1. 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)

1. Specifics in the examination, beyond the general examination and vital signs are:

• Anthropometric
• Weight, height and BMI calculation
• Arm circumference
• Triceps skin fold thickness

2. Clinical:

• 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
• Neck: Thyromegaly
• Extremities: loss of muscle mass (arm circumference, bitemporal wasting), loss subcutaneous fat (triceps skin thickness), bone tenderness (Vit D)
• Neurologic: Peripheral neuropathy, reflexes, tetany, mental status, handgrip strength 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.

Other investigations:

• • Anaemia with Fe levels, or B12 / Folate if macrocytic.
  • Vitamin and trace elements
  • Ca, PO4, Mg, Glucose, UEC are all non-specific
  • Retinol binding protein

2. Pathophysiology of Re-feeding Syndrome

Reintroduction of glucose into diet after a considerable period of fasting 

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)

Discussion

Nutritional assessment:

History:

• 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)

Examination:

• 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
  • eg. neuropathy for Vitamin B12 deficiency

Anthropometry

• BMI
• Ideal body weight
• Lean body mass

Biochemistry and physiology:

• Cholesterol and triglycerides
• Random BSL
• HbA1C
• Serum cortisol
• TFTs
• FBC for lymphocyte count
• Albumin and prealbumin
• Transferrin
• Calculation of nitrogen balance
• Micronutrient levels:
  • Fat-soluble vitamins A, D and E
  • Thiamine
  • Zinc
  • Selenium
  • Vitamin B12
  • Folate
• Delayed hypersensitivity skin-testing

  Refeeding syndrome pathophysiology:

• Total body phosphate depletion occurs during starvation:
  • Exogenous sources of phosphate are inadequate to supplement the daily phosphate requirements
  • Intracellular phosphate stores are used to synthesise ATP (using protein and fat as fuel)
  • Homeostatic mechanisms maintain serum concentrations of these ions at the expense of intracellular stores
• With recommencement of nutrition:
• An abrupt conversion of body fuel use from a catabolic starvation state to a normal anabolic state occurs.
• Whereas during starvation fat catabolism was the chief source of energy (requiring no transmembrane electrolyte shifts), carbohydrate metabolism requires an intracellular migration of electrolytes (predominantly phosphate, which is required to trap glucose inside the cells).
• Thus, the insulin surge associated with the reintroduction of carbohydrate metabolism results in a sudden and massive intracellular movement of electrolytes.
• All the clinical features of refeeding syndrome are the result of extracellular electrolyte depletion, and the failure of normal concentration gradients.
• Clinically, this will result in heart failure due to hypophosphataemia, and arrhythmias due to hypokalemia.