Re-Feeding Syndrome Flashcards

1
Q

What is the defintion of Re-feeding syndrome?

A

Potentially fatal shifts in fluid and electrolytes that may occur in malnourished patients following re-feeding (whether enterally or parenterally)’. Leads to

  • Hypophosphataemia
  • Hypokalaemia
  • Hypomagnesaemia
  • Hyperglycaemia
  • Thiamine deficiency
  • Sodium retention
  • Fluid overload
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2
Q

What are the hormones released by Prolonged Fasting?

A
  • Glucagon
  • Cortisol
  • Growth Hormone
  • Adrenaline
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3
Q

Who is at risk of Re-feeding syndrome?

A
  • Patients with anorexia nervosa
  • Patients with Chronic Alcoholism
  • Oncology patients
  • Postoperative patients
  • Elderly patients (comorbidities, decreased physiological reserve)
  • Patients uncontrolled diabetes mellitus
  • Patient with Chronic Malnutrition
  • Long term users antacids (magnesium and aluminium salts bind phosphate)
  • Long term users of diuretics (loss of electrolytes)
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4
Q

What are functions of Phosphate?

A
  • Component of biological molecules: Nucleic acids, Phospholipids, Cellular organelles
  • Intracellular messaging – cAMP
  • Bone mineralisation (hydroxyapatite)
  • Hydrolysis of ATP – aerobic energy source
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5
Q

What are the consequences of Hypophosphataemia?

A

0.35 – 0.8 mmol/L

  • Mild
  • Chronic - osteomalacia

<0.35 mmol/L

  • Confusion
  • Seizure
  • Coma
  • Impaired muscle contractility
  • Rhabdomyolysis
  • Ileus
  • Red blood cell fragility
  • Impaired platelet & leukocyte function
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6
Q

What are the patient at risk of Hypophosphataemia?

A

Decreased Intake

  • Alcoholics
  • Severe malnourished
  • Eating disorders

Decreased GI Absorption

  • Intestinal Failure
  • IBD
  • Radiation enteritis

Increased Renal Losses

  • Hyperparathyroidism
  • Fanconi’s
  • Chronic diuretic use
  • Renal tubular acidosis
  • Oncogenic osteomalacia

Genetic

  • X-linked hypophosphataemic rickets
  • Autosomal dominant hypophosphataemia
  • Hereditary hypophosphataemic rickets with hypercalciuria
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7
Q

What are functions of Potassium?

A
  • Protein synthesis
  • Glycogen synthesis
  • Determinant of resting membrane potential (Em): Muscle contraction
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8
Q

What are Consequences of Hypokalaemia?

A
  • Muscle weakness
  • Cramps
  • Tetany
  • Impaired contractility
  • Rhabdomyolysis
  • Ileus
  • Nausea/vomiting
  • Constipation
  • Arrythmias
  • ECG changes
  • Heart block and cardiac arrest
  • Impaired urinary concentration
  • Increased ammonia production and urinary acidification
  • Increased HCO3 reabsorption
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9
Q

What are the patients at risk of Hypokalaemia?

A

Decreased Intake

  • Alcoholics
  • Severely malnourished
  • Eating disorders

Increased Cellular Uptake

  • Metabolic alkalosis
  • Insulin – Refeeding
  • Periodic paralysis

Increased Extra-Renal Losses

  • D + V
  • Intestinal fistula
  • Chronic laxative abuse

Increased Renal Losses

  • Loop / Thiazide diuretics
  • Hypomagnesaemia
  • Conn’s / Cushing’s
  • Barter’s
  • Liddle’s
  • Gitelman’s
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10
Q

What are functions of Magnesium?

A

Enzyme co-factor

  • Energy metabolism
  • Neuromuscular excitability
  • Protein/nucleic acid synthesis
  • Control Ca/K channels

Co-factor for ATP

Regulation endocrine secretion – PTH, Aldosterone, Insulin

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11
Q

What are consequences of Hypomagnesaemia?

A
  • Muscle weakness
  • Cramps
  • Tetany
  • Impaired contractility
  • Ileus
  • Nausea/vomiting
  • Constipation
  • Arrythmias
  • Heart block and cardiac arrest
  • Hypocalcaemia
  • Hypokalaemia
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12
Q

What are patients at risk of Hypomagnesaemia?

A

Decreased Intake

  • Alcoholics
  • Severely malnourished
  • Eating disorders

Decreased GI Absorption

  • IF
  • IBD
  • Radiation enteritis
  • Long term PPI

Increased Cellular Uptake

  • Post DKA
  • Post MI
  • Acute pancreatitis

Increased Renal Losses

  • Loop / Thiazide diuretics
  • Hyperparathyroidism
  • Gitelman’s
  • Nephrotoxic drugs:
  • Cisplatin. CsA. Gentamycin. Tobramycin
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13
Q

What are the functions of Thiamine?

A

Thiamine co-factor of thiamine pyrophosphate (TPP). TPP co-factor for

  • Transketolase - Pentose phosphate pathway
  • Pyruvate Dehydrogenase - Flux from glycolytic pathway through to Kreb’s cycle
  • α-Ketoglutarate Dehydrogenase - Kreb’s cycle

During rapid re-feeding, induction of CHO metabolism causes utilisation of already depleted thiamine stores

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14
Q

What are the consequences of Thiamine Deficiency?

A

Wernicke-Korsakoff Syndrome

  • Wernicke’s Encephalopathy - Acute onset
  • Korsakoff’s Syndrome - Chronic neurological complications associated with WE
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15
Q

What are signs and symptoms of Wernicke’sEncephalopathy?

A

Neurological lesions

  • Vascular congestion
  • Demyelination
  • Gliosis
  • Haemorrhage

Encephalopathy

  • Disorientation
  • Indifference
  • Agitation

Oculomotor dysfunction

  • Nystagmus

Gait ataxia

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16
Q

What are Associated Conditions of Thiamine Deficiency?

A
  • Re-feeding in malnourished patient
  • Chronic alcoholism
  • Anorexia nervosa
  • Hyperemesis of pregnancy
  • Malignancy
  • Transplantation
  • Hemodialysis and peritoneal dialysis
  • AIDS
  • Measurement of Thiamine?
17
Q

Why is Thiamine not measured in clinical practice?

A

Relatively unstable in blood.

  • Long turnaround time (sent to Glasgow) and expensive ~£30
  • Thiamine non-toxic so administer and monitor response.
  • Never wait for result of lab test to decide whether to replace
  • Look for? Neurological abnormalities on MRI, Unexplained unconsciousness/coma in malnourished patient, Acute delirium/ataxia
18
Q

What can happen with glucose in Re-feeding?

A

Excessive administration of glucose may lead to hyperglycaemia in early stages of re-feeding. Can cause:

  • Hyperosmolarity
  • Osmotic diuresis
  • Dehydration
  • Ketoacidosis
  • ? increased CO2 production – hypercapnia & respiratory failure
19
Q

What can happens with sodium and water during re-feeding?

A

Re-introduction of CHO leads to rapid decrease in renal Na+/H2O excretion + additional fluid repletion may lead to:

  • Volume overload
  • CCF
  • Pulmonary oedema
  • Arrhythmia