15.4.7 Malnutrition Flashcards
Define Malnutrition
- Malnutrition, as defined by WHO, encompasses macro- and/or micro-nutrient deficiencies or excesses, imbalances, and impaired utilization, including both overnutrition (related to overweight/obesity) and undernutrition (acute/chronic malnutrition, micro-nutrient deficiencies)
- Undernutrition occurs predominantly in children <5 years of age living in low-and middle-income countries
Causes of malnutrition
Multifactorial
- feeding practices
- child factors
- recurrent infections
- maternal
Slide 5
Classification of malnutrition
Underweight
- acute (wasted)
➡️ Moderate (MAM)
➡️ Severe (SAM)
- chronic (stunted)
Overweight
Slide 11 + 12
Severe acute malnutrition with/without oedema
- The term severe acute malnutrition with oedema has replaced ‘protein–energy malnutrition’ or ‘kwashiorkor’, which was used to describe children with severe wasting and nutritional oedema.
- The term severe acute malnutrition without oedema has replaced the term marasmus to describe children with severe wasting without nutritional oedema.
Malnutrition diagnosis
- Leads to anthropometric failure on the growth chart, and is
- Associated with clinical signs
➡️due to metabolic/physiological decompensation
➡️2’ to protein, energy (CH), electrolyte, mineral, trace element deficiencies
Severe acute malnutrition
Defined and measured by
- Mid-Upper Arm Circumference (MUAC) of less than 11.5cm in children aged 6–60 months (circumference of child’s left upper arm).
- Weight-for-Height (WFH) or Weight-for-Length (WFL) below - 3 standard deviations (SD) or z-score <-3
- The presence or not, of bilateral pitting pedal oedema (nutritional oedema)
Moderate acute malnutrition
Defined and measured by
- a WFL between -3 and -2 SD below the median of the WHO child growth standards/ z- score between -3 and -2
- MUAC between 11.5cm and 12.5.
- The child doesn’t have any oedema and has a good appetite.
WHO def: slide 17-18
New classification system for severe acute malnutrition
Slide 19
Severe acute malnutrition (SAM)
General
Diagnosis
Clinical signs
- severe impaired physiology (multi- system)
- pre-death
- multi-system (slide 23-24)
Diagnosis
- Anthropometric failure (MUAC, growth chart)
Associated clinical signs + deficiencies
- due to metabolic/physiological decompensation
- 2’ to protein, energy (CH), electrolyte, mineral, trace element deficiencies
- hair changes (discolorisation, sparse, flag sign -> amino acid and copper)
- Skeleton (rickets) - > Vit D, calcium
- Angular stomatitis (subcutaneous fat preserved, but muscle not) -> protein
- Subcutaneous fat and muscle bulk loss
- oedema -> low albumin{protein}
- corneal clouding -> vit A
- bitot spots -> vit A
- corneal ulceration -> vit A
- dermatosis (take the nappy off)
- mood (miserable, irritable, apathetic)
Invisible / physiological changes in SAM
- Total body water: increased due to decrease in fat and muscle, leads to rise in extra-cellular fluid
- Liver: can’t cope with large amounts of protein in diet, makes less glucose (gluconeogenesis)
- Pancreas: decreased exocrine secretion (lipase) and endocrine function (decreased peripheral uptake of glucose)
- GIT: atrophy, decreased disaccharide enzymes (digestion), malabsorption, increased enteric infection (gut flora)
-
Cell walls: ‘leaky’ due to free radical membrane damage with K+ and Mg2+ leaking out and being excreted; Na+ leaks in
– Low K+ and Mg2+, high Na+ leads to oedema - Kidneys: can’t get rid of excess fluid and sodium
- Immune system: less efficient with decreased cell-mediated and humoral immunity, decreased complement proteins, decreased polymorphonuclear functions = predispose to infection
- Cortisol: levels increased with abnormal glucose tolerance
In state of starvation
- Short-term starvation/fasting:
➡️Free fatty acids (FFAs) and ketone bodies primarily oxidized using available fat stores from adipose tissue, and myofibrillar proteins can be broken down into amino acids, which can be converted into glucose (through gluconeogenesis). - After several days of starvation (when body fat has been depleted): ➡️Myofibrillarproteinsareextensivelybrokendowntomaintain
essential metabolic processes. - The short-term regulation of macronutrient oxidation and synthesis depends on insulin and glucagon, whereas the long-term regulation of these processes is mediated by other hormones, such as growth hormone, thyroid hormones, catecholamines and corticosteroids.
- In addition, cytokine release in cachexia, especially the release of tumour necrosis factor (TNF), IL-1 and IL-6, reduce appetite and food intake, and have direct catabolic effects on skeletal muscle and adipose tissue.
- Results in subcutaneous fat loss and muscle wasting
Oxidative stress
- Reduced levels of antioxidants, including vitamin E and glutathione.
- Combination of reduced intake and synthesis.
- An imbalance between reactive oxygen species production and detoxification by peroxisomes results in mitochondrial damage, which ultimately reduces ATP production and impairs cellular function in the liver.
- Mitochondrial dysfunction and ATP depletion together with specific nutrient deficiencies might influence the response to an intercurrent infection and contribute to the development of multi-organ failure
Hepatic function
- SAM with oedema associated with changes in hepatic metabolic function with the presence of hepatic steatosis (fatty liver).
- Not related to the impaired secretion of lipids (in the form of very low-density lipoproteins) by the liver.
- An increase in fatty acid release from adipose tissue that could be taken up by the liver observed in some but not all children
- Impaired hepatic lipid oxidation mainly due to impaired mitochondrial function. Also affecting hepatic synthetic pathways and reduced glucose synthesis.
Enteropathy
- one of the most common complications
- Diarrhoea, secretory and/or osmotic, common
- Poor nutrient digestion resulting from impaired hepatobiliary and pancreatic exocrine function could contribute to nutrient malabsorption and diarrhoea.
- Malnutrition leads to small intestinal villous blunting, thereby reducing intestinal absorptive capacity, including impaired monosaccharide and disaccharide absorption, which could contribute to osmotic diarrhoea.
- Distinct alterations in intestinal microbiota that can affect intestinal inflammation and function.
Cardiac function and haemodynamics
- Some studies reported cardiac muscle atrophy and decreased cardiac output
- Other studies reported normal cardiac output when corrected for body surface area with impairments observed only in the most severely ill children, probably related to sepsis.
