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:
Biochemistry and physiology:
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:
Or, the diagram.
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