With respect to nutritional support in the critically ill:
a) Outline how you would assess the nutritional status of a patient with suspected malnutrition. (70% marks)
b) Outline the pathophysiology of severe re-feeding syndrome. (30% marks)
a) Assessments of nutritional status:
This is notoriously unreliable as there are many conditions that can alter the non-specific markers of nutritional status.
A good history should include the circumstances of poor intake (duration, cause, etc.), a background of previous eating behaviours, and GIT symptoms (nausea, vomiting diarrhoea, weight loss)
a. Specifics in the examination, beyond the general examination and vital signs are: Anthropometric
Weight, height and BMI calculation
Triceps skin fold thickness
Hair: Hair loss or abnormal distribution (lanugo),
Skin: Conjunctival pallor and skin pallor, xerosis (dry skin, A), spooning of nails (Iron), ecchymoses or petechiae (C or K), pressure ulcers, poor wound healing
Mouth: Glossitis (Niacin, Folate, B12, B2, B6), bleeding or sores on the gums and oral mucosa (C), angular cheilosis or stomatitis (B2, B6), leucoplakia, poor dentition
Extremities: loss of muscle mass (arm circumference, bitemporal wasting), loss of subcutaneous fat (triceps skin thickness), bone tenderness (Vit D)
Investigations to assess protein status for protein calorie malnutrition, must all be taken in context of other evidence of acute and chronic illness and will alter as part of acute phase response.
Serum albumin (longest half-life at 18 – 20d)
Serum transferrin (half-life of 8 – 9d), but also reflects iron status, and low transferrin should be considered an indicator of protein status only in the setting of normal serum iron.
Serum pre albumin (half-life at 2 – 3d) - responds quickly to the onset of malnutrition and rises rapidly with adequate protein intake, but altered in the acute phase response due to acute or chronic inflammation.
o Anaemia with Fe levels, or B12 / Folate if macrocytic.
o Vitamin and trace elements
o Ca, PO4, Mg, Glucose, UEC are all non-specific
o Retinol binding protein
b) Pathophysiology of Re-feeding Syndrome
Reintroduction of glucose into diet after a considerable period of fasting with a low BMI
Insulin in response to glucose load moves the glucose into cells (with K and Mg)
The first step of glycolysis is the phosphorylation of glucose. This holds the glucose in cells. This leads to sudden and precipitous fall in phosphate that is the hallmark of refeeding syndrome
Severely reduced phosphate is available for ATP, cAMP
Failure of tissues with high energy requirement - heart, kidney, muscle (rhabdomyolysis), brain, respiratory (diaphragm)
Untreated leads to death
Additional Examiners' Comments:
Poorly answered, with no specific details about the relative importance of measures of nutritional status. Candidates were expected to comment that nutritional assessment in the critically ill is difficult with many of the objective measures confounded by the consequences of the acute illness. A simple list of anthropometry, clinical signs and investigations was not sufficient as it missed the point that a careful history is crucial.
An approach to the assessment of nutritional status:
- Premorbid weight and the pattern of its change
- Premorbid nutritional routine
- Diseases affecting gastrointestinal function (eg. coeliac disease)
- Disease affecting satiety control (eg. Prader-Willi syndrome)
- Factors influencing metabolic substrate utilisation (eg. thyroid dysfunction, hypoadrenalism, Cushings disease or corticosteroid therapy)
- Observed quality of nails and hair (an indicator of chronic protein intake)
- Subcutaneous fat measurements (triceps)
- Muscle bulk and muscle tone of quadriceps and deltoids
- Presence of oedema and ascites
- Evidence of any specific micronutrient deficiency
- Ideal body weight
- Lean body mass
Biochemistry and physiology:
- Cholesterol and triglycerides
- Random BSL
- Serum cortisol
- FBC for lymphocyte count
- Albumin and prealbumin
- Calculation of nitrogen balance
- Micronutrient levels:
- Fat-soluble vitamins A, D and E
- Vitamin B12
- Delayed hypersensitivity skin-testing
Though the pathophysiology of refeeding syndrome can expressed as a stupidly complex flowchart, the non-insane candidate may wish to make use of a logical point-form description:
- With starvation, less carbohydrate becomes available
- As the result of this, there is a switch to fatty acid and ketone based metabolism
- This switch is in part mediated by a decrease in the insulin levels
- Low oral intake also means decreased phosphate intake
- However, there is a daily requirement for phosphate (for ATP synthesis)
- This phosphate is not replenished by the poor oral intake
- As a result, intracellular phosphate is depleted
- Homeostatic mechanisms maintain a normal serum phosphate in spite of this
- As carbohydrate is reintroduced, the secretion of insulin results in a large-scale uptake of phosphate into the tissues
- As the intracellular phosphate is depeleted, there is nowhere to mobilise more phosphate from, and hypophosphataemia results.
Or, the diagram.
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