Malnutrition
Description
- Deficiency (or excess/imbalance) of energy, protein or micronutrients with measurable adverse effects on body composition, function and outcome
Types
| Marasmus | Energy deficiency. Wasting, no oedema, preserved albumin |
| Kwashiorkor | Protein-deficient. Oedema, hepatomegaly, dermatitis (typically perioral/perianal), flaky-paint rash, hair changes |
| Marasmic kwashiorkor | Both |
| Disease-related malnutrition | The hospital problem: inflammation + reduced intake + increased requirement |
| Sarcopenia | Loss of muscle mass and function - independent predictor of mortality |
- Micronutrient deficiency occurs at any BMI - obesity does not exclude malnutrition
Epidemiology
- ~30-40% of Australian hospital inpatients are malnourished or at risk - largely undocumented
- Highest in older adults, cancer, chronic liver disease, IBD, CKD, COPD, dementia, alcohol use disorder
- Malnutrition independently predicts longer length of stay, more infection, more readmission, higher mortality
Aetiopathogenesis
Four mechanisms - usually more than one at once
1. Reduced intake - anorexia, dysphagia, nausea, depression, dentition, social isolation, fasting for procedures
2. Impaired digestion/absorption - pancreatic insufficiency, coeliac, short bowel, cholestasis
3. Increased requirement/losses - sepsis, burns, surgery, malignancy, high-output stoma, dialysis, protein-losing enteropathy
4. Impaired utilisation - inflammation-driven catabolism (cachexia), insulin resistance
Refeeding syndrome - the mechanism, then the numbers
- Starvation -> catabolism, intracellular phosphate/K/Mg depletion despite normal serum levels
- Refeeding -> inc insulin, dec glucagon -> anabolic switch: glycogen, fat and protein synthesis
- Consumes phosphate, magnesium and thiamine
- Drives potassium, magnesium and phosphate intracellularly
- -> Hypophosphataemia is the biochemical hallmark, plus hypokalaemia, hypomagnesaemia, sodium and fluid retention, disturbed glucose/protein/fat metabolism
- Clinically: arrhythmia, cardiac failure, respiratory failure, rhabdomyolysis, seizures, Wernicke encephalopathy, death
Diagnosis
Screening then assessment
- Screen every inpatient: MST, MUST or NRS-2002
- Assess: Subjective Global Assessment, or GLIM criteria - at least one phenotypic plus one aetiologic criterion
- Phenotypic: unintentional weight loss, low BMI, reduced muscle mass
- Aetiologic: reduced intake/absorption, disease burden/inflammation
Examination - deficiency signs worth knowing
| Sign | Deficiency |
|---|---|
| Angular stomatitis (cracks at the corners of the mouth) | B12, B6, folate or iron |
| Glossitis | B12, folate, iron, niacin, riboflavin |
| Perifollicular haemorrhage, friable bleeding gums, loose teeth, poor wound healing | Vitamin C (scurvy) |
| Corkscrew hairs | Vitamin C |
| Nystagmus, ophthalmoplegia, ataxia, confusion | Thiamine - Wernicke encephalopathy |
| Peripheral neuritis, hoarseness (laryngeal nerve), vomiting/apathy/irritability | Chronic thiamine - beriberi |
| Dermatitis, diarrhoea, dementia | Niacin (pellagra) |
| Oedema, hepatomegaly, perioral/perianal dermatitis | Protein (kwashiorkor) |
| Perioral and acral rash, alopecia, poor healing, diarrhoea | Zinc |
| Night blindness, Bitot spots, xerophthalmia | Vitamin A |
| Bone pain, proximal myopathy | Vitamin D |
| Temporal, interosseous and quadriceps wasting; loss of subcutaneous fat | Energy/protein |
Investigations
- Weight, BMI, weight trajectory, hand grip strength, mid-arm circumference
- FBE, UEC, phosphate, magnesium, calcium, LFT, CRP, glucose
- Iron studies, B12, folate, vitamin D, zinc, thiamine where relevant
- Albumin is a negative acute-phase reactant, not a nutritional marker - do not use it to diagnose or track malnutrition
- Cause-directed: coeliac serology, faecal elastase, TSH, HIV, malignancy workup
Refeeding risk stratification - the examinable list
HIGH RISK if ANY ONE of:
- BMI <16
- Unintentional weight loss >15% in 3-6 months
- Negligible intake for >10 days
- Low potassium, phosphate or magnesium before feeding
HIGH RISK if TWO OR MORE of:
- BMI <18.5
- Weight loss >10% in 3-6 months
- Negligible intake for >5 days
- History of alcohol misuse, or use of insulin, chemotherapy, antacids or diuretics
Management
1. Identify and treat the cause
- Dysphagia -> speech pathology, texture modification
- Nausea, pain, constipation, oral thrush, dentition, depression - all reversible barriers
- Pancreatic enzyme replacement; gluten-free diet; treat the sepsis or the tumour
- Review drugs - opioids, metformin, digoxin, SSRIs, chemotherapy
2. Choose the route - "if the gut works, use it"
| Route | Use |
|---|---|
| Oral | Food fortification, frequent small meals, oral nutritional supplements between (not with) meals |
| Enteral (NG/NJ/PEG) | Functioning gut but inadequate oral intake. Preferred over parenteral - preserves mucosal integrity, fewer infections, cheaper |
| Parenteral | Only when the gut cannot be used: obstruction, short bowel, high-output fistula, severe ileus. Central line sepsis, cholestasis, metabolic complications |
- PEG in advanced dementia does not improve survival, aspiration risk or pressure injuries - discuss goals of care rather than defaulting to it
3. Prevent refeeding syndrome
- Give thiamine (and a B-complex/multivitamin) BEFORE and during the first days of feeding - the single most important step, and the one most often forgotten
- Start feeding low and slow: ~10 kcal/kg/day in high-risk patients (5 kcal/kg/day in extreme risk), building to full requirements over 4-7 days
- Check phosphate, potassium, magnesium daily for at least 3 days and replace aggressively
- Do not stop feeding when phosphate falls - replace it and continue at the current rate
- Monitor fluid balance, weight, glucose, ECG in high-risk patients
- Restrict sodium and fluid initially
4. Special situations
- Decompensated cirrhosis with sarcopenia (no encephalopathy): high protein 1.2-1.5 g/kg/day + adequate energy, frequent small meals and a late-evening snack
- Reduces the prolonged overnight catabolic fast that characterises cirrhosis
- *Protein restriction is obsolete and harmful* - it worsens sarcopenia without preventing encephalopathy
- Perioperative: 7-14 days of preoperative nutrition in severely malnourished patients undergoing major surgery
- Anorexia nervosa: highest refeeding risk; medical stabilisation, cardiac monitoring, multidisciplinary care
- Alcohol use disorder: parenteral thiamine before any glucose-containing fluid
5. Monitor
- Weight, intake charts, grip strength and function (not just weight)
- Electrolytes, glucose, LFT
- Dietitian review; discharge nutrition plan
Associations
- Sarcopenia and frailty - independent predictors of mortality
- Pressure injuries, delayed wound healing, surgical site infection
- Impaired immunity, higher infection rates
- Osteoporosis and osteomalacia
- Depression, cognitive impairment
- Cirrhosis, cancer cachexia, COPD, CKD, heart failure, IBD - disease-related malnutrition
- Anorexia nervosa; alcohol use disorder
- Post-bariatric surgery - thiamine, B12, iron, calcium, vitamin D, copper deficiency
- Older age, polypharmacy, social isolation, poverty, food insecurity
Natural history & complications
- Malnutrition is independently associated with mortality, longer stay, more complications and readmission - and improves with treatment
- Refeeding syndrome peaks in the first 72 hours of feeding and can be fatal
- Wernicke encephalopathy: only ~10-16% show the complete triad - treat on suspicion, not on the triad
- Untreated -> Korsakoff syndrome, which is largely irreversible
- Muscle mass recovers slowly and requires resistance exercise alongside protein - nutrition alone rebuilds fat, not function
- In cancer cachexia, nutrition support alone does not reverse the catabolic drive - treat the tumour and the inflammation
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