read more → (heart tracing) is more worrying with a slow heart rate, electrolyte disturbance, or a lengthened QTThe QT interval, a measurement on a heart tracing that some psychiatric drugs can lengthen.Read more → (a measure on the ECG that, when too long, can trigger dangerous heart rhythms). Purging by vomiting causes a low-potassium, low-chloride alkalosis (blood that is too alkaline), dehydration, swollen salivary glands and dental erosion. A patient with severe anorexia and an already slow heart rate is at added danger if started on a QT-prolonging drug, so baseline heart rate and electrolytes must be checked first.

How to spot it

  • A woman with bulimia nervosa who vomits daily has recurrent presyncope. An ECGElectrocardiogram, a recording of the heart's electrical activity.Read more → (electrocardiogram) shows a prolonged QTc interval. Which mechanism explains this?
  • A 13-year-old girl develops anorexia nervosa before her first period. Two years later she remains prepubertal with short stature. Which mechanism explains this?

Tell it apart

  • Refeeding syndrome, hypophosphataemiaA lower than normal level of phosphate in the blood.Read more →, hypokalaemia and hypomagnesaemia on reintroducing food, unlike the bradycardia of chronic starvation.
  • Russell's sign, knuckle calluses from self-induced vomiting, rather than a feature of restricting anorexia.
  • Hypokalaemic metabolic alkalosis, from vomiting, whereas laxative misuse can instead cause a metabolic acidosis.
  • Anorexia nervosa, low BMIBody mass index, a measure of weight relative to height used to classify weight status.Read more → with bradycardia and osteoporosis, unlike bulimia's usually normal weight.

Watch for

  • Anaemia from vomiting is not typical and does not directly prolong the QTc interval.
  • Hyperthyroidism is not a recognised consequence of bulimic vomiting behaviour.
  • Growth hormone deficiency here is acquired from starvation, not a congenital condition.
  • Diabetes mellitus is not the mechanism linking anorexia nervosa to delayed puberty.
  • Coeliac disease is a separate condition not implied by this starvation history.

Use it again

  • Extract the defining phenomenology, duration, severity and functional-impact clues.
  • Match the pattern to the most specific diagnostic or assessment construct.
  • Actively test the closest look-alike against the missing or contradictory clue.
  • Choose the precise term rather than a broader category that is merely compatible.

In detail

In this lesson

  1. Why the physical complications matter more than the psychology here
  2. Plain definition
  3. The critical caveat
  4. First principles: building it from the ground up
  5. Structured walk-through: the complications, system by system
  6. Look-alikes and differentials
  7. Diagnosis: how these complications are actually identified
  8. Management: what is actually done
  9. Exam pearl
  10. In one line

In this lesson

  1. Why the physical complications matter more than the psychology here
  2. Plain definition
  3. The critical caveat
  4. First principles: building it from the ground up
  5. Structured walk-through: the complications, system by system
  6. Look-alikes and differentials
  7. Diagnosis: how these complications are actually identified
  8. Management: what is actually done
  9. Exam pearl
  10. In one line

Why the physical complications matter more than the psychology here

Eating disorders are psychiatric diagnoses, but the thing most likely to kill a patient is physical, not psychological: cardiac and electrolyte complications, and, paradoxically, the act of refeeding itself if done too fast. This topic is about recognising those physical dangers early and understanding exactly why refeeding must be cautious.

Plain definition

Anorexia nervosa involves severe restriction of food intake leading to a dangerously low body weight, while bulimia nervosa involves cycles of binge eating followed by compensatory behaviours such as self-induced vomiting or laxative misuse. Both produce physical complications, but through different routes: anorexia through prolonged starvation, bulimia largely through repeated purging. A patient can be normal weight and still have life-threatening electrolyte disturbance from purging alone.

The critical caveat

Most candidates assume the biggest danger in anorexia is simply 'being underweight'. It is not: the biggest killer is cardiac. For example, imagine a severely malnourished patient started on full-calorie feeding too fast who develops a dangerously low blood phosphate level within days and becomes acutely unwell. That specific danger is exactly why refeeding must start cautiously and slowly.

First principles: building it from the ground up

During prolonged starvation, the body downregulates its metabolism to conserve energy: heart rate slows, blood pressure and temperature drop, and the body draws on its own fat and muscle for fuel. Crucially, intracellular stores of phosphate, potassium and magnesium become depleted even though blood levels can look falsely normal, because the body is not actively processing carbohydrate. The moment carbohydrate is reintroduced, insulin surges, and insulin drives phosphate, potassium and magnesium out of the blood and into cells all at once. Blood levels of these electrolytes then crash, which is the entire mechanism behind refeeding syndrome.

Structured walk-through: the complications, system by system

Cardiovascular: bradycardia (slow heart rate), hypotension (low blood pressure), a shrunken heart on imaging, and a prolonged interval on the (a measure of the heart's electrical recovery time that, when too long, can trigger dangerous, sometimes fatal, heart rhythms).

Endocrine and bone: amenorrhoea (loss of periods) from switched-off sex hormones, and osteoporosis (thin, fragile bones) from prolonged oestrogen deficiency and malnutrition.

Haematological and hepatic: low blood counts (anaemia, low white cells) and raised liver enzymes, both from starvation itself.

Purging-specific complications: self-induced vomiting causes a hypokalaemic (low potassium), hypochloraemic metabolic alkalosis (blood that is too alkaline), dehydration, painless swelling of the parotid salivary glands, and dental erosion from repeated stomach acid exposure. Laxative misuse instead tends to cause a metabolic acidosis, the opposite direction, an important exam distinction.

Refeeding syndrome: the hallmark is (dangerously low blood phosphate), alongside hypokalaemia and hypomagnesaemia, carrying risk of abnormal heart rhythms, heart failure, weakened breathing muscles, delirium and seizures.

Look-alikes and differentials

Refeeding syndrome (, hypokalaemia, hypomagnesaemia appearing WHEN food is reintroduced) is distinguished from the baseline bradycardia of chronic starvation (present before any feeding starts) by timing relative to refeeding. Russell's sign (calluses or scarring on the knuckles from repeated contact with the teeth during self-induced vomiting) points specifically to purging behaviour, not to restricting-type anorexia. Vomiting-related hypokalaemic alkalosis is distinguished from laxative-related metabolic acidosis by checking the direction of the blood pH and bicarbonate.

Diagnosis: how these complications are actually identified

Baseline and serial bloods (full blood count, urea and electrolytes, phosphate, magnesium, liver function) are essential before and during refeeding. A 12-lead identifies bradycardia and prolongation before starting any QT-prolonging medication. Weight, and vital signs (heart rate, blood pressure, temperature) are tracked serially, per NICE eating disorder guidance, to flag a patient moving into the medically high-risk range.

Management: what is actually done

Refeeding follows a slow, cautious, monitored protocol, starting well below full calorie requirements and increasing gradually, with daily electrolyte checks and thiamine (vitamin B1) supplementation from day one, per Maudsley and NICE guidance, to prevent and refeeding syndrome. Electrolyte abnormalities are corrected proactively rather than reactively. Cardiac monitoring is used for patients with significant bradycardia or prolongation, and any QT-prolonging medication is avoided or used with extreme caution.

Exam pearl

When a vignette describes a severely malnourished patient about to start feeding, the exam is almost always testing whether you know to go slowly and check phosphate, not whether you know the definition of anorexia.

In one line

The physical danger in eating disorders is cardiac and electrolyte, and refeeding done too fast can be as dangerous as the starvation it is meant to treat.

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