Clinical malnutrition

The nutritional status of a healthy person is qualified by how the person is fed; both the quality and quantity of the food matter. A disease can also influence the nutritional status, and the other way around: the nutritional status influences the patients reaction to the disease.

 

Definitions of clinical malnutrition

ESPEN Guidelines for nutrition Screening (2002)

According to the Espen Guidelines a severe risk on disease-related malnutrition occurs when  at least one of the next criteria is met: 

• Weight loss  > 10-15% within 6 months
• BMI < 18.5
• Subjective Global Assessment grade C
• Serum-albumin < 30 g/ l (and no proof for liver or renal disturbances)

More information:

• ESPEN Guidelines for nutrition screening van J. Kondrup, S.P. Allison, M. Elia, B. Vellas en M. Plauth (2002);
• Defining malnutrition: A plea to rethink van P. Soeters, F. Bozetti, L. Cynober, A. Forbes, A. Shenkin en L. Sobotka (2016) 

 

Malnutrition

Malnutrition is often defined as 'a short on nutrients leading to a diminished biological function'. In this definition there is the assumption of an inadequate nutritional intake. No attention is paid to the effect of the disease-process on the nutritional status of the patient. Not only the food intake influences the nutritional status, but also the presence of a disease. Also, the nutritional status influences the patient’s reaction to the disease.

Clinical Nutrition (2008)

In an article of P. Soeters et all in Clinical Nutrition (2008) malnutrition is defined as: ‘’ A subacute or chronic state of nutrition in which a combination of varying degrees of over- or undernutrition and inflammatory activity have led to a change in bodycomposition and diminished function’’. Important in this definition is taking into account the degree of inflammation.

Chronic and acute malnutrition (Konstantinides 1998)

A difference must be made between chronic and acute malnutrition.The chronic form may occur in patients prior to hospitalisation as a result of disease or medical conditions that lead to low energy and protein intake and poor food choices. During hospitalisation the acute form may occur as a result of reduced or absent food intake due to illness, drug therapy or depression. Moreover, the acute form may also occur from increased energy expenditure in hypermetabolic states such as trauma or surgery.

Malnutrition or depletion?

Malnutrition caused by lack of intake shows Marasmus signs. The person is thin. When disease plays a part, you often see Kwasiorkor: the weight loss is being masked by fluid retention in the body.

 

 

 

Consequences of malnutrition

Loss of lean body mass has a negative effect on the organ function, wound healing, immune response to infections, healing and a longer hospital stay.Complications as a result of malnutrition:

• Decreased wellbeing;
• Depressed behaviour;
• Weight loss;
• Muscle loss, less activity, less lung-function and less heart-function;
• Increased infection-rates;
• Increased complication-rates;
• Negative side effects of therapy (radio- and chemo-therapy);
• Decreased wound-healing;
• Increased risk for pressure-ulcers;
• Gut dysfunction;
• Extended length of stay.

  

Prevalence of malnutrition in a clinical setting

Studley (1936) was the first who showed that weight loss is a risk factor for post-surgery complications. In post-surgical patients weight loss of more than 20% was associated with a higher mortality level: 33%. Mainly as a result of increased infection rates. Ever since many studies have been published that showed that in developed countries malnutrition occurred in a lot of hospitalised patients. 

Mean prevalence

According to Tierney (1996) the mean prevalence is 41% (variation 23%-62%) in surgical patients and 44% (variation 29%- 59%) in non-surgical patients (Naber, 1997). In older patients the prevalence varies from 5% to 46%. 

Variation

The large variation is caused by the use of different definitions of depletion.

 

Refeeding syndrome

The refeeding syndrome is a dangerous disorder. It was first descibed in far east prisoners of war after WWII. Eating after a period of prolonged starvation, seemed to precipitate cardiac failure. The pathophysiology of refeeding syndrome has now been established. Clinical symptoms are:

• hypophosphataemia, hypopotassemia en hypomagnesemia;
• glucose-intolerance;
• thiamine (B1) deficienty;
• organfailure and oedema.

The refeeding syndrome can occur with parenteral as well as enteral feeding. Patients with anorexia nervosa, cancer, alcoholism and some patients after operations have a high risk of refeeding syndrome. Also patients with neurological dysphagia who are being fed through a tube are at risk. 

Recommendations for prophylaxis

1. be alert for the existance of the syndrome and recognise patients at risk;
2. Screen and supplement phosfate and if nessecary magnesium, potassium and thiamine before restarting nutrition 
3. Start with a caloric intake < 20 kcal / kg per day
4. consult a dietician;
5. when caloric intake increases;
6. evaluate bodyweight daily in case of oedema; 
7. slowly increase the volume, monitor heartf requency and fluid balance;
8. monitor phosphate, potassium, magnesium and glucose.

Advice for supplementation

• Serum-phosphate < 0.65 mmol/l: 25mmol / 24 h, iv;
• Serum-phosphate < 0.4 mmol/l or a decrease of 0.2 mmol/l: 50 mmol / 24 h iv, max 10 mmol/h;
• Serum-magnesium < 0.7 mmol/l: oral supplementation (unless diarrhea) magnesiumoxide or magnesiumcitrate;
• Serum-magnesium <0,55 mmol/l: magnesiumsulfate, iv;
• Serum-potassium < 3.5 mmol/l: oral KCl-drink or  40-80 mmol/day iv;
• Vitamin B1 (thiamine) supplementation without checking the blood (takes too long and is expensive), max 50 mg/day iv of oral supplementation.