ENDONUTRICIÓN

Marthe Bricard
marthe.bricard@anahuac.mx

Para proteger el microbioma es importante dar probióticos.

Es la hermanita de becerril → les maman las bacterias.

SISTEMA DE EVALUACIÓN
- Examen escrito : 5% (​first 10 if you come to class​) +7 points → necesitas 3 en el
examen para el 10 jajaja (solo poner el nombre y ya tienes 3)
- Examen departamental (midterm) 20% → esa semana tenemos clase y examen el
VIERNES en la tarde. Todos los grupos hacen el examen al mismo tiempo.
- Prácticas 15%
- SGA (video making the questions) → 10 cuestionarios y te grabas. Lo
hacemos a 1 persona y tiene que escuchar su voz y nos grabamos
namas y luego 9 cuestionarios mas a otras personas sin grabarnos.
- Nos va a dar un ejemplito.
- The due is probably one month and a half from now, she gives us
a lot of time to perform the activities.
- Pregunta en español en tu video jajaja
- Calculations (your own: energy, macronutrientes ) se hacen en clase y lo
subes a BS
- MNA (5) elders → se lo pasas a los viejitos y ves qp.
- Participación en clase (nearpods → small exams): 10% Se pueden hacer antes de
clase si mando un artículo o después para ver si pusimos atención.
- ESTOS TE DAN PUNTOS EXTRA. Reward a todos si le echas ganitas.
- Resolución de Problema o Caso (third exam) 10%
- Exam is more related with diseases
- Acumulativos
- Examen colegiado en linea 20%
- Trabajo final 20% Algorithm (follow the rubric) → ta cabron ):
Any hospital patient
is my patient at RISK of undernutrition?
→ Screening tool (SGA → Weight loss, diet … NRS 2002)
- No, it isnt at risk → you do nothing at that momento → do the screening in 7 days
again
- YES he is at risk → assess → with what → you need to explain everything.

- Undernutrition → feed → does the (gut) work? HAHAHAHA

otra vez voy a tener que apagar la camara jajajajaajaj
- Yes → enteral nutrition
 - No → parenteral nutrition
Mete fórmulas, principios éticos, todo el temario alv.

Aprender a reconocer la undernutrition → malnutrition

- We will screen for malnutrición (all people) → inside the hospital.
- The most important screening tool → subjective goals assessment → what
brought the px to the hospital, physical exam…
- Tarea → ask 10 adultos y un video donde veas si los pacientes están en riesgo de
malnutrición y te vas a grabar.
- Other screening → NRS 2002, NRS, MUST
After the screening is the assessment.
tools such as anthropometry, body composition (how much fat), labs (albumin,
cholesterol), functional test (strength → loss of muscles). The interpretation of tha
assessment tools is not the same as someone in the ICU. Afterwards you figure out wtf is
going on and treat it.
Treatment → food JAJAJAJA
- Indications
- Contraindications, tubes in the stomach, how do we choose the entrada alv.
Venas, qp, parenteral nutrition.
- Formulas, etc.
- Prevent complications
Second activity → calculate → GS → calorimetría
Ecuaciones predictivas, esto ya lo vimos en cálculo jajaja iono
Ay nmms true jajajaja esta de huevis. Bueno pa mi, chance a ti te gusta.

Mira covix en el temario.

Enfermedades específicas → casos clínicos → nutrientes específicos que hacen que los
tratamientos médicos mejoren. OMEGA previene mets. come tu pescao
Remove encephalopathy → lactulose y aa.
Pharmaconutrition → food as drugs

CHAMACOS
- Una clase pa que te lo aprendas cabron.

GERIATRICS → How to screen them. Mini nutritional assessment.

Después de los 80 años el 50% tiene sarcopenia → fragilidad → mortalidad.

ETHICS COMO SI NO LO VIERAMOS PINCHES FOREVER.

The most important things → CPR (en el hospital)
ETHICAL PRINCIPLES → remove water and food in nutrition. Justo estaba leyendo esto,
no se mueren porque no comen, dejan de comer porque se van a morir.

MANY BOOKS.
- Fisiología de la nutrición McGraw-Hill 2012
 - Endonutrición apoyo nutricio ta chido
- El Gottschich es la biblia.
- Arenas para ale. Nutrición enteral y parenteral.

MALNUTRITION
- Obesity
- Undernutrition
Undernutrition → ​deficit ** macro (lipids, proteins, carbs), micro (minerals (trace
elements), vitamins) nutrients, ​partial or total, seen in hospital patients, with
consequences: body composition change (mass lost, ​40% muscle → 100% RIP)​,
functional changes.
**Due to a lack of intake, lack of absorption, digestion or metabolism
→ Not enough intake → malnutrition. Pero igual si te alimentas mal.

Examples:
Vitamin C: total: scurvy (pirates: teeth lost), partial: bleeding gums, joint edema; vitamin
D: osteopenia, cancer
B complex, B1, C,D, A,Zn, proteins, lipids, vitamin, K, K, Mg, PO4
Prevalence: 48% in hospitals Mex, 35-35% EU, 35-50% USA

Malnutrition usually refers to undernutrition, they use it interchangeably when it

shouldn't be. Mos obese people are also undernourished. Excess of macronutrients but a
micronutrient deficiency.

Undernutrition is a deficit of nutrients. A deficit happens if you don’t eat (not enough
intake will lead to a deficit), also because you don't absorb, digest or metabolize
nutrients. Deficit of micronutrients that could be partial or total.
Ex:
- If you have a deficit of vit C a total one then you get scruvy (escorbuto pa ale).
- If you have a partial deficit you have bleeding gums
- Continued deficit→ joint pain and joint oedema, tooth loss.
Si en 3 meses no tienes vitamina C → escorbuto → pasa rápido el pdo
- Vitamin D (ADEK liposoluble) stays from 6 months to 1 year in liver.
 - Osteopenia, osteoporosis, fractures,
- Vitamin D is an immune modulator to reduce inflammation and avoid
infections.
- Long term you get cancer.
- In short term you get more infections

Micronutrients→ minerals (trace elements?) y vitaminas.

Deficit of macro and or micronutrients that could be partial or total → definition of
undernutrition. This is seen in hospitals, like everywhere. The prevalence is huge. 50% of
patients inside the hospital have malnutrition.
Obeso con deficit of protein → undernutrition.
La Medicina en Europa está muy relacionada a prevenir y aquí en México pues no.
MEXICO MAGICO.

- Structural consequences and functional consequences of nutrient deficit.

- Cell loss, body composition change
- If you lose 40% of your muscles you die
- 20% of your heart it goes to shit → heart failure
- If u lose cells of your kidney → kidney failure
- ORGANIC FAILURE
- Immune system → u dont create immune cells → you get infections →
sepsis → CHOC → death

ARTÍCULOS
- ESPEN
- GLIM CRITERIA
ah caray nos mando articulos?
apenas nos va a mandar creooo

ESPEN criteria in a chart

UNDERNUTRITION CONSECUENCES​_________________________________
1. Impaired immune response: Impaired ability to fight infection.
2. -----Reduced muscle strength and fatigue: Inactivity, and reduced ability
to work, shop, cook and self-care. Poor muscle function may result in falls,
and in the case of poor respiratory muscle function result in poor cough
pressure-delaying expectoration and recovery from chest infection.
3. Inactivity: In bed-bound patients, this may result in pressure ulcers and
venous blood clots, which can break loose and embolize.
4. Impaired temperature regulation: hypothermia
5. Impaired wound healing: Increased wound-related complication, such as
infections and un-united fractures.
6. Impaired ability to regulate salt and fluid: Predispose to overhydration, or
dehydration
7. Impaired psycho-social function: Apathy, depression, introversion,
self-neglect, hypochondriasis, loss of libido and deterioration in social
interactions.
8. Low vitamin D levels (<20 ng/ml): Pooter physical performance, greater risk
of future nursing home admission and are independently associated with
an increased risk of falling in older people, particularly in those aged 65-75
years.
9. Increase morbidity in acute and chronic disease: Development of pressure
ulcers, poor wound healing and post-operative complications; acute
kidney failure, pneumonia and respiratory failure.
10. Higher mortality: Wide variety of patient groups and in younger patients.
11. Infections: The risk of infection is more than three times greater among
hospitalised malnourished patients than well nourished patients → sepsis
→ shock
a. neumonia, diarreas (c. difficile)
12. Organic failure
13. Longer hospital stays
14. hipoalbuminemia
a. Edema
b. lesser therapeutic response
15. Dysbiosis- lose good bacteria
16. Increased risk mortality
 17. Neuropathy
CLINICAL SIGNS OF DEFICITS OF MACRO & MICRO NUTRIENTS​________________

Micronutrients Macronutrients

❖ Vitamins ❖ Carbohydrates:
➢ A: rashes and typical ocular effects (eg, fatigue, constipation
xerophthalmia, night blindness) (bowel movement <
➢ B: 3 times a
■ Thiamine B1: ​beriberi, wernicke - week),headaches,
korsakoff syndrome nausea and bad
breath (because of
■ B2 Riboflavin:​ dermatitis, cheilosis and
cetosis:<130gr)
glossitis (magenta tongue & smooth)
❖ Proteins: ​Skin, hair
■ B3 Niacin: ​Pellagra
and nail problems,
■ B6 pyridoxine: ​Isoniazid. neurologic
loss of muscle mass,
symptoms with > 2g /day
increased risk of
■ B9 folic acid: ​ micro and megaloblastic
bone fractures,
anemia and neural tube defect
bigger appetite and
➢ C Ascorbic acid: scrurby and antioxidants, increased calorie
dehiscences, (prevents cronic disseases intake, risk of
such as coronary heart dissease & cancers) infections, fatty liver,
➢ E: mainly mild hemolytic anemia and may inhibit proper
nonspecific neurologic deficits. body growth in
➢ D: Heart disease and high blood pressure, children.
Diabetes, Infections and immune system ❖ Fats: ​dry scaly rash,
disorders, Falls in older people.Some types of decreased growth in
cancer, such as colon, prostate and breast infants and children,
cancers. increased
➢ Multiple sclerosis. susceptibility to
❖ Minerals infection, and poor
➢ Calcium: muscle aches, cramps, and spasms. wound healing.
pain in the thighs and arms when walking or Symptoms of an
moving. numbness and tingling in the hands, omega-3 fatty acid
arms, feet, and legs deficiency include
➢ Iron: Anemia →weak and tired, pagophagia, visual problems and
➢ Magnesium: fatigue, weakness sensory nerve
loss of appetite, nausea, vomiting disorders
➢ Potassium:muscle cramping and weakness,
constipation, bloating, or abdominal pain.
➢ Zinc: loss of appetite, taste, or smell. Decreased
function of the immune system and slowed
O -

severidad se mide
La
Fenotípicamente

growth

ESPEN
There has to be a risk to begin with & then you can evaluate the BMin order to
make a diagnosis. Free fat mass index: by dexa or bioimpedance→ no one in Mexx
has this shit in hospital settings, you barely weigh your patients.

GLIM CRITERIA
You need 1 from the phenotypic and 1 from etiology.
 ★ Etiologic criteria →
significant decrease of
ingestion (absorption or
ingestion) and
inflammation due to
chronic illness (obesity) and
acute inflammation
(gordito con accidente).
★ Phenotypic criteria → due to
weight loss (check criteria)

*If the patient has ONE severe criteria, then the classification is SEVERE.*

If you have nausea, vomit, diarrea, GI symptoms more than 2 week → malnutrition
1. Don't eat
2. Eat but don't absorb
3. Inflammation
Severity​_______________________________________________

=
EE
-

WHY DO WE LOSE MUSCLE MASS? ​(metabolic response to starvation you adapt,

with a metabolic response to stress you don’t adapt)
● Glucose dependent: ​brain cells, kidney (medulla), blood cells (red and
white)
○ They energy only depends on glucose, in starvation (when you don't
eat) your liver makes changes in the hormones, insulin goes down,
glucagon goes up.
○ We need them to be alive
○ Metabolic response to starvation (18hrs don´t eating):
metabolically you have changes if you don't have access to food
■ It starts when you star destroying your own muscles to obtain
glucose​ (catabolism)
● Insulin down, glucagon up → liver glycogen (only last 18 to 24hrs), liver
activate → gluconeogenesis (​carbons ​to create a new glucose molecule)
When you are at starvation, you use live glycogen, but it only last few hours
○ Cori cycle to make lactate to glucose.
○ Glycerol you need to break the ácidos grasos.
○ Lo más fácil es el catabolismo.
● Deficit glucose→ metabolic response to starvation→ gluconeogenesis→
catabolism (AA, muscles) ​AA: COO-NH
○ Importance of liver: start gluconeogenesis → break down muscles to
obtain proteins → aminoacids → break down aminoacids → carboxil
● → 24 HRS→ 72 HRS: ​300 gr of muscles​→ to produce ​75 gr AA
○ Your heart could die
○ in 3 days you lose 1kg of muscles when you are starving
● 100% mortality if you lose 40% loss of muscles
 ○ No hay reserva de músculos, cuando se pierden ya valio para 100pre
● Example: 13-15 kg of muscles: 1kg/3days, ​40% muscles→ die, 5 kg→ 3*5=​15
days to live
○ Days without food→ 30-40
● Adaptation (72 hrs) 3 days → 75gr of AA
○ After the adaptation → Only 25 gr AA (100 gr muscles) Con la
adaptación podemos sobrevivir 5 semanas sin comer
○ Brain adapts:​ ketones ​(70%)
○ Butyrate increases insulin sensitivity. (fiber→ butyrate with a normal
microbiome) helpful for the immune system (stimulate apoptosis).
■ The brain don´t use glucose as main resource of energy,
instead it uses ketones → that is why we reduce AA used
■ We can create ketones from lipids
■ Starving is an adaptation, glucagon goes up when there is a
stress response. So Starvation is a low stress response, but this
inflammation doesn't kill you. They were catabolic in the stress
response, the lost muscle mass and the consequences are
that they keep with fatigue and adinamia.
● They use steroids because of the inflammation.
○ Basal metabolic rate goes down 25%
■ Less energy to survive
○ When we have ​inflamation​, you ​don't have adaptation
■ That's why in UCI only survive 10 - 15 days
● Muscles=proteins=functions, homeostasis
● Measure catabolism​→ UUN (24 hour urine collection) Ureic Urinary Nitrogen
○ Provide: ​UUN x 6.25 ​=amount of exact proteins (16% of a gram
protein=the nitrogen) that you will have to give to the patients to
reduce catabolism.
○ it measures the proteins we are losing
○ 10-12 normal, women: 8-10 grs N, men: 10-12 grs Nitrogen/ day,
hypercatabolic (anabolism and catabolism):14-20 grams of UUN
○ The end product of catabolism is carboxyl and amines (COO- and
NH)
● RCP (PCR) to measure inflammation
● Glucose, TG
*NO water no Food→ 5 days / NO food but water→ 5 weeks*
SCREENING​_____________________________________________
● Prevalence 50%
● Screen 100% inside a hospital, easy, fast, not expensive
● Questions: weight, diet, acute disease (inflammation): coma, BMI
● Subjective Global Assessment
○ B: at risk, moderate undernutrition → assessment

Significant Weight Loss (ESPEN):

● Chronic: ​6 months​ (>10%) example: 70 kilos, lost 8kg
3 months​ → >7.5%,
1 month​ → >5% aba
Means that they are at risk. Do an assessment
● Acute:​ ​2 weeks ​→ >2% → risk → do an assessment.
● BMI 70/1.74/1.74 = 23 (ideal in men), BMI 77.5/1.76/1.76 =25
● (ESPEN criteria: RISK, <18.5, BMI <20 when <70 years old + significant weight
loss = undernutrition)
Para hacer la tarea hay que hacer el cuestionario
- Primero preguntas si puedes hacerle el cuestionario que valora la nutrición.
Mirelle puede estar en riesgo porque la pérdida de peso fue muy rápida.. Se llevo
10 kilos en 6 meses, amonooos. & because she has reduced intake.
se tardo 10 min
Form:
https://nutritioncareincanada.ca/sites/default/uploads/files/SGA%20Tool%20EN%
20BKWT_2017.pdf

6 kilos
➔ What´s your weight?
➔ Nutrient intake
◆ Have you reduced your intake?
● Yes, how long?
○ Significant mean less than 50% usual plate for more of
7 days → RISK → assess
● Time and quality
◆ What do you eat? Solid diet or fluids?
○ Solid (suboptimal) or liquids (like in swallowing
problems)
◆ In hospitals → water, tea and diluted juice → no
energy → acaloric diet.
◆ Energy: Supplements → ta bien.

➔ Weight
◆ Lost weight for the past ​6 months​?
● To know if it is​ chronic
● >10% → significant weight loss
◆ Past ​2 weeks​ lost weight?
● To know if it is ​acute
● > 2% is significant
➔ Symptoms
◆ Anorexia, diarrea, vomiting, nausea → medical impact
◆ How many times?
 ◆ GI symptoms ​MUST ​be present 2 weeks to have an impact in
nutritional status
◆ NUTRITIONAL CONSEQUENCES ARE AFTER 2 WEEKS, MEDICAL
CONSEQUENCES CAN BE AFTER 2-3 DAYS.

➔ Functional Capacity
◆ Do you consider you have a functional capacity? Make your life all by
your own
◆ Ask:
● Do you feel tired? You cannot prepare your food?, how long?
You can bathe on your own?
◆ Ambulatory people
● Do everything at home, they can't concentrate, you don't do
exercise, but you still wake up, and up, etc.
● Bed ridden → always in bed (read, poop, eat)

➔ Metabolic requirement
◆ What´s the reason you are in the hospital? NOT THE COMORBIDITIES.
◆ You search for metabolic stress, inflammation.
◆ Trauma : Associated with stress
● Severe stress: Head trauma
● Mild stress: urinary infection, 1 elective surgery (like liposuction,
sth small), small broken bone
● Moderate stress: pneumonia, mayor surgery (abdomen,
thorax), long bone fracture
● Severe stress: traumatic brain injury, multiple trauma, burns
and sepsis
➔ Physical examination​ (subjective)
◆ Lost muscles?
● Check arms and legs
○ Deltoid.
○ Legs → crural
○ You have to put x/xx/xxx acording your experience
about how severe it is. Mild, moderate or severe.
◆ Lost of fat mass
 ● Can you see te spaces between the ribs (yo see all the ribs
SEVERE)
○ Few? Moderate
○ All? Severe
● Or in the face
◆ Do you have edema/Ascites?
● Check wave sign
● Godet´s sign

➔ SGA Rating
◆ A​: Normal
● Normal treatment/ nothing
● 7 days later still at hospital:
○ Repeat the screening assessment
○ Because its probable that he had a complication, and
half people in the hospital is undernourished
◆ B​: at risk or with moderate undernutrition → assess
● if you have 1 significant risk (weight loss, GI symptoms,
disease)→ you can say is B
◆ C​: Severe undernutrition → assess.
● if you have 3 significant risk (weight loss, GI symptoms,
disease)→ you can say is a C
● not eating sign, disease, high stress B
● TBI, weight lost
● Stress + weight loss or bad alimentation
Screening during a party
● Oficial significant weight loss:​ More than → risk of undernutrition → assess
○ 20% in 1 year
○ 10% in 6 months
○ 7.5% in 3 months (​ESPEN criteria: 5%) → to make an earlier diagnosis
(with 5% you make an assessment, its more sensitive ) You get more
false positives. You can check false positive.
■ Prevalence of undernutrition in Europe: 25%
■ Its better to exaggerate in screenings
○ 5% in one month
○ 2% in 2 week
● Intake: ​eat ​<50% ​usual plate for more than 7 days, puts you at risk (NO
MAMES) y tienes que hacer assess
● Girls 1500/1600 kcal / day, boys 1800-2000 kcal/day

You perform this in people in the hospitals → usually they have inflammation →
stress → many problems. If they have lost weight and they get stress → more risk
of undernourished.

Tarea: hacerle el global assessment al otro.

Perform a complete nutritional history→ Timeline → weight loss
Si la hacen de a pedo pa comer les das nutrición parenteral. O sea si tienen
estrés de ver la comida, la “escondes” en la nutrición parenteral.

Usually the patients with anorexia nervosa die from heart failure. They lost their
muscles, > 40% → death.
The first muscle to be lesionado is the Heart is rich in glutamine so it's easier to
incorporate in the krebs cycle (se condensa el acetil co a y el oxalacetato).
What else do u eat? vitamins, supplements, drugs, etc.
→ Drug / nutrient interactions.

- Supplements, OTC, vitamins, minerls, prescription drugs; drug/nutrient

interactions
 - Grapefruit + drug → reduces metabolism (inhibe citocromos) →
increase eventos adversos
- Coffee + analgesics → agonism (improves absorption of AINES)
- Antiepileptics (valproic acid) + vitamin D → fractures for the long
term, because is antagonic with vitamin D, you cannot absorb
vitamin D, they compete. Supplement with vitamin D
- Quinolones + diary → 99% no absorption, antibiotics + food
(proteins) → no absorption (60-80%), dysbiosis → probiotics
- No dar Ab con comida.
- Ab should be taken fasting. But they can give you gastritis
because they cause destruction of pathological and
beneficial bacteria → dysbiosis (change bacteria, because
they kill them)
- To improve absorption give no food, but to don't lesionate
them given them probiotics during ab treatment and 15 days
after (every 8 hours).
- YES → antibiotics + probiotics (SB Saccharomyces boulardii) 3 times
/ day with or without food. During antibiotic treatment and 15 days
after. To every human in your consult.
- SB is a yeast
- 2 kind of probiotics: yeast (levadura) and bacteria
- Yeasts 3 times a day when you prescribe antibiotics.
During ab treatment and 10 days after.
- With or without food
Our microbiome develops when we are 3-5 years old so avoid antibiotics.
- Bacteria (fasting), yeast (SB)
- When (what time of the day), how many, with or without meals
- Article in BS → drug/nutrient interactions

Bioelectrical impedance
Machine that will measure you body mass with electricity, this electricity can’t
pass through the fat.
● 2 compartiments body fat​ : fat mass, free fat mass (muscle, bones, water)
○ This is how we know how amount of fat we have
○ 3-Bioimpedance: resistance fat mass
 ■ Before the test: Remove all metal, 4 hours fasting, not on
menses, no alcohol, no party (don't be awake too long), no
marathons, no drugs (diuretics) → because everything here
changes water content.
■ Contraindications: pace makers
■ Girls don´t have to be on their days → andrés
■ NOT​ the gold standard
○ 2→ “Bodpod”; air plethysmography. Density→ fat mass
■ You have the same amount of air between the 2
compartments. You take space and push the air,
the machine senses this air movement.
■ Air pressure in the front and back is different
● Measures density of the body
● Gives you fat mass and free fat mass
● Gold Standard of 2 compartments. JAJAJAJAJAJAJA
WEY NO PUEDO CON ESOT JAJAJAJAJAJAJAJAJAJAJJAS
■ Less
○ 4-Futrex
■ triceps fat→ all fat mass
■ near infrared ray
● 3 compartment
○ Gold Standard: ​fat mass, muscle, bone mineral
mass
○ DEXA: double energy x ray absorptiometry
(densitometry) → habia uno en CT
■ Measure density of the masses
■ Te dice bone mass.
■ For dual energy x ray
● 1 compartment: 5-Plyconometry (skin folds). Fat mass. Sensitive to water
changes→ Amount of fatness. It can be hurtful if it's not done properly.
○ Anthropometry (circumference) edema changes “body
composition”
● air preassure in the front and back is different
○ gives

★ 1st option: DEXA

 ★ 2nd air plethysmography
★ 3rd Bioimpedance
★ If it is not available: BODPOD
★ Then Bioimpedance
★ Futrex
★ plyconometry
Nutritional History
● Supplements, OTC, vitamins, minerals, pres
○ Grapefruit with ​any drug​: inhibit metabolism of drugs
○ Cofee + analgesics: agonism
○ Antiepilectics (valproic acid) + vit D → fractures
○ Quinolones + dairy→ no absoptioin, anntibiotics + food→ no
absorption (60-80%) dysbiosis
■ You need to be fasting with antibiotics
○ Yes: antibiotics + probiotics (SB, Saccharomuces bouladii)
■ Give to the patients
○ When (what time of the day), how manny, with or without meals

DESDE ACA NO SABEMOS QUE PEDO

Malnutrition Universal Screening Tool (MUST) for adults
Nutritional history:
Diet:
● Fruits​: 3 - 5 day: ​red​ (except watermelon - because glicemic excess)
○ A lot of berries
○ Tomatos
○ They have a lot of polyphenols → superfoods
■ Resveratrol
○ Fiber and polyphenols foods
■ Pear: it peel has a lot of fiber
○ Avoid high glycemic index: melon, papaya, mango, watermelon,
pineapple and juices
● Vegetables: 5/day ​raw, ​green​, other colors (carrots → cooked to reduce
glicemic index)
○ Green and raw are the best ones
○ → Ruminococcus (fiber) → microbiome
■ Rumino sound like cow → eat grass → the more
Ruminococcus you eat is better
● Cereals: ​avoid white (because they are simple carbs): rice, potatoes, pasta
simple carbs (not too many), ​Brown​ 1-3/day. Oatmeal
○ Fiber
● Seeds​ (chia), almonds, nuts;
○ We search for ​OMEGA 3
■ It protects against cardiovascular events and cancer
○ 2 gr EPA
● Proteins ​(3 per day): white fish, tuna, salmon. 5/week
○ At least 3 per day
○ Vegans don't have access to iron and b2
○ Best animal to eat: white fish
● Meat 1/week, poultry 1/week
● Eggs​ (one/day)
● Dairy:​ yogurt, kefir (Ca, vit D, probiotics) 1 - 3 /day
○ yogurt: Ca, vitamin D and probiotics
○
 ● Soy
○ Protein and
● H2O: 30 ml/kg

HASTA ACA QUIEN SABE QUE ONDA.

NUTRICIONAL HISTORY

One year ago he lost 10 kg in 1 month → 8.3% → it is significant → lost water,

muscles and bones. .
But one month ago que regained 12 kilos → fat.
- Second context he also lost 12 kilos for the past year, he lost fat → he is not
going to rebound. Its better to lose weight slowly.

1. You need to make a timeline first,

 2. Then, you do the 24 hour recall.

3. Search for signs of specific deficits

PCR → It is an acute-phase protein of hepatic origin that increases following

interleukin-6 secretion by macrophages and T cells. Its physiological role is to
bind to lysophosphatidylcholine expressed on the surface of dead or dying cells
(and some types of bacteria) in order to activate the complement system via C1q
→ you don't know where the inflammation is coming from.
- no tiene inflamacion porque esta debajo de 1mg/dl
→ if you suspect infection, search for procalcitonina.

Cuando hay inflamación el hígado tiene prioridades, está es la PCR, apoya el

proceso inflamatorio para salvaguardar el cuerpo.

Negative acute phase hepatic protein— whenever you have an inflammatory

process, the liver doesn’t s it, the values go down (​albumin, prealbumin,
transferrin, retinol binding protein​)
Albumin: (producida por el higado) ​ it maintains oncotic ;) pressure, lifespan 28
days
- Transporta proteínas
- Transporta hormonas
- Transporta medicina

→ Minimal amount of albumin that we should have is 3.5gramos → debajo de 3.5

es undernutrition
3-3.5 mild undernutrition
3.5-2.5 moderate undernutrition.
Less than 2.5 is severe undernutrition
Habla de desnutrición crónica por el lifespan, que es de casi un mes → 28 días
dura la albúmina.
A very low albumin tells us that mortality is higher
Puedes tener desnutrición con albúmina normal.
La paciente toma muchísima agua → 4 litros por dia → y diluye la concentración
de albúmina. Mucha pipi → pierdes water and electrolytes → se deshidrata por
perder electrolitos.

Cuando te deshidratas, las cosas se concentran. La albúmina se adapta, también

en px con anorexia, etc.
→ la interpretación es tricky.
En este caso, entonces, no usas la albúmina.

Prealbumin
Prealbumin is a protein made in your liver. Prealbumin helps carry thyroid
hormones and vitamin A through your bloodstream. It also helps regulate how
your body uses energy.​ Life span: 2-3 days → it's acute → what you were eating 2
days ago
→ Minimal normal amount 20 mg/dL
You can classify undernutrition with this one
Severity: 15-20 → mild under, 10-14.99 → moderate under, <10 mg/dL → severe

It is acute undernutrition, because the lifespan is only 2-3 days.

If it is more than 20, the person was being fed correctly at least 2-3 days ago.
Transferrin
8-10 days → Lifespan
<200 mg/dl → acute desnutrition
Transports IRON (ferritin). Iron deficit → transferrin up.
Example: a child lost in the forest → many people.
Anemia → ferritin increases because there is no iron, so the body senses to make
more transferrin to bond to iron. that’s why ​you cannot use transferrin for
undernutrition diagnosis.
Eating for the past 10 days?
Severity: 200-151 mild 150-100 mod less than 100 severe

It is acute → 10 days ago my patient was eating fine when more 200mg/dL
It interprets the way you where eating 10 days ago.

Retinol binding protein ​ (lifespan 12 hours) → ask the patient what he has eating
12 hours ago what thepatien was eating just ask, dont test this shit.
Retinol-binding protein (RBP) is the most sensitive measure of protein status. RBP
does not seem to be affected by the acute inflammatory response, like
prealbumin or albumin.
As its lifespan is 12 hours you better ask, not use it.

Para el assess
Prealbúmina is going to tell you cómo funciona tu tx de hace 2 días.
Transferrina la puedes ocupar para ver como va tu nutritional assessment de
hace 10 días
Si quieres ver un cambio en albúmina, necesitas esperar un mes de tratamiento.

Para asses you treatment use one of the ones que mide las agudas →
transferrin or prealbumin.
When you classify with proteins, and they don’t match regarding severity, you
take the worst classification.

If there is a patient in the ICU, and all three (albumin, prealbumin, transferrin) are
down it just means you have an inflammatory process, it doesn’t really mean the
patient is undernourished yet.
Low BUN (<6 → low protein intake, >20 → dehydration, high protein intake, kidney
failure).
the amount of urea nitrogen found in blood, it is a reflection of ​protein
catabolism​. → the amount of proteins
Normal es entre 6-20
● <6 es que no comen suficientes proteínas
● > 20 → they eat a lot of proteins → or ​dehydrations​ or kidney failure pero
para eso sacas la depuración de creatinina también.

Creatinine, the amount of creatinine is the result of muscle you have. -davila 2018,
true. La viejita mamada con creatinina de 1.3 JAJAJAJA X2 JAJAJAJA NMMS TANTO
TRAUMA QUE ME ACUERDO PERFECTO HAHAHAHAHAHA no mames . Sueño con el 1.3
JAJAJA jajajajajajajaaj HAHAHAHAHAHA taba mas mamada cuando era vegana
expliquenme eso, más que la viejita ??? mi creatinina era 763576523765
hahahahahahaha

Creatinine​ 0.5 (0.8-1 gr)

When you feed → verify that you made the correct calculations
Nutritional treatment response: transferrin (10 days), prealbumin (2 days)
- You expect the prealbumin/transferrin to go up after 2/10 days when you
want to assess the nutritional treatment, it goes up if it works.

Total cholesterol​ 100 mg/dL ​(​<150 mg/dL)​ ​→ steroids, hormones, cell membranes
(structures, fluidity)
TC Normal: 150-200
LDL- Cholesterol → atherogenic (risk of heart attack). Este debe estar menor 100.
Células espumosas, trombos, infartos.
HDL- cholesterol ​and TBI—> ​<25mg/dL​—> increased mortality risk (​sepsis, severe
TBI​). Este lleva colesterol de tejidos al liver para la depuración.
Normal is >60 mg/dL
→ Less HDL increases death. En px con sepsis aumenta el riesgo de
mortalidad.
 - You could use it in ICU for prognosis of your patient
- Obese people have lower HDL-c wow :(
- Less than 25 HDL they die

En ICU → Apache, others

- If in 24 h your HDL drops 50% you have a 50% chance to die, dierect
association between drop of hdl and death
- yo tengo HDL de 80 jajajajajajaj → eso mamonaaaa
OMEGA 3 es lv, su intake esta relacionado con HDL.
Aumentas HDL si comes omega 3, si comes fibra >21 gr al día, polifenoles (están

en frutos rojos, vino rojo) → ​regalenle vino rojo a ale pa que le

suba el HDL hahahaha porque borraste lo otrohaha
me caer re bien hahahaha te amo si te regalo es mi
bebida favoritax2 ACEPTO
porque se me hizo muy salvaje JAJAJAJAJAJA. Si regalame, lo podemos tomar
juntas.

JAJAJAj q es esto Una frase de vida.

Ponte a sartre y esto ya llegara a otro nivel de vida.

Cuando hay inflamación, las enzimas que cambian TGC y ester colesterol se
activan o desactivan. En inflamación HDL mantiene los TGC dentro. Las enzimas
que promueven que el colesterol vaya dentro de HDL se detienen, se llena de TGC,
es inútil.
apo A adentro tiene lípidos → LDL tiene TGC, HDL tiene free fatty acids and ester
cholesterol

Si das OMEGA 3 → activas anti inflamación → promueves las enzimas que hacen
que el HDL trabaje.

Obesidad → inflamación → reduce HDL → aumenta riesgo cardiovascular

in presence of inflammation, HDL stops being HDL, HDL is filled with triglycerides
and it stops working → the function changes

<<Si bajas de peso muy rápido, todo se desbalancea, debe ser poco a poco.
→ Dinamómetro → strength → >20kg mujeres, >30kg hombres.
Abajo de eso es undernutrition.

Diagnosis

Agudo <3 meses, crónico > 3

Si es inflamatorio o no
Mild, moderate or severe.

El px era chronic, severe undernutrition, without inflammation

→ indications and contraindications

access
Next week:

Enteral nutrition
Indications and contraindications → chapter 10
Check the access
Drug nutrients-interactions
Fasting blood glucose
Catabolism → break muscles—> AA—> C, COO-, ​NH2.​ Urinary Ureic Nitrogen (urine
24 hour collect) →women: 8-10 grams/day N, Men: 10-12 grams/day
16% of a protein=Nitrogen,​ ?? How many proteins do I give??—: ​UUn*6.25​ (is that
number because 16% of a protein is nitrogen) (1/16*100=6.25)

Recap_
Nutritional history:
Time line→ one year have you lost weight
Significant?? % (1 year, 6, 3, 1, 2 weeks)
Patient: 120 kilos one year ago
1. Year ago 10 kilos (during one month → 8.3%(significant)) → ​lost FFM (water,
muscles, if you adapt correctly then fat),​ some fat _____ gained 12 kilos →
fat mass (rebound!!!). Consequences: osteopenia, osteoporosis—>
fractures, sarcopenia
2. 10 kilos in one year (1kg/month)—> loss ​Fat mass
 ENTERAL NUTRITION INDICATIONS
Anyone that doesn’t achieve his/her nutritional goal by mouth for the past 5 days
(ESPEN), 7 days (ASPEN)
Reasons:
1- Cannot
2- Don’t want to
3-SHouldn’t eat polymeric nutrients

If the gut works, use it

If the gut works partially, use it partially→​ Benefits​ of using the gut
- When you stimulate the structure of the gut you stimulate the function, the
organs attached to the GI tract. Microbioma, etc.
- Si alguien tiene CA de esófago, no das IV, solo te saltas el esófago y usas el
gut.
Minimal enteral nutrition​: 10-20mL/hour/day (240-480 mL/day, ​1 glass of
nutrition to your patient in 24 hours​). Even if you don't eat everything by the GI
tract, you give minimal so you have all the benefits of using the gut.
ASAP (As soon as possible)​: Early enteral nutrition: ​first 48 hours ​after hospital
admission→ Reduces catabolism→ Reduces mortality. Tienes 2 días para
empezar el nutritional treatment.

Calorimetry: so you can know how many calories does your patient eat.
Oral supplement
Gastrointestinal tubes
Anybody not achieving the nutritional goal by mouth more than 5 days (ESPEN
guidelines) or 7 days (ASPEN guidelines).
Retrospective (more than 5 days ago) o prospective (for the next 5 days,
example: coma)
Gold Std: study: indirect calorimetry→ measures exact energy needed. Respiratory
Quotient: balanced diet or not??
Have you reduced your intake?, clinical symptoms, anemias or nutritional
deficits→ when you assessed the patient.

Enteral indications (patients who cannot achieve nutritional goal):

● Glasgow <8
● Severe head trauma
● Coma
● Tongue cancer
● Pharynx cancer
 ● Larynx cancer
● Neurological → Multiple sclerosis, Parkinson, Cerebral palsy, Amyotrophic
lateral sclerosis (ELA), huntington. duchenne, Guillain Barre.
○ Swallowing issues.
● Proximal upper GI malignancies, head and neck cancers,?
● ERGE
● EVC → 60% of patients have swallowing problems → micro bronchial
aspirations → chemical pneumonia
○ After a vascular event people persist with problems swallowing 60%
● Microbroncoaspirations
● Airway burns (hypercatabolic patients)
○ People that need a lot of energy so they don't accomplish the
nutrients needed
● Hypercatabolic patients (burns, severe trauma, stress, sepsis​,
Hyperthyroidism, some cancer patients ​)
● Traumatic brain injury
○ Coma
● Intubation and enteral nutrition
○ Stress related with any injury or with hypercatabolism
● Pregnancy is absolute contraindication
● Obstructive paraesophageal hernia - you have to go to the ileum
● Short bowel syndrome
○ You need 2 years to stimulate after surgery - intestinalization colon -
you stimulate constantly with nutrients.
○ Colon intestinalization → ametaplasic colonocitos → le das minimal
enteral nutrition → para que absorban nutrientes y el colo no pierda
esa capacidad.
● Metaplastic change involving the absorption of nutrients
● Achalasia.
● Severe gastroparesia → post pyloric nutrition
● Pyloric stenosis.

People who don’t want to achieve nutritional goal: (neurological diseases and
psychiatric diseases)
● Psychiatric disorders
● Pica
● Rabies
● Anorexia
○ Anorexia nervosa
 ○ Anorexia of the age: geriatric patients
● Bulimia
● Eating disorders
● Depression
● Dementia and delirium
● Terminal alzheimer (because of psychotic events)--> they think you want
to poison them
○ Organic issue: problem swallowing
○ Hallucinations
● Munchhausen syndrome
● Hypothyroidism
● Psychotic patients
● Psychiatric patients
● Toothache
● Anxiety
● Cachexia
● Hipotiroidismo
● Drug users → los choco hongos? tas busy en el viaje → el peyotaxo deli

Enteral indications: People who shouldn’t eat polymeric food

● Severe undernutrition
● Severe Pancreatitis
○ You use the gut as soon as possible but with a different formula
(elemental formula and not polymeric formula)
■ Necrosis es contraindicación → ahí no usas el gut.
● Cirrhosis
● Active CUCI or Crohn or Celiac (active proinflammatory issues)
○ You have to use minimal enteral nutrition to stimulate peristalsis and
prevent adhesions
○ If you give specific nutrients you stimulate anti inflammatory
processes
■ You stimulate good microbiome if you give the good nutrients
○ 10 mL/hr/day to stimulate the minimal
○ CUCI bleeds→ avoid pooping by avoiding fiber. ​Use an elemental
formula (no fiber) that you can absorb.
○ Celiac disease → you give specific nutrientes que absorben rápido y
no necesitan digerirse y das probióticos.
TIENE EN COMÚN LA INFLAMACIÓN → cuci, crohn y celiac disease
Das vitamina C, D (directo antiinflamatorio contra IL-10), Zn, Se, OMEGA 3 →
immunotherapy → + probióticos que regulan el Sistema inmune
● Phenylketonuria →some metabolic diseases you cant give them some
nutrients.
● GI fistulas
○ Colon - colostomy - you can use the gut
○ Yeyunum high output fistula is the only contraindication - you can’t
use the gut because you don’t have the absorption right
● Post surgery
○ ERAS (early recovery after surgery) protocol, to reduce
complications→ reduce catabolism→ reduce death
■ Pre and postoperative→ you feed them
● Bariatric surgery → careful
● After GI Bleeding → primero ayudas y ya luego que haga el fasting
● Metabolic diseases
● Post transplant
● Paralytics ileus → después de anestesia
Minimal enteral nutritions → motilin (hormone) → peristalsis
- Bacteria y agua lo estimulan, cuando tienes hambre tu gut se mueve y
aumenta sonidos

Given by her:
● Elemental formulas (AA: glutamine: MCT, no fiber) hydrolyzed formulas
● Malabsorption
● Active CUCI (low residue)- pseudocolitis , you give elemental formulas do
absorb in yeyunum. Remove fiber but you can still use gut
● Celiac : give nutrients that can be absorbed easily and probiotics
● Crohn (pseudo-obstruction → peristalsis), celiac
D,C Zn, Se, omega 3 → immunotherapy. This plus probiotics to modulate the
immune system. (for cuci, crohn, celiac)

● Chronic hepatic and kidney failure, transplant patients

● Severe pancreatitis
● Short bowel syndrome
● Diarrhea (colitis pseudomembranosa)

ERAS PROTOCOL
Surgery: ERAS protocol
○ → lesser catabolism, postsurgical complications
 ○ Control group:​ usual tx in GI surgeries: fast 3 to 5 days
○ Experimental: ​8-12 hours after surgery started EN (elemental
formulas: AA, peptides, maltodextrina, MCT→ predigested food→
absorbed, minimal enteral nutrition)
○ ??: lesser ​dehiscence of GI wounds ​(surgical injuries open)?? →
experimental group→ why? → because of aa, proteins will help you
heal→ energy→ cells heal, GAP
○ Before surgery: 8 hours feed with solids, drink liquids 2 hours before
surgery, 2 hours before→ you give an oral glucose shot ​50 grams
glucose + 200 ml H2O
■ To reduce catabolism
○ During: anesthesia → avoid postsurgical ileus (gastric: 24 hours,
jejunum; 8 hours​, colon: 72 hours -that’s why you ask patients if they
have gone to poop-)
■ Entre más esté el paciente con anestesia, pero va a ser el
paralytic ileus → avoid prolonging surgery
○ After surgery: feed 8-12 hours with elemental formulas ​10-20 ml/hour
(slowly minimal enteral nutrition)
■ No meats, fruits, vegetables, solids etc. 10 ml/hour minimal
enteral nutrition, a few drops of AA, that will maintain
homeostasis and you avoid post surgical complications.
Entre el antes, durante y después es más de un día sin alimentación → stress
response → catabolismo → gluconeogénesis.
Produces 5-6 L de saliva al día fisiológicamente. Liquid enzymes saliva que va al
gut. Si le damos en esos 6 L minimal nutrition → 1 glass → da aa, energía para
mantener homeostasis. Promueves healing, GAP junctions, etc. jajajaja se
contesta las preguntas sola y yo las repito JAJAJAJA es bien tierna
Cortas el gut, una sutura las junta pero las GPA junctions, new tissue es lo que
hace que se pegue haces esto por medio de la alimentación. Das energía.
Si esperas 5 días se atrofia, disbiosis, complicaciones.
*Hay un archivo en bs de esto

Contraindications: at risk of death if you use it (you can harm the patient if you
use the gut
If I use the gut I could kill/ hurt my patient:
● High Output Jejunal Fistula (more 500mL/day)
● “Obstruction” , “isquemia”, “Peritonitis” (appendicitis)→ Tx: surgery→After
surgery: Enteral Nutrition
● Mayor bleeding (during the bleeding, active bleeding)
● Terminal patients (autonomy) → if they don't want to receive enteral
nutrition
● Shock, hemodynamic instability → lack of oxygen → homeostasis →
maintained with energy (ATPasa Na/K) → complication: ischemia, necrosis
of the gut.
● Necrotic pancreatitis
○ Severe pancratic acute disease you can use the gut with some
formulas
● Uncoercive/ Vomiting a lot
 ○ Chemoterapia
○ Bulimic patient
○ Hyperemesis Gravidarum(pregnancy)
● Uncoercive diarrhea
○ You cannot treat it so you can’t use the gut
■ Chemotherapy
■ Radiation
■ Celiac disease
■ IBD
■ Clostridium difficile
■ Cholera
● Crohn y CUCI puedes usar el resto del gut, you only
need to avoid fiber, removing fiber and steroids from
formula, but if then they still have diarrhea you can
classify it as contraindication.
● MO transplant (immunity abolishes) → we need 100 neutrophils to feed the
patient
● Risk of dehydration and electrolyte imbalance
● Caustic burns
● Frozen Abdominal (catastrophe)→ las frozen, las frozen son lesbianas
jajaja así se les dice? jajajaj ya vist el
video?​https://www.youtube.com/watch?v=UD4 TSql pc do ):
mandamelo→ this happens in trauma, instead of open the patient you
frozen it, if you put them in the stress of surgery, they die, so you pack the
patient and when they are stabilized they open them
● Severe paralytic ileus (more than 5 days)→ abdominal sepsis → “ileo
paralítico- adios dice pulido”
● NCE (children)
● Burns
● Abdominal trauma/visceral perforation
● Active upper bleeding, inferior bleedin: after therapy you can use the gut

Formulas → esto no no lo dio

● Polymeric: complex food (fiber: prebiotics, LCFA, proteins) needs digestion
● Oligomeric: semi digested food: MCT, di/tri peptides, di/tri saccharides
● Elemental (hydrolysis): digested; peptides:AA, dextrin, MCT
● Alitraq, Peptamen jr, inmunes
● Proteins: hypo/hyper, 15% normal, 6%, 18-21%
● Kcal: normocaloric 1kcal/ml, hyper 1.2-2 kcal/ml
 ● AA: glutamine, arginine, BCAA
● Dextrose
● Lipids: oils (MCT), olive oil, omega 3

EXAM IS UP TO ​INDICATIONS
Nos mandará lista de temas

Bones, muscles and fat are the 3 compartments

Benefits for Using the Gut; minimal enteral

nutrition
10-20ml/hour/day
Maintain Structure
● Enterocyte → absorption
● GAP junctions (zinc) → lo mantenemos con proteínas (aminoácidos y zinc)
○ Gap junctions are a specialized intercellular connection between a
multitude of animal cell-types. They directly connect the cytoplasm
of two cells, which allows various molecules, ions and electrical
impulses to directly pass through a regulated gate between cells.
● Translocation → infeccion, celiac deseas.
● Goblet cells → sintetizan mucosa
● Parietal cells → ácido clorhídrico (función de defense against bacteria)
○ la acidez activa los fármacos, las enzimas, etc.
● GALT (B cells maduran a→IgA)→ Immune tissue. It produces
Immunoglobulins (especially IgA)
○ The absorption area in our gut is equivalent to a football field
● Microbiota (90% bacteria, the rest is fungus, dr says its almost 99)
● Organs:
○ Pancreas
○ Gallbladder→ if you don’t use it
○ Liver
○ Brain

Maintain Function
 ● Enterocyte → Absorption
● Gap juntion -->Against→ translocation→ bacterial→ sepsis, food
translocation→ antigen→ food allergies, celiac disease (bacteria crosses
intestinal barrier, it predisposes to infections)
● Mucosa
● Parietal cells → Synthesis HCl→ against bacteria. These are stimulated by
acidity:
○ Activate proteinase→ protein digestion (it gets broken down)(carbs
and nutrients don’t, acidity blocks their digestion9
○ Absorption of cations (Mg, Cu, Se, Fe)
○ Activation of drugs
● GALT → IgA synthesis en mucosa GI→ circulation → other mucosa:
respiratory tract genito/urinary
○ Alimentalos bien y ya no les da neumonía ni infecciones urinarias en
hospitales.
● Microbioma → Against opportunistic bacteria (​C. difficile​), (​microbiome gut
brain axis​), neurological system → 95% synthesis → sacaromyces no se
que is the treatment for c difficile
○ Por eso la colitis se asocia a la depresión
● Protects against disease (DM), con lactobacillus → induce transformation
of complex carbs (Fibra) → butirato → aumenta sensibilidad a insulina.
● Vit k, B complex, BCAA synthesis

BENEFITS OBTAINED BY USING THE GUT

ORGANS
● Pancreas → Digestion, hormone synthesis
● Bile→ absorptions lipids, liposoluble vitamins (ADEK
● Gallbladder: If we don’t use it→ stones
● Liver: First step metabolism (drugs, nutrients)
● Brain: Microbiome gut brain axis (enterochromaffin produces serotonin 9)

Enteral Access. How to choose the access

1- Time?
a) ​< 4 weeks​ ➝ ​Temporal Access
Access through face:
● Nose→ ​Nasoenteric tubes (Gold standard)
 ● Mouth ➝ if nose “not working”, just if there are problems like:
○ Nose obstruction (tumors, polyps, adenoids) or septal deviation
■ If you pass there will be epistaxis
○ Trauma, Fx in the base of the skull and nose ➝ ​Through the nose the
tube could go into the brain
○ Severe traumatic brain injury
■ Glasgow < 8​→ We could have fracture base skull→ “brain
nutrition”
■ Fx that cannot be localized on the TAC ➝ Wait 3 days to see if
it appears in the TAC

b) ​> 4 weeks ​➝ ​Permanent Access

● Directly access the gut→ cut the gut (stomach or jejunum)
○ By endoscopy: ​PEG​ (Percutaneous endoscopic gastrostomy push or
pull​)
○ PEJ → no se usan porque ponen al px en riesgo. Puedes perforar el
gut
○ Surgery: gastrostomy (stamm, Janeway, Witzel) or jejunostomy.

2- Bronchoaspiration risk?
❏ Contraindications to use the stomach (use jejunum): Cancer, ulcers,
bariatric surgery, pyloric stenosis, ​severe reflux​, gastroparesis by chemo.
i) Taking space of the stomach (tumores, balloons)
ii) Increase intraabdominal pressure (pregnancy, ascites)
iii) Cannot protect airway (coma, lethargy, somnolence, severe
gastroparesis, encephalopathy)

a) NO→ Gastric (physio)

★ Could I feed stomach with a bronchoaspiration risk? Yes, if:
○ Head >60ª
○ Prokinetics
○ Feed slow continuous infusion

b) If YES ➝ jejunum​ ➝ endoscopy - What does it involves?

★ Note: ​we need resources→ sedation, endoscopy, special tube, formula
(elemental), nursing time, slow slee, pump avoid complication: ​dumping
 syndrome​ (vagal syndrome→ complex nutrients, too fast in your bowel→
diarrhea + syncope), use: continuous infusion to feed.
○ If you feed too fast theres a compilation (dumping sindrome)
★ We cannot use it to give drugs (its alcalin). Complication: not activating
drugs, obstruct the tube.

If temporal:
NAso gastric→ bed
Naso jejunal (temporal)→ endoscopy

VIDEO
Collocation of nasogastric tube
- Chest X-Ray ➝ GOLD STANDARD
- If you’re not sure of the collocation because there’s no way to use an X-Ray,
DON ́ T PUT the nasogastric tube

HASTA ACA NOS QUEDAMOS

• After collocation wait 8 - 12 h (ASPEN criteria) to tie minimal enteral nutrition

The reality is that you could just wait 2 h

Pemanent access
➔ Percutaneous endoscopic gastrostomy (PEG) ➡PEG with jejunal extension
(PEGJ). You cut
Gastric
For stomach, there is pull and push technique
● Push→ you have more complications (its with needle, when you pull them
they open, it could go to the peritoneal cavity)
● Pull→ its preferred
○ Wait 4-6 hours so it doesn't bleed
Access by endoscopy or by surgery
Surgery when there is contraindication for endoscopy
● Surgery (stamm, janeway, witzel)

Jejunum
 ● PEJ (don’t use it)
● Surgery: jejunostomy

Case: severe TBI, coma patient, for 12 months. What access would you choose?
Enteral or Parenteral? Does the gut function? yes→ use it→ Enteral
Time? Permanent
Bronchoaspiration→ yes → jejunum
Drugs? yes→ NOT IV for 12 months→ sepsis. Drug enteral access→ jejunum→ no,
we need gastric access

We use ​PEGJ

Semi elemental, elemental → alitraq, peptamen jr, inmunex

polymeric: harder for the gut to assimilate (food in liquid form)
- If you only have polymeric you can use it but you have to start very slowly (10ml/h).

elemental semi elemental its prehydrolyzed nutrients(predigested, absorption is faster)

Contraindications, benefits gut, complications and formulas.
Examen hasta indications
 ULTIMA CLASE PARA MEDIO TERMINO
• After collocation wait 8 - 12 h (ASPEN criteria) to tie minimal enteral nutrition
The reality is that you could just wait 2 h

Pull technique → endoscopio, needle, jalas hasta la boquita, le pones como el

seguro y lo jalas hasta que quede como así

y lo sacas jalandolo alv, porque no necesitas suturas

The push technique seems easy but it's not.

Complications: insertar esto en la cavidad peritoneal, es más difícil.
Yo digo que si esta dificil es JAJAJA tqm chivis que no ma como no se te sale a
menos que te la jales alv ta asqueroso hahaha te quiero mucho
PEJ:

Permanent access
➔ Percutaneous endoscopic gastrostomy (PEG) ➡PEG with jejunal extension
(PEGJ). You cut
- Tome (cut), direct enteral access: by endoscopy, by surgery
- Gastrostomy: ​PEG​ (percutaneous endoscopic gastrostomy). How to take it
out: pull, surgical (Stamm, Janeway, Witzell) → they involve: sutures → 2
surgeries → 2 $$$
- Preferred: PEG: ​pull​, push technique → sedation, easy to to, remove by
pulling
- Do it by surgery if ​contraindications to it by endoscopy​: ascites (increase
risk of infections), (pregnancy: none), obesity (because you don't see the
light), cannot pass by endoscope: tumor, achalasia, if you perform another
surgery
 - Jejunostomy: ​PEJ​ (it exist but don't use it → you can perforate the gut),
surgical​ (x2 surgeries)
- Note: temporal nasojejunal tube →​ endoscopy, permanent ​jejunostomy →
by ​surgery

Entre la abdominal wall y el estómago hay fatt

Entre la abdominal wall y el yeyuno hay fat, órganos. En cadáveres el intestino se
ve como en los libros, vivo se ve como una maraña, si intentas perforar para el
yeyuno, vas a perforar intestinos.

Gastric
For stomach, there is pull and push technique
● Push→ you have more complications (its with needle, when you pull them
they open, it could go to the peritoneal cavity)
● Pull→ its preferred
○ Wait 4-6 hours so it doesn't bleed
Access by endoscopy or by surgery
Surgery when there is contraindication for endoscopy
● Surgery (stamm, janeway, witzel)

Jejunum
● PEJ (don’t use it)
● Surgery: jejunostomy

How do you take gastrostomy out?

PEG you just pull it out. Remove the bumper outside the skin and pull you could
use anesthetics but not necessarily.
We only need a light sedation, we rather use the pull technique

● Gastrostomy with sutures needs surgery

● Jejunostomy is a permanent access, you have to access by surgery (to
remove it too)

Case:​ severe TBI, coma patient, for 12 months. ​What access would you choose?
Ask each questions…
Home, prescription drugs.
Enteral or Parenteral?​ Does the gut function? yes→ use it→ ​Enteral
Time?​ ​Permanent
Bronchoaspiration​→ yes → ​jejunal
Drugs? ​yes→ NOT IV for 12 months→ sepsis. ​Drug enteral access→ ​jejunum→ no,
we need ​gastric access
- (acidity, not obstruction of jejunal tube)

Percutaneous Endoscopic Gastrostomy with Jejunal extension → excellent :)

gastrostomy is cool → drugs, water, y tambien si quieres to remove thing for

aspiration (secreciones por un tumor, las sacas para que no hagan
broncoaspiration)

Se pone por pull technique

Lavar los tubos con awa, para evitar la obstrucción con los tubos.

PEG
Skin and next to it the percutaneous gastrostomy
Endoscope is still there so you can watch everything
Through the endoscope you can grab the tube and take it with you so the come
together and reach together the jejunum and then you remove the endoscope
 ● Today there's a jejunal port, gastric port for 3 things:
1. Supply drugs (you cannot do it through jejunum you can make an
obstruction because there is no acid there)
2. To provide something fast (If you feed too fast the jejunum you have
Dumping Syndrome)
3. Suction

Gastric residue only measured in the stomach → EXAMEN

Complications: Prevention
- Broncho-aspiration​: jejunal Access, If i need to feed the stomach →
prokinetics, continuous infusion, ​gastric residues every 6 hours in the
stomach ​(just before next bolus feed, or 2 hours after feeding), head at
>60%

- Why not measure the residue in all patients receiving gastric nutrition? you
are taking out nutrients (like eating your own vomit) → ​risk of
undernutrition
- no lo quitas en todos porque tambien les quitas nutritientes (food)
and acido

Gastric Residue
- Gastrostomy is close → you change o something
- you open to give food in → dentro del estómago (la comida se
acumula en el estómago) cuando la alimentación se acaba tienes
que esperar 2 horas para que llegue al duodeno
- paciente con riesgo de broncoaspiración la comida va para arriba y lo que
hacemos es medir el residuo (abrimos el tubo y aspiramos el contenido) →
succionas → lo que este es el residuo gástrico.

62.5 ml/hr/day (infusion rate) with an enteral pump

Estómago → puedes hacer lo que quieras (bolus, intermitente o continuo)

Jejunum → continuous (bolus no puedes dar por la velocidad) dumping
síndrome si lo das en bolus.

Types of Feeding
- 3- Bolus feed:​ ​40 min to one hour​, 300-500 ml, 4-6 feeds per day → ​375
ml/hour ​- ONLY IN STOMACH, TO AVOID dumping syndromes in jejunum
- 2- Intermittent feeds​: feed ​5 hours per one hour “rest” 4 times per day: 24
hours → tolerance? → ​4 hours feed per 2 hours rest 4 ​times per day →
tolerance ​(gastrointestinal hemodinamic cool) → 3 hours feed + 3 hours
rest*4 per day. Example: 375 ml in 3 hours →​ ​125 ml/hour. → intermitent
- Feed 5 hours rest 1 hour
- 1- Continuous infusion: all the time (24/7): start ​20 ml/hour/day (minimal
enteral nutrition)​ → ​every 8-12 hours verify ​tolerance (ESTA ES LA MÁS
TOLERADA) → por que es lenta
- (GI tolerance, metabolic tolerance: glycemia, triglycerides, kidneys.

Hemodynamic tolerance ​→ the most important → blood pressure. If the patient is

in shock we can not feed him/her) → increase amount 20-40 ml/hour for 8-12
hours, after this verify tolerance and if it is okay → increase 20-40 ml/hour → 1500
kcal/day → 1500 ml/day, divided by 24 hour in a day →​ 62,5 ml/hour/day ​(we
reach the amount of food that the patient need).
- We need to feed the patient as soon as possible
(hemodynamic stability)
- Is the slowest and the most tolerated ​(tolerance is associated
with speed and osmolarity)

Empiezas con minimal enteral nutrition.

Ve si está hemodinamicamente
- Si está intolerante → BP dropping, HR muy alto, saturación baja, fiebre, es
un shock y te esperas para alimentar.
- Si todo esta bien 8.12 hrs después aumentas la MEN a 20-40 ml.
 Formulas
★ Polymeric: ​complex food (fiber: prebiotics, long chain fatty acids→
absorption with bile, proteins)
★ Oligomeric ​(semi elemental): semi digested food: to reduce energy
needed for digestion; Medium chain triglycerides (they cross membranes
no problem without bile) , di/tripeptides, di/tri saccharides. NO fiber
★ Elemental (hydrolysis): ​completely digested: peptides, AA, dextrin, medium
chain triglycerides (passive transport) → digestion nor energy nor
carnitine (transporter for mitochondria) needed → absorbed directly (by
passive diffusion)
○ Examples: Alitraq, Peptamen junior, inmunex (IMX, enterex)
○ SCFA passive (synthesis by microbiome)
■ We dont need to eat short chain fatty acids, we produce it
★ Proteins:
○ hypoproteic (​6%​): ​example: kidney failure without dialysis and
hepatic encephalopathy
○ ​15% of the formula protein is ​normal protein (of the formula),
normoproteic,
○ Hyperproteic 18-21% (burns, trauma, hypermetabolic, sepsis,
malnourished, sarcopenia, chronic kidney patient with dialysis→
relationship ​stress and proteins​). ​Measure: BUN/creatinine (take
care of the kidney always)
★ Measure urinary ureic nitrogen NUU*6.25=proteins needed, ask?? BUN¿¿
★ Kcal: normocaloric 1 kcal/ml, ​hypercaloric ​1.2-2 kcal/ml ​of the formula
(patients: water restrictions ascites, kidney, hepatic, heart failure anasarca)

- Modules: one nutrient (modular nutrition), you decide that you want one
specific nutrient that aren’t on formulas
- Proteins: casein (you add it when normocaloric is not enough)
- AA: glutamine, arginine, BCAA (Leu, Val, ILeu)
- Dextrose: maltodextrine
- Lipids: oils (MCT oil), olive oil, omega 3
Short chain fatty acids are produced by the microbiome.

Complications -
dijo a Nosotros
NO nos

pero pues
el examen espacio
todos
pa
.
 ★ Mechanic: ​during insertion of the tube, with the presence of the tube→
inflammation, ulcers, infections, sinusitis, otitis, mucosa necrosis: respect
time, adjust tubes. Obstruction of the tube (tube for drugs)--> prevention:
flush the tube before and after using it with 20 mL warm water. Treatment:
in/out movement 20 ml warm water.
★ Metabolic: ​dehydration, electrolytic unbalance, glycemia (up or down),
BUN (proteins), hepatic enzymes (they go up if you don't use enteral).
★ Refeeding Syndrome: (severe electrolyte and fluid shifts associated with
metabolic abnormalities in malnourished patients -there’s a bad tolerance
to food during WW2 in the camps they had refeeding syndrome (after 5-7
days of not receiving nutrients), you cannot feed them to fast because
when you give glucose, it enters to the cell and it does with sodium -) to
take out Na you need K, if there’s not outside the cell there’s hypokalemia.
○ undernutrition (5 days), glucose → enters cell with Na, H2O →
maintain homeostasis → exit Na, enter K by ATPasa → K goes in, Mg ,
ATP (phosphate) → hypokalemia, hypomagnesemia,
hypophosphatemia (if phosphate goes outside the cell very quickly),
vitamin B! (thiamin) It needs Pyruvate dehydrogenase so it catalyzes
the reaction of pyruvate and a lipoamide to give the acetylated
dihydrolipoamide and carbon dioxide to enter into the Krebs Cycle.
→ heart failure and neurological syndromes
★ K (1-2mEq/kg/day, not more than 10 mEq of K per hour), Mg (1 gram every 12
hours), PO4 before feeding, thiamin (300 mg), start at 50% of energy
requirements. YOU NEED TO GIVE K, MG AND THIAMIN.
★ GI symptoms: associated to speed, osmolarity of formula. Differential
diagnosis: C. difficile (prevention and treatment: give Saccharomyces
boulardii).

If they gain weight → obesity but no undernutrition

If you have a complication of diabetes of infection then you add mild stress
Having chemo/radio increases stress
ASPEN is for diagnosis no screening
% of weight loss
70 kilos -100%
2 kilos
 PARENTERAL NUTRITION

Not achieving nutritional goals by enteral nutrition for more than 5 days (ESPEN), 7 days
(ASPEN)

Difference Total
- Total → give everything (macro, micro, water, vitaminas, lípidos, si damos potasio
→ por la vena - excepto (fibra) carbohidratos complejos.

Partial parenteral nutrition indications

- To complete enteral nutrition con partial parenteral
- Use it: Time 5-15 days
- Osmolaridad en los brazos → (<900 Osm)
- Through basilic and cephalic veins
- Active CUCI, CROHn, celiac
- Ulcerative colitis
- Chemotherapy (diarrhea, increased energy demands): chemotoxicity prevention:
C, Zn, Se, D, w3, probiotics. → depending on the amount of diarrhea, if it affects
the absorption of nutrients you can have total or partial parenteral nutrition.
- Upper GI bleeding
- Paralytic ileus (from surgery) for more than 5 to 15 days: minimal EN + PPN

Se usa la vena cava que es un acceso central.

Total parenteral nutrition indications

Indicaciones total nutrition
Ind: someone not achieving nutritional goal by enteral nutrition for more (5 days / 7 days)
- GI cancer + undernourished + obstruction/pseudo won't let you use the gut→
perioperative nutrition: 10 days before surgery.
- Anorexia nervosa (they feel better because they only see a catheter not food)
- Jejunal High output fistula (6 weeks)
- Necrotic pancreatitis
- Short Bowel Syndrome
- Severe Paralytic Ileus → frozen abdomen → abdominal trauma, sepsis.
- Uncoercive diarrhea and vomit (hiperemesis gravidarum)
- Abdominal sepsis
- Intestinal failure
- Bone marrow transplant

Parenteral nutrition contraindications

- Shock (hemodynamic unstability) → glucose reaches the gut but the gut does
not have O2 → si no hay O2 para metabolizar → gut isquemia
- Hyperosmolarity → DM, coma, acidosis
 - Glycemia >300 mg/dL Tx: HO2, insulin, K
- TG >400 mg/dL (dont give lipids in PN, still give glucose and AA)
- BUN >100 (CKF). Tx dialysis
- Refeeding Syndromes: Tx give him K, Mg, PO4, Thiamin, unbalance in
electrolytes→ hay hipofosfatemia, hypokalemia → heart failure and heart
attacks
- Glucose to fast → worst refeeding syndromes
- Inability to obtain venous access → coagulopathies (patients receiving
anticoagulants) → partial contraindication
- Terminal illness (doesn't want to be feed)
- When risks of PN exceed potential benefits
- Severe renal/hepatic failure
- They need dialysis
- If the gut works (functioning GI tract)
- If the patients needs < 5 days with parenteral nutrition

Total parenteral nutrition

Temporal <4 weeks por central access

through the neck ya me perdi jajaja
- Juyularis interna
- Subclavia → the best technique, less infections.
- You take an x ray to see where the catheter is.
- Seldinger technique (atraummatic needle) guided by ultrasound
and ecg
- Cephalic

Permanent, tunnelized and Hickmann

Time > 4 weeks
Skin tunnelled
Subclavia → cava; at the same time subcutaneous tunnel in the tórax
The exit in the torax
Tunneled access with 1 entrance and 1 exist (10 cm in between)

Exit in the skin in the tunnelized is down, you have space between the entrance, you use
it when you need more time of use → prevent sepsis.
Use it in dialysis. You don't puncture the skin every time you need the dialysis (which is
constantly)

Sepsis associated to:

- Staph aureus
- Epidermitis.
- Faecalis

Subcutaneous inserted ports

- TAMBOR
It is use in chemotherapy (does not need to be used daily)
- Under skin and it is perforated with atraumatic needles

Case: Patient that needs 3 weeks total parenteral nutrition by a central catheter but
you cannot use the neck to access. How would you access the upper cava vein?
● Peripherally inserted central venous catheters (PIC) → we can use it less than 1
month. Enter by basilic or cephalic vein.
● Long catheter
● Temporal: distance between skin perforation and vein perforation (less distance it
could be infected)
● Its temporal because of the risk of INFECTION: Aureus, enterococcus faecalis,
pseudomona and candida
● Venodiseccion
Design the nutrition → compounding system “all in one” → EXAM
- you design the parenteral nutrition formula → ya te vi raquela jajaja
- The best one
JAJAJA TQM no mames yo pense que era mas caro jajajaja

2 chambers: glucose and aa

3: glucose, aa and lipids.
Metabolic bone disease: long term complication of vitamin D def
Glucose triglycerides electrolytes → refeeding syndrome → metabolic bone disease (Vit D
deficit)

Complications
Septic: impregnated catheter (chlorhexidine: BACTERIA and silver: FUNGI)
1. Aureus and epidermidis
2. Faecalis
3. E. coli
4. Pseudomona
5. Candida

- Metabolic: glucose, triglycerides, electrolytes, enzymes → refeeding syndrome,

metabolic bone disease (Vit D deficit → Fractures), copper, chrome
- If you don't use the gut: infections, atrophy, translocation, diarrhea, dysbiosis, C
difficile, stones, elevations of enzymes (X2 for 2 weeks), pancreatitis, don't have
first step metabolism, depression
- Mechanic: perforate, lacerate, bleeding, hemopneumothorax, chylothorax,
tamponade
- How you insert the catheter → pneumothorax, hemopneumothorax,
tamponade
- Drug interactions ( NEVER MIX NUTRIENTS AND DRUGS IN THE SAME
CATHETER ) → embolism

DON’T USE CATHETER FOR ANYTHING ELSE BUT NUTRITION.

You actually have 3 catheters in one
At the tip you have 3 hoyos

White catheter for nutrition

 Inflammation Impact on Nutrient Metabolism

Metabolic response to starvation

● Catabolism is high
● In 3 days we can lose a kilogram of our weight
● Increase in gluconeogenesis the brain uses ketone bodies in 75%
● With stress we have more hormones, cortisol, glucagon, everyday they’re going to
be high
● Even if you feed the patient, he or she is going to be in the same situation because
we don't adapt
● By day 3, we adapt, we form ketone bodies
In metabolic response to stress then ketone bodies go down
Stress response normal is to activate gluconeogenesis
● Gluconeogenesis goes up
● Liver changes its function
● We need lipolisis
● There’s a synthesis of + acute phase hepatic proteins such as PCR
● If we dont adapt to ketone bodies we die in 7-10 days because we loose proteins
and functions with this
Lactate can be transformed into glucose by the Cori cycle.
● Whenever we have stress (inflammatory process)
● Even if we have insulin (there's TNF-alpha, IL-1, IL-6) there is a change in the
receptor that induce a change in amino acids giving you insulin resistance
● Obese people develop insulin resistance in a medium term because of the
inflammatoty process
● Glucose comes into GLUT 4 and tries to enter
● Inflammation gives direct inhibition of GLUT-4
● Acetyl CoA enters into the Krebs cycle
● Whenever we have inflammatory process pyruvate is not going to transform into
Acetyl CoA (pyruvate dyhidrogenates is a 3 molecule enzyme)
● TNF-alpha, IL1 IL6 estimulartes TRY→ SER (which inhibits enzymes)
● Increased glucocorticoids and growth factor and stimulate cinas synthesis
○ There's resistance in GLUT force
○ Pyruvate won't be transformed into acetyl coa
● What we look IN ICUS we measure lactate and we get hyper lactate because
pyruvate is not transformed into acetylCoA and instead it is converted into lactate

Gluconeogenesis is activated in the liver (lactate glucose) = Cori cycle. Nevertheless,

energy is needed, Cori cycle becomes extremely expensive because PDH isn’t useful and
glucose production can’t be used as e ectively

● Insulin resistance
● Block of PDH due to PDHK → any kinasa inhibe enzimas → oberactivated aquí.
○ No se transforma piruvato a Acetil Coa y no hay ciclo de Krebs
■ Piruvato → lactato
● Hyperglycemia and hyperlactatemia & hypertriglyceridemia
El hígado sigue estimulando gluconeogénesis.
Se hace el Cori cycle para pasar de lactato la glucosa. Pero necesita mucha energía.
Desperdicias energía acá. → glucose is useless → It wont give you energy
● Block of Glut4 due to TNFalpha

Stimulate insulin → Glut 4 to membrane, access to more glucose.

In ICU we have proinflammatory cytokine, receptor w/ change in structure, change in
expression of receptor, change in order of aa, changes blinding → insulin resistance →
glut 4 does not function because of inflammatory process
PDH is very important to transform pyruvate into Acetyl coenzyme A

Cytokines induce PDH kinase 4 (inhibits enzymes) overly activated→ you don’t activate
krebs cycle→ lactate→ hyperglycemia, hyperlactatemia, hypertriglyceridemia
- Liver needs to stimulate gluconeogenesis (Cori cycle) expensive, you need a lot of
energy

Hyperglycemia + Hyperlactatemia + Hypertrigliceridemia (excess of glucose transformed

into fatty acids)
Inflammation reduces the production of lipoprotein lipasa
Glucose

LIPID METABOLISM
Lipid metabolism
Normal px → broke by LPL - fatty acids → carnitine transporter → mytochondria → beta
oxidacion → energia.
● Lipoprotein lipase breaks down glycerol into free fatty acids. Free fatty acids are
needed to get inside the inner membrane of the mitochondria along with carnitine
→ beta oxidation → a lot of energy

Inflammation (TNF-alpha, IL-1, IL-6)

● Hormone sensitive
● TNFAlpha inhibits expression of lipoprotein lipase. No free FA, no accessing to
mitochondria because TG don’t break down to FA
● Inflammation stimulates hormone sensitive lipase (enzyme in adipose tissue that
allows triglycerides to exit the adipose tissue).
● Inflammation also blocks carnitine (inhibits synthesis of carnithine)so fatty acids
can’t enter mitochondria. Aside from the function of carnitine as transporter, it is
also an anti-inflammatory molecule. We cannot synthesize enough so we have to
give it to the patients (40 mg/kg/day) becoming an essential aminoacid during
stress
● Inflammation reduces synthesis of carnitine
● Carnitine function as an anti inflammatory
● We don't have glucose, lipids nor carnitine so we need to use proteins if you give
too much there’s going to be kidney failure
● Search aminoacids which enter to the krebs cycle besides from glutamine
Glutamine 0.3-0.5 g/kg

The more severe the problem, the lesser the nutrients u can use

Proteins
Proteinuria→ albuminuria→ RKF
● Glutamine gets transformed into Alphacetoglutarate. Nevertheless Acetyl CoA is
needed to activate Krebs Cycle.
● Parenteral nutrition
● Indication: anyone who doesn’t achieve nutritional goals by enteral nutrition

In hyperglycemia treatment is insulin the problem is that it inhibits keto adaptation

Hyperglycemia comes with hypertriglyceridemia which is also and inhibitors of keto
adaptation

Excess of glycemia associated with TG, HTG, HG, Insulinemia, inhibits direct keto
adaptation.
Minimal enteral nutricion reduce catabolism, you also need to find the source of
inflammation

Calculation Class
● Basal metabolic rate maintains vital signs and temperature (most important
because that’s how proteins work.) You measure this one as soon as you wake up.
Minimal amount of energy needed to survive Measure it just after sleeping, fasting
state.
● Resting metabolic rate (RMR): (BMR) includes basal metabolic rate + nutrient
thermogenesis (energy needed to digest, transport, absorb, digest ; energy needed
to transform nutrients into energy) = 7-10% of the total amount of energy needed
daily
○ Measured after breakfast.
● Total metabolic rate resting metabolic rate + work out (2 hours/day) or stress
factor (mild stress: 20% moderate: 40-60%, severe 60-100%)

1 molecule of oxygen you synthetase 1 molecule of carbon dioxide in glucose metabolism

With proteins 1 molecule of oxygen in protein metabolism is 0.82 → 1 oxygen you synthetize
0.82 of carbon dioxide
Lipids: 1 molecule of oxygen produces 0.72 of carbon dioxide

3 Main Products
Water (breathe, pee)
Carbon dioxide
Energy (ATP)

Glucose oxidation
Glucose 6 oxygen = CO2 + 6 Water + ATP
Thus heat production can be calculated from 02 consumption or co2 production nitric
oxide nitrogen how much kilocalories need to ingest.
Measure energy (heat):
● DIRECT CALORIMETRY: sensors everywhere → you touch everything.
○ Research.
○ Al heat measured
○ ATP, heat can be measured by direct calorimetry
 ● EVAPORATIVE heat losses (breathing) → how do we loss heat
○ Non evaporative heat losses conduction (touch something cold), convection
(cold breez) and radiation (thinking uses a lot of energy)

To put attention we also perder calor por radiación

Si los comiéramos diariamente sabremos que cantidad de alimento tendríamos que
comer porque es la energía que perdimos.

Direct calorimetry: senses heat you lose (room where you put the person and measure in
24 hours everything that they lose),. We only do this for research purposes.

INDIRECT CALORIMETRY AND WEIR EQUATION:

Metabolism End products:

● Glucose: 4 kcal/g
● Lipids: 9 kcal/g
○ Produce less carbs?
● Proteins: 4 kcal/g
If you go to the gym you can use the indirect calorimetry

GLUCOSE OXIDATION

Ketogenic bodies <0.67

If you eat too much carbs, they are transformed into lipids = lipogenesis
If you don't eat you dont produce carbon dioxide
If you eat much the index is >1= (1.1)

Predictive equations
● Harris-Benedict (RESTING METABOLIC RATE: it includes nutrient thermogenesis it’s
included)
● Stress HB* stress factor (Mild stress: 1.2-1.4, Moderate stress: 1.5-1.7, Severe stress:
1.8-2) OR Harris B* Activity factor (1 hour exercise: 1.1, 3 hours: 1.2-1.3)

The best way to approach ICU patient if you don't have indirect calorimetry (Gold
standard) you feed with 25 kcal/kg per day

What weight should we use?

Hospital patients we want to improve their health not their weight
● If you feed ideal weight in undernourished patients you overfeed and if he’s
undernourished you create refeeding syndrome USE ACTUAL WEIGHT
○ Between ideal and actual weight its water
○ You want to heal the patients, you want them to survive, the priority is not to
increase his weight
○ Overfeed patients → hypertriglyceridemia, sepsis, etc.
● BMI 18.5 to 26.9 → ACTUAL weight

● Obese patient (BMI >27), 115 kg, height 1.70

○ Does fat use the same amount of energy than muscles? No
○ Adipose tissue also needs energy
○ Losing weight inflammation (not good in hospital setting)
○ If you feed ideal weight → undernutrition
○ If you feed actual weight → overfeeding (heart attacks, sepsis), because you
would be feeding him as he had a lot of muscle, but he had a lot of mass
instead.
○ USE ADJUSTED WEIGHT
■ Ideal + ((actual-ideal) * 40)
■ Ideal= BMI ideal*Height2
● BMI ideal women 21.5
● BMI ideal men 23

Next week
● BMI
● Which weight would you use
○ If BMI >27 adjusted weight
○ <27 we use actual weight

HOMEWORK
● We need to make energy calculations applying harrison benedict, thumb equation
and mi in or ireton jones.
○ You invent yourself a disease
NEXT WEEK
● We are going to review how much energy how much macronutrients, lipids,
proteins?

CALCULATIONS APUNTES DE RAQUEL PORQUE SE PERDIÓ EN LOS DE ARRIBA

Nutrient thermogenesis is 7-10% of the metabolic rate.

In hospital patients we add the stress factor.
3 end products of metabolism: water, co2 and atp

How do we measure the heat that we lose, its measured by two things: evaporative heat
losses (measured by breathing). Another way to lose our heat i by touching something (you
conduct the heat). Radiation is another way (existing) we radiate our heat.

Direct calorimetry: senses heat you lose (room where you put the person and measure in
24 hours everything that they lose),. We only do this for research purposes.

What we actually do to measure the energy we use is indirect calorimetry.

In real life the indirect calorimetry is done with a machine with a mask. You breathe
through your mouth and pinch the nose.

Weir equation: volume of oxygen, the co2 we expel and the urinary ureic nitrogen. = the
amount of energy you need per day.

The respiratory quotient take into consideration the volume of co2 (the amount you are
synthetizing /the volume of 02 you are using.
- For each molecule of glucose you use you produce 1 molecule of co2
- Proteins→ 1 of o2 you synthetize 0.82 molecule so the quotient is 0.82 (because
- Lipids→ 1 02 you synthetize 0.71. So the quotient is 0.71.

If you don't eat you don't create carbon dioxide → <0.67 → ketone bodies (ketogenesis) →
keto diet, alcohol,
1-1.2 → eating too much carbs → lipogenesis (transformamos glucosa a lípidos)

Non proteic RQ: goes up if they eat a lot of carbs, goes down if you eat a lot of lipids.
BUN<6 → not eating proteins.

PREDICTIVE EQUATIONS
If you don’t have indirect calorimetry use the thumb equation.

SU mamda de patricio
 1. Which weight should we use ?
a. Actual weight (the one you use for calculations)
b. Ideal weight→ if you use this you overfeed patients and can cause a refeeding
syndrome.

Patricio gordo

2. Which weight should we use ?

a. Actual weight→ you would be overfeeding
b. Ideal weight → But what would happen if you only feed the ideal →
undernutrition because fat needs energy to survive. He would lose weight
and we don’t want him to do that.
i. WHAT DO WE DO?
 1.
2. Ideal weight =BMI x h2
a. In between ideal weight.

Normal BMI you dont adjust your weight.

WE ONLY ADJUST FOR PEOPLE WITH BMI >27. People undernourished you use actual.
More than 27 we use adjusted.

Haris benedict, thumb equation and ireton.

De raquel:
Harris benedict: 2380 kcal
Thumb: 1750-2100 kcal
Ireton:

https://www.mdapp.co/ireton-jones-equation-calculator-442/

Holis hoy somos solo tu y io ay no Ay no? Tu cola yo tmbn te amo

Obese (BMI > 27)→ ideal you wouldnt give him enough put if you use actual weight you are
giving the patient too mucho (hyperglicemia, hipertrigliceridemia, fatty liver etc)--> you use
adjusted weight too perform the energy calculations

Examples calculations
● Man, 30yrs old, weight 120kg, 1.65m
● BMI: 44.11 OLV
● weight for calculation: Adjusted
● Make a calculation with 25 kcal/kg/day → 25x85.6=2140 kcal (3,000 noo???) do c ):
perame

Adjusted weight = ideal + (actual - ideal) * 40%

Ideal = ideal BMI * Height 2

Ideal: 23*1.65*1.65 = 62.62

BMIi women: 21.5, men 23

Adjusted weight = ideal + (actual - ideal) * 40%

Adjusted weight = 62.62 + (120- 62.62) * 40%
Adjusted weight = 85.57 kg

If you want to be extremely precise

● When you have obesity 1 or 2 we adjust with 25%
● When you have obesity 3 we adjust with 50%
But for something generalized we take the 40%
Make a calculation with 25 kcal/kg/day → 25x85.6=2147.5 kcal
MACRONUTRIENTS
● Kcal: 25 kcal / kg / day (when we don't have indirect calorimetry, we use this the first
days in UCI; ist accurate, similar to indirect calorimetry)
● 2147.5 kcal
● Divide this amount of energy between the macronutrients → 50/30/20
● 50% carbs/ 30% lipids/ 20% proteins)
● 50% → 1,073.25 kcal in carbs
○ Grams? You divide them en 4
■ 1073.25 /4 = 268.3 grams → is this amount okay?
● Verify glucose metabolic rate (Max 4 mg/kg/minute or 7
grams/kilo/day) →its the amount that can be metabolized→ to
avoid hyperglycemia → avoid infections (bacteria love sugar)
○ Hyperglycemia associated with hypertriglyceridemia
● Max: 2.5 mg/kg/min → in DM, insulin resistance and in severe
brain trauma (because of the edema, if you give them more
sugar → osmolarity increases → dehydrated neurons)
● Grams glucose / weight / 1440 (minutes in one day)* 1000 =
○ 268.3 grams /85.9/1440 * 1000 = 2.17 mg / kg/ min
● Grams glucose / weight
○ 268.3 grams /85.9 = 3.1 grams /kg/day
○ Enteral glucose: 4 kcal en 1 gram
○ Parenteral dextrose: 3.4 kcal per gram (it has to be diluted in water, anything
injected has to be diluted), but the water doesn't give you energy, the gram
has the same molecular weight but it has water
● 30% lipids→ 644.25 kcal
○ 1 gram of lipids → 9 kcal
○ 644.25/ 9= 71.58 g
○ Verify:
■ Maximum: 2 gr/kg/day; usual amount→ 1 gr/kg/day
■ Grams of lipids / weight
● 71.58 / 85.9 = 0.83 gr/kg/day → ITS OKAY (:
*If my patient has COPD you need to reduce carbs and increased lipids because of the CO2.
No cache lo otro que dijo pero sintetizas menos CO2 con lípidos.

● 20% proteins→ 429.44 kcal

○ 1 gram of proteins → 4 cal
○ 429.44/ 4 = 107.36? Yeap
○ Verify: grams of proteins /weight (max 2 gr/kg/day; usual amount 1 gr/kg/day)
■ 107/85.9 = 1.25 gr/kg/day (stress)
 PROTEIN CALCULATION GR/KG/DAY

Renal failure 0.62 Less proteins: CKF

non dialysis
Long term 1.0
Hepatic:
Hospitalized 1.2 to 1.4
encephalopathy (0.8
Start up or minor surgery 1.5 to 1.7 grams/ kilo 48
hours)
Mayor trauma 1.7
AKF, nephrotic sx
Sepsis 2.0

Burns 2.2 Metabolic diseases

Urinary ureic nitrogen* 6.25 = amount of proteins to in children
give

Urinary Ureic Nitrogen * 6.25 = total amount of proteins to give (exact amount they need)
somos inclusivas jajaja lit no, es que ella siempre dice his/he (por traducir) jajajajaja tqm
acepto el they
- Means how many muscles are we destroying
- Collect pee in 24 hours, take UUN * 6.25
1g of Nitrogen= 6.25g of Protein

ICU Calculations
START: Proteins exact:
Measure catabolism → Urinary ureic nitrogen (normal: 10+/-2 gr/day, girls 8-10, boys: 10-12
gr). Most of the nitrogen lost in urine

Nitrogen balance: Nitrogen intake - (nitrogen catabolism: UNN + 2 )= 0 to -2 (they are

acceptable within this limit)

UUN * 6.25 = amount proteins to give in one day

One protein: 16% of a protein is nitrogen → 1/16% = 6.25
UUN 12→ → ? proteins → 12 * 6.25 = 75 grams /day

With inflammation we cannot use the carbs and lipids → catabolic

80-100 non proteic kcal: 1 gr of nitrogen

Kcal non protein (carbs and lipids): nitrogen → 80:1 → because the patient is under
severe stress
 - How many carbs can i give in relation to the nitrogen lost
- The lesser, the better → 80 non protein kcal for each gram of nitrogen → 80:1
UUN 12→ 80*12 (the UUN) → 960 kcal (carbs and lipids): 12 gr Nitrogen
- 960 → Then half and half, half from carbs and half from lipids
12*6.25=75 gr proteins → 75*4= 300 kcal from proteins
Total: 960 + 300 = 1260 kcal (permits: hypocaloric diet → permissive hypocaloric diet)

100-120 kcal (coming from carbs and lipids): 1 gram of nitrogen (if they get better)

When they get better nitrogen goes down, and carbs and lipids up.
- At the beginning you give a lot of nitrogen
According to the evolution of the patients you adjust this.

We have to feed people ASAP → minimal enteral nutrition → step by step → start slowly→
that is why the permissive hypocaloric diet → reaching a balance in a few days.
- Too much is worse than too little.
- But dont starve people → catabolism
QUE NO ENTIENDES QUE NO LES DESDE COMIDA ALV JAJAJAJA
Jajajajajaj

Water calculations
- Water: 30ml/kg (weight)
- 30 ml * 85.9 = 2568 ml
- 2143 kcal of enteral nutrition → formulas (one can standard polymeric: 1 kcal/ml),
75-80% of a formula is water =
- Our patient was receiving 2143 nel frank esta pendejo
- Si dijo eso nooo revisa arriba si eran 46.5 casi 47 JAJAJAJjajatedije :o
- 2143*80% = 1712 ml H20
- 2568 - 1712 (enteral nutrition) = 856 ml use for IV drugs, enteral water (flush the
tubes 20 ml warm water), IV solutions, anything that get in the vein

- Liquid balance
- End of day: in / out (urine, “non measurable” losses of water (breathing, sweeting,
etc), increase 7% per each degree °C)
The normal in the body
Extracellular and intracellular
 Anahuac Mexico University
North Campus

Faculty of Health Sciences

Bachelor’s Degree in Medical Surgery
Eight Semester

January-May 2021

Endonutrition
NRC 13408 | S 10:00h

Dra. Marthe Alice C. Bicard González

Arantza González Carrillo, 00321265

Vivian Rodríguez Siguenza, 00317908
Mariana Martinez Mercado, 00312008
Frank Alexei Ruggeberg Castillo, 00327903

Activity
Clinical Cases

April 8th, 2021

Cancer case: American 81 year old female with colorectal cancer, treated surgically two months
ago, receives chemotherapy by a subcutaneous port. She used to eat a western diet. She refers
nausea for the last month and vomit for the last 5 days (reason that explains why she hasn´t been
eating well). She was diagnosed with intestinal obstruction due to adherences and she had to be
re-intervened (resection of 100 cm of jejunum and 90 cm of terminal ileus).

On physical examination she looks pale with thin legs and edema of lower limbs.

Actual weight: 54kg, previous (6 months ago): 61 kg, height 163 cm.

Labs: K 3.5, PO4 2.2, Albumin 2.8, NUU 12, BUN 15, creatinine 1.

1- Define cancer

● “The term "cancer" is a generic name that includes a group of hundreds of different
diseases whose common characteristic is the uncontrolled growth of abnormal cells.”
(Hernández R, & Gómez Á, 2018)
● Pathological hyperplasia

2- What is the relationship between cancer and a western diet?

● The Western dietary pattern is often composed of red and processed meats, sugary
beverages, refined carbohydrates and salty snack
● The previous figure shows the typical Western dietary pattern (red) vs a prudent dietary
pattern (blue)
● A Western dietary pattern has been consistently associated with increased risk of
colorectal cancer mainly but also with breast cancer, prostate cancer and pancreatic
cancer.
● A Western dietary pattern has been as well associated with increased incidence of
metabolic syndrome
● Western-style diet high in fat and scarce in fiber and vitamin D increase risks of
colorectal cancer
● Dietary fat has been implicated in the increase of colorectal cancer risk, and associations
have been found between colorectal cancer incidence, saturated fat intake, and high
consumption of red and processed meat
● This type of diet has been shown to promote important oncogenic processes in colon
tissue, apoptosis, proinflammatory stimulus, and increased neoplastic growth
 ● Artificial sweeteners feed the wrong bacteria. By changing the microbiome, it increases
the risk of cancer. Bacteria in colon can break down bonds, they eat the sugar
○ Too much bacteria = ↑ gas
○ It transforms fiber into a short chain of fatty acids.
○ Not nonsugar coke, it has sweeteners
■ Diabetes, obesity, HTA, Parkinson, Alzheimer, many complications
associated with sweeteners
● Butyrate promotes apoptosis.
● Inflammatory process → stimulation of arachidonic acid → promotes oxidative stress →
damaging DNA
● To compensate the excess of meat, one must eat a lot of fiber → counteract effect
● Western Diet has 20 omega 6 :1 omega 3
○ We actually should be eating: 2:1 → W6:W3 → To prevent cancer: 1 W6: 2W3

3- What is cachexia?

● Cachexia is a multifactorial process of skeletal muscle and adipose tissue atrophy

resulting in progressive weight loss. It is associated with poor quality of life, poor
physical function, and poor prognosis in cancer patients
● The etymology of the word cachexia is associated with poor prognosis: it is derived from
the Greek kakos andhexia which means“bad condition” and has been recognised as a key
sign in many cancers
● Loss of greater than 5–10% of body weight is usually taken as a defining point for
cachexia
● Pathophysiological changes and clinical consequences of cachexia are summarised in the
next figure:
 ● Undernutrition + inflammation (catabolism)

4- How do we screen cancer patients? Does the patient have a nutritional risk?

● There are different tools to screen cancer patients:

○ Subjective Global Assessment (SGA)
■ (A) → Well-nourished
■ (B) → Mildly/moderately undernourished
■ (C) → Severely undernourished
○ Nutrition Risk Screening (NRS-2002): It takes into account the impaired
nutritional status of the patient and the severity of the disease.
■ If the patient is 70 years old or older, then one must add 1 to the total
score.
■ If the final score is 3 or more, the patient is at-risk, which means a
nutritional care plan must be initiated.
 ■ If the final score is less than 3, then the patient must undergo a weekly
screening.
● Results
○ SGA:
■ Weight change: The patient lost 7kg in 6 months → 11.47 % of body
weight
■ Dietary intake: not specific “ she hasn't been eating well)”
■ GI symptoms: nausea for the last month; vomit for the last 5 days
■ Functional capacity: not specific; progression getting worse.
■ Physical findings: Thin legs (muscle wasting) and edema of lower limbs
Disease and its relation to nutritional requirements
■ Disease and its relation to nutritional requirements: Dx. colorrectal cancer
(Metabolic demand: high)
■ Overall SGA: C → severely malnourished
○ NRS- 2002:
■ Initial screening:
● BMI < 20.5 → yes
● Has the patient lost weight within the last 3 months? → yes
● Has the patient had a reduced dietary intake in the last week? →
yes
● Is the patient severely ill ? (e.g. in intensive therapy) → yes/no
■ Final screening:
● Impaired nutritional status: Mild Score 1 → Wt loss 45% in 3
months or Food intake below 50–75% of normal requirement in
preceding week
● Severity of disease: Moderate Score 2 → Major abdominal surgery
■ Total Score: 3 + 1 = 4 → the patient is nutritionally at-risk and a
nutritional care plan is initiated nosotros
● Malnutrition and a loss of muscle mass are frequent in cancer patients and have a
negative effect on clinical outcome. All cancer patients should be screened regularly for
the risk or the presence of malnutrition.

5- Why is undernutrition an independent prognostic factor in cancer patients?

● Weight loss, impaired physical performance, and systemic inflammation in patients with
cancer are all independently associated with an unfavourable prognosis, increased
toxicity of anticancer treatments resulting in reductions or interruptions of scheduled
treatment, and reduced quality of life.
● Regardless of the TNM classification, the nutritional status of the patient will affect their
prognosis. This is going to have an impact on their morbidity and mortality.
 ● Prognosis: morbidity, mortality. If the patient is undernourished, independently of the
TNM classification, his morbimortality is going to be increased.
6- Why do cancer patients get undernourished? Is the patient undernourished?
● Malnutrition and a loss of muscle mass are frequent in cancer patients and have a
negative effect on clinical outcome. They may be driven by inadequate food intake,
decreased physical activity and catabolic metabolic derangements.
● Catabolic alterations in cancer patients:
○ Inadequate nutritional intake is frequently observed in patients with cancer and is
associated with weight loss, which may be severe.
○ Muscle protein depletion is a hallmark of cancer cachexia, severely impinging
quality of life and negatively impacting physical function and treatment tolerance.
○ A systemic inflammation syndrome is frequently activated in patients with cancer.
This can vary in degree but impacts all relevant metabolic pathways.
○ Systemic inflammation is associated with the development of fatigue, impaired
physical activity, anorexia, and weight loss.
● According to the SGA and NRS-2002, the patient is undernourished.

● Malabsorption
● Surgery → longer hospital stay → higher risk of undernutrition
● Depression
●
Proteolytic factor: like an enzyme, destroys muscles to get aa
Lipolytic factor: someone stimulating Hormone sensitive lipase, extracts TG from adipose tissue
to obtain FFA
When you get aa and FFA you transform those into energy

7- “Feeding the patient is to feed the tumor”?

If we stop feeding the patient, the tumor is going to keep feeding itself, it won't stop growing.
It's better to feed the patient because otherwise he will be undernourished.

Remove omega 6, proteins coming from animals, give them vegetable proteins, cetogenesis
causes undernutrition, stop giving easy glucose but you still need to give them complex carbs

8- What kind of nutrition would you give? (several options possible)

a. Total Enteral nutrition

 b. Total Parenteral Nutrition: because in this case, the organism behaves like a
short bowel syndrome, and in that case he must be fed entirely through the
vein. It involves a central catheter and guarantees adequate osmolarity.

- Not enough gut → Because of the major abdominal surgery the px went
through, her organism behaves as if she had short bowel syndrome.
- Permanent access → More than 1 month → subcutaneous port

c. Minimal enteral nutrition (trophic): Stimulates the intestine and keeps it

working. Clinical benefits include improved feeding tolerance, better weight
gain, improved bone mineralization, reduced systemic sepsis and shorter
hospital stay; moreover minimal enteral feeding facilitates a smooth and rapid
transition from parenteral to enteral nutrition.

- Trophic: stimulation

d. Partial parenteral nutrition

- Restrictions: osmolarity, amount liquids, time (15 days) → you can’t

achieve the nutritional goal in this time
- Access: peripheral vein

9- What is EPA? Why do we recommend it for the treatment of cancer patients?

As a supplement, EPA is most commonly used for heart disease, preventing adverse events after
a heart attack, and depression, it inhibits proteolytic factors, produced by the tumor cells
(catabolism). EPA is commonly used as a prescription medicine to reduce triglyceride levels. The
majority of cancer patients experience weight loss as their disease progresses and, in general,
weight loss is a major prognostic indicator of poor survival and impaired response to
antineoplastic therapy. EPA is an omega 3 with several effects such as anti-inflammatory
(reduces catabolism), inhibits proteolytic factor, reduces endothelial adhesion (that reduces risk
of metastasis), and reduces chemotoxicity. The patients stop losing weight.

→ Prevention and treatment dosage is 2-4 g of EPA daily

● Eicosapentaenoic acid (EPA) is one of several omega-3 fatty acids

● Omega 3 → reduces pain, fibrosis, and risk of metastasis
● Anti-inflammatory (reduces catabolism), inhibit proteolytic factor, reduces endothelial
adhesion → risk metastasis, reduces chemotoxicity
● Omega 3 makes chemo more effective → you could reduce dose → reduces side effects
→ less likely that patients will stop treatment
○ More sensitivity towards tumoral cells
● Prevention and treatment: 2g EPA

10- What other micronutrients would be useful in patients undergoing chemo and
radiotherapy?
 ● Vit. E: (Recommended dietary allowance) 15 mg/dl (Tolerable Upper Intake Level) 1000
mg/dl
○ To prevent peroxidation of lipids, reduces pain
○ In combination with n-3 polyunsaturated fatty acid reduces fibrosis from radiation
treatment, and decrease oral mucositis associated with chemotherapy
■ N-3 can reduce tumor growth
● Vit. D-3: (AI) 5 microg/d for ages 19–50 y, 10 microg/d for 51–70 y, and 15 microg/d for
>70 y (UL) is 50 microg/d
○ Suppresses the growth of tumors, inhibitors of cancer cells
● Vit. C: (RDA) 90 mg/d for men and 75 mg/d for women (UL) 2000 mg/d
○ Protection against chemotherapy-induced mutagenesis, increases function of NK
cells and LcT and LcB
● Selenium: (RDA) 55 microg/d (UL) 400 microg/d
○ May enhance the effectiveness of various chemotherapeutic agents, tumor cell
apoptosis, scavenger for products of oxidation reactions
● L-carnitine
○ increases lean body mass, improves total daily physical activity, functional status,
and cancer cachexia symptoms
● Oral zinc sulfate: 3x45 mg/d
○ As a taste modulator in RT
● If necessary; monitorization and substitution of Potassium, Phosphate and Magnesium
○ To prevent refeeding syndrome

11- Why is arginine contraindicated in patients with active tumors?

L-arginine, a different form of an aminoacid called arginine is used to produce nitric oxide (a
ROS) by different enzymes (nitric oxide synthases) which are found in various tissues of our
body. It is believed to be a free radical that can potentially be beneficial and work as an
antioxidant, and a mediator for the immune system, BUT, when the concentrations of this
metabolite are too high they react rapidly with superoxide (another ROS) and form peroxynitrite,
“a potentially damaging nitrogen species which can react through several mechanisms, including
the formation of an intermediate through a reaction with a hydroxyl radical”. Active cancer is a
pure catabolic state, thus, disturbing the balance of the generation and antioxidation of ROS.
Added to this, there is a mixture of substrates for oxidation; “Polyunsaturated fatty acids
(PUFAs), transition metals, and oxygen are present in abundance”. When there is inflammation
or disease (cancer), tissues break down and free transition metals and iron, reacting with ROS,
these metabolites can negatively affect the patient. To adapt to these changes, “the body alters the
transport and distribution of iron by blocking iron mobilization and absorption, and stimulating
iron uptake from plasma by liver, spleen, and macrophages”, creating acute phase reactions to
protect itself, leading to alterations like iron starvation and cellular uptake of iron potentiated by
ROS like nitric oxide.

Kidney failure case:

● 55 year old man with long term Diabetes (20 years since diagnosis) and chronic kidney
failure treated for the last 3 years with peritoneal dialysis (2.5% dextrose 1.5 L every 6
hours).
● He has lost 8 kg in the past 4 months (usual weight 65kg, actual 57 kg, height 1.72m), he
refers nausea and vomit for the last 2 weeks.
● Diet: hypocaloric solid diet for 2 weeks, fasting for the past 2 days.
● He refers fever for the last 3 days.
● Hb 9.6, Leu 15, BUN 134, Creatinine 4.5, PO4 5.3, K6, Albumin 2, Urinary Ureic
Nitrogen 14
● PERITONEAL culture with S. AUREUS
● Gastric emptying study: severe gastroparesis
● Tx: hemodialysis

Questions
1- What causes chronic kidney failure?
● Primary causes:
○ Uremia is the primary cause of CKD
○ Diabetes Mellitus
○ Systemic arterial hypertension
○ Glomerulonephritis
○ Obstructive nephropathy
○ Cystic disease
○ Secondary glomerulonephritis or vasculitis
○ Cancer
○ Uncertain
2- Explain Chronic Kidney Failure physiopathology
● As a result we get an irreversible loss of nephrons
● The physiopathology depends on the cause of the CKD, in this case we might assume that
DM was the cause.
● When there is excess glucose in the blood it starts sticking to proteins in the blood which
is a process called non-enzymatic. This process of glycation particularly affects the
efferent arteriole and causes it to narrow, this process is called hyaline arteriosclerosis.
This creates an obstruction that makes it difficult for blood to leave the glomerulus, and
increases pressure within the glomerulus leading to hyperfiltration. In response to this
high-pressure state, the supportive mesangial cells secrete more and more structural
matrix expanding the size of the glomerulus. Over many years, this process of
glomerulosclerosis, once again, diminishes the nephron’s ability to filter the blood and
leads to chronic kidney disease
● The persistence of the hyperglycemic state, the filtration of proteins, growth factors in the
tubular system trigger oxidative stress and consequently a state of persistent cortical
interstitial inflammation that results in hypoxia and tubulointerstitial fibrosis that largely
determine the progression of the renal disease.
● The next image shows factors and pathways contributing to the progression of renal
disease:
3- Why do kidney patients get undernourished?
● The causes are multifactorial and include reduced food intake due to effect of uremia,
reduced absorption of nutrients from oedematous gut, metabolic acidosis, increased
protein loss during dialysis, inflammation, oxidative stress, carbonyl stress and hormonal
disorders. Accumulative impact of these factors results in decreased nutrient intake.
● Decreased protein and energy intake due to anorexia, increased protein catabolism,
decreased anabolism, chronic inflammation, metabolic acidosis and hormonal imbalances
have all been linked to protein energy wasting as etiological factors.
● Anorexia is common in patients with CKD and may result from alterations in orexigenic
(appetite stimulating) and anorexigenic (appetite inhibiting) hormones, accumulation of
metabolic waste products in the body in kidney failure, abnormal taste and the effect of
medications on taste buds. Accumulative impact of these factors results in decreased
nutrient intake.
● The result of a chronic inflammatory state in CKD is an increase in resting energy
expenditure, which promotes protein catabolism and decreased anabolism. Protein
catabolism, in addition to increased protein losses (mostly amino acids) through dialysis
 techniques and decreased synthesis of albumin leads to a state of negative nitrogen
balance and muscle wasting

● The most important factor associated with undernutrition → UREMIA

○ Avoid uremia at all costs
● Infections,stress, complications associated with their pathologies (DM/ HAS)
● Inflammation → anorexia → catabolism

4- How does peritoneal dialysis work?

● Peritoneal dialysis is based on the exchange of solutes between blood in the peritoneal
capillaries and the dialysis fluid is introduced in the peritoneal cavity and subsequently
drained.
● Peritoneal dialysis solutions contain glucose or another sugar to achieve fluid removal.
● It uses the lining of the abdomen to filter the blood through a catheter. The dialysis
solution flows from a bag through the catheter into the abdomen.While the dialysis
solution is inside, it absorbs wastes and extra fluid from the body. After a few hours, the
solution and the wastes are drained out of the abdomen into the empty bag

5- How do you treat peritoneal infections?

Infections within the abdominal cavity arise because of inflammation or disruption of the
gastrointestinal tract, gynecologic or urinary tract. These infections are usually polymicrobial
and result in an intra-abdominal abscess or secondary peritonitis, which may be generalized or
localized (phlegmon). Antibiotic therapy is used to prevent local and hematogenous spread of an
intra-abdominal infection and to reduce late complications. Treatment agents depend on whether
the infection is community acquired or health care-associated. Source control such as removal of
appendix, closure of perforation, resection of gangrenous bowel, drainage of abscess and
image-guided percutaneous catheter drainage may be required to control the infection.

6- Does this patient need nutritional support? (make a nutritional screening).

Subjective Global Assessment Form
● Nutrient intake
○ Duration of inadequate intake: 2 days.
■ Minimal intake, clear fluids or starvation.
○ Nutrient intake in past 2 weeks:
■ No improvement or inadequate.
● Weight
○ Non fluid weight change past 6 months: 8 kg weight loss.
■ 8.7% loss without stabilization or increase.
○ Weight change past 2 weeks unknown.
● Symptoms
○ Nausea and vomiting.
● Functional capacity
○ No dysfunction.
7- What is his Nutritional diagnosis?
Weight loss in last six months: 12.3%, reduced intake 2 weeks, fasting 2 days, nausea and
vomiting for the last 2 weeks, disfunction, gastroparesis, peritonitis, elevated stress, ascites, loss
of fat, proteins, carbs
Albumin <2.5
C: Severe chronic and acute undernutrition
● Severe chronic undernutrition → disease
● Infection + catabolic state → bad prognosis → severe acute undernutrition
● With inflammation
8- What would be the prefered nutritional access?
Because of severe gastroparesis, it is preferred to use a nasojejunal tube. 10-20 ml/h/day. But due
to hemodialysis, it is recommended to use PN; “Intradialytic parenteral nutrition (IDPN) shall be
applied in malnourished non-critically ill hospitalized patients with CKD and KF on
hemodialysis, or the same patients if at risk of malnutrition that fail to respond or do not tolerate
ONS or EN”

● Parenteral nutrition → it is safe

○ Start slowly

9- What are his protein demands?

Thumb equation: 25 kcal x 57 g=1425 kcal
1425 kcal (0.15%)=213.75 kcal
213.75/4=53.4375 g (wo Kidney failure)
Kidney failure:
0.62-0.7 kcal/kg/day
0.62x57=35.34 g CKD w/ no dialysis, AKF w dialysis, nephrotic sx
0.7 x 57= 39.9 g
1.2 g → hemodialysis
1.5 → peritoneal dialysis (we lose more proteins)

● Because of the BUN → we star with 0.62 kcal/kg/day

As soon as BUN goes down, give more
We have to be careful w/ UUN because in KF we don’t have urine
BUN up probably you’re giving too much proteins
Animal proteins are bigger and have proinflammatory lipids, they come w/ saturated fats, omega
6 (too big and with inflammation)
Other objective is to reduce uremia and worsening of KF (by changing the quality of proteins)
- Instead of giving animal proteins, we give the pxs vegetable proteins
- To reduce damage to glomeruli, (animal proteins reduce glomerular filtration
worst than ever)
- Branching aminoacids (BCAA)→ they give energy, ease to metabolize → 2-6 grams
(during stress) reduce anabolism
10- What micronutrients do we need to supply and why?
● Folate, Vitamin B6, Vitamin C, Vitamin E, Thiamine, Zinc, and Selenium.
● Because some micronutrients may be removed/lost during peritoneal dialysis, we need to
supply them.
● The depurative mechanisms at the basis of dialysis modalities along with a variable
amount of hemofilter adsorption may increase the risk of vitamin and trace element
deficiency

● Don’t give B12 + Folic Acid at the same time→ they compete with the receptor
One in the morning and the other one at night
● Kidneys activate D-3, it is given activated

● Carnitine → anti inflammatory

● Mn and Mg → important for glycolysis
References:
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group recommendations for action against cancer-related malnutrition. Clin Nutr [Internet].
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2. Mahmoud AM, Ali MM. Methyl donor micronutrients that modify DNA methylation and
cancer outcome. Nutrients. 2019;11(3):1–30.
3. FAO, World Health Organization. Vitamin and mineral requirements in human nutrition
Second edition. World Heal Organ [Internet]. 1998;1–20. Available from: www.who.org
4. Arends J, Bachmann P, Baracos V, Barthelemy N, Bertz H, Bozzetti F, et al. ESPEN
guidelines on nutrition in cancer patients. Clin Nutr [Internet]. 2017;36(1):11–48. Available
from: http://dx.doi.org/10.1016/j.clnu.2016.07.015
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& Meneses-García A(Eds.), Manual de Oncología, 6e. McGraw-Hill.
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doi:10.1155/2011/601434
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A%20Western%20dietary%20pattern%20has,but%20cohort%20studies%20reporting%20no
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45 year old female, with a history of alcohol and NSAID abuse, arrives to the emergency room due to
coffee ground emesis for the past 2 days. She has a slurred speech, is disorientated and combative.
Her sister refers that the patient has had long term poor appetite, nausea for the past month, vomit for the
past 2 days, intermittent steatorrhea for the past 6 months.
At physical examination she presents jaundice, asterixis, abdominal pain, hepatomegaly, ascites and
edema up to both knees.
Previous weight 122 kg (3 months ago) , actual: 116 kg
Labs: Hb 12, WBC 17 000, Na 124, K 5, BUN 30, creatinine 1.8, albumin 2.1, total bilirubin 3.7, AST
320, ALT 124, AF 195, INR 1.8, glucose 115 mg/dl
Upper endoscopy showed esophageal varices with active bleeding and were treated with banding.
Respiratory Sputum gram stain shows gram positive cocci (pneumococci).

1- What are the diagnoses of the patient?

● Pneumonia
● Esophageal varices → due to portal hypertension
● Digestive tract bleeding
● Chronic kidney disease
● Liver disease
○ Decompensated cirrhosis → Portal Hypertension
○ Hepatic encephalopathy Type 2
○ Alcoholic cirrhosis
● Suggestive values of insulin resistance
● Hyponatremia
○ Dehydration

Severely undernourished

2- What is the alcohol byproduct that causes damage to mitochondria in the liver?
● Acetaldehyde
○ Long-term ethanol consumption changes the structure of mitochondria because
mitochondria are enlarged, misshapen, appear swollen, or elongated with disrupted
cristae
○ Levels of glutamic dehydrogenase or mitochondrial aspartate aminotransferase are
elevated in alcoholics
○ A breath test measuring CO2 production after administration of 1-14C-α-ketoisocaproic
acid showed mitochondrial dysfunction in alcoholic patients
○ Ethanol promotes oxidative stress, both by increasing ROS formation and by decreasing
cellular defense mechanisms
○ Acetaldehyde is a highly reactive and toxic byproduct to hepatocytes that may contribute
to tissue damage because it forms a variety of protein and DNA adducts that promote
glutathione depletion, lipid peroxidation, and mitochondrial damage.
○ Long-term consumption of ethanol decreases mitochondrial protein synthesis
it forms a variety of protein and DNA adducts that promote glutathione depletion, lipid peroxidation, and
mitochondrial damage.

3- What are the metabolic changes associated to the excess of NADH secondary to ethanol
metabolism?
● Ethanol consumption leads to an accumulation of NADH. This concentration levels of NADH
inhibit gluconeogenesis by preventing the oxidation of lactate to pyruvate
● The consequences may be hypoglycemia and lactic acidosis.
● The NADH also inhibits fatty acid oxidation. An alcohol consumer's NADH needs are met by
ethanol metabolism. Triacylglycerols accumulate in the liver, leading to “fatty liver”
Production of an excess of both NA+ and acetaldehyde.

During fasting there is a risk of hypoglycemia → destruction of muscle → catabolism

Due to the inflammatory process, we cannot use fat tissue

4- Why is malnutrition associated to hepatic disease? (metabolic consequences)

Patients with hepatic disorders are exceptionally vulnerable to developing malnutrition because of the key
role played by the liver in regulating the nutritional state and the energy balance. Moreover, the presence
of chronic liver disorders could reduce the appetite and thus influence the nutrient intake. Affection in
vitamin synthesis.

Steatorrhea → loss of vitamins and nutrients

Everything in liver disease leads to a px being undernourished

● Anorexia
● Muscle destruction
● Pxs cannot use fat
● Pxs cannot feed themselves
● Acidosis
● Excess of inflammation → malabsorption of nutrients
5- What is the best tool to assess these patients? (analyse all assessment tools)
● RFH-NPT (Royal Free Hospital Nutritional Prioritizing Tool): It follows two steps and in the
second one there are three questions that will add to the final result
○ THIS IS THE GOLD STANDARD
○ First Step: we must know if our patient is a transplant candidate/recipient
■ If the answer is NO go to step 2
■ If the answer is YES → High risk
○ Second step: Does the patient have fluid overload?
■ NO: BMI (0, 1 or 2), Weight loss % (0, 1 or 2) and any acute disease that has
compromised their nutritional state? (2)
■ YES: Are the meals completed (0 or 2), a 50% decrease in dietary intake the last
5 days (0, 1 or 2) and Weight loss (0, 1 or 2)
○ The addition of each score provides the information of each range
■ 0 → low risk
■ 1 → moderate risk
■ 2-7 → high risk
● GMS (Graz Malnutritional Screening): it has 5 variables and each one gives a score. It provides
its own list of diseases and their risk
○ Weight loss 3 months (0-2)
○ BMI (0-2)
○ Change in dietary intakes (0-3)
■ Loss of appetite
■ Nausea/vomiting/diarrhea
■ Chewing and/or swallowing problems
○ Severity of disease (0-2)
○ Age > 65 (1)
● NRS-2002 (Nutritional Risk Screening): using four quick questions we can decide whether our
patient needs further examination.
○ First step: BMI, weight loss, dietary changes and severely ill
■ Age is important as well, taking 70 years old as the limi
○ If any of those give alarm sings then we could divide it between mild, moderate and
severe → both nutrition and illness states are important
● MNA-SF (Mini Nutritional Assessment-Short Form): it evaluates the nutritional state using a
timelapse of three months
○ Ask if the patient has decreased their food intake due gastrointestinal problems
○ Weight loss ○ Mobility
○ Psychological stress ○ Neuropsychological problems
○ BMI
■ If it’s not available we can use CC (calf circumference)
Undernutrition → independent mortality risk → if pxs go into surgery → they could die
● Albumin → prognosis
○ Nutritionally speaking, it won’t give you the severity of undernutrition
(you can’t use hepatic proteins, neither cholesterol)

SGA → very good tool to make the assessment

6- What would be the best route of nutrition support?

Parenteral nutrition: naso-yeyunal
● Risk of bronchoaspiration
● We have to use the gut
● Minimal enteral feeding

7- What micronutrient deficit is associated to the encephalopathy?

Deficits are most commonly seen with thiamine, vitamin B12, folate, vitamin D, vitamin E, and copper
deficiencies. The neurological findings observed with these nutritional deficiencies are variable and
include encephalopathy, optic neuropathy, myelopathy, polyradiculoneuropathy, and polyneuropathy.
-Vitamin and mineral supplementation should be considered for all patients with ESLD because of the
essential role of the liver in nutrient transport, storage, and metabolism, in addition to the presence of
nutrient depletions due to drugs. Vitamin deficiencies can contribute to complications. For example, folate
and vitamin B12 deficiencies can lead to macrocytic anemia. Deficiency of pyridoxine, thiamin, or
vitamin B12 can result in neuropathy. Confusion, ataxia, and ocular disturbances can result from a
thiamin deficiency.
Vitamin and mineral deficiencies occur in alcoholic liver disease as a result of reduced intake and
alterations in absorption, storage, and ability to convert the nutrients to their active forms. Steatorrhea
resulting from bile acid deficiency is also common in alcoholic liver disease and affects fat-soluble
vitamin absorption. Vitamin A deficiency can lead to night blindness. Thiamin deficiency is the most
common vitamin deficiency in people with alcoholism and is responsible for Wernicke encephalopathy.
Folate deficiency can occur as a result of poor intake, impaired absorption, accelerated excretion, and
altered storage and metabolism. Inadequate dietary intake and interactions between pyridoxal-5-phosphate
(active coenzyme of vitamin B6) and alcohol reduce vitamin B6 status. Deficiency of all B vitamins and
vitamins C, D, E, and K is also common. Hypocalcemia, hypomagnesemia, and hypophosphatemia are
not uncommon among people with alcoholism; furthermore, zinc deficiency and alterations in other
micronutrients can accompany chronic alcohol intake.
Liver disease → The liver plays a crucial role in maintaining systemic Zn homeostasis.
-Zync: Chronic liver disease, such as chronic hepatitis, liver cirrhosis, or fatty liver, impairs Zn
metabolism, and has resulted in Zn deficiency, which in turn has caused multiple metabolic abnormalities,
including insulin resistance, hepatic steatosis and hepatic encephalopathy.
Alcoholism → Micronutrient deficiencies are commonly encountered in alcoholic patients, not only
explained by a decrease of global dietary intake, but also because of maldigestion, malabsorption,
impaired hepatic activation and an increased breakdown and excretion.
-Vitamin B1: Among water soluble vitamins, the vitamin B1 (thiamine) deficiency has been the most
frequently described and feared, potentially leading to Wernicke’s encephalopathy and its well-known
triad (delirium, oculomotor abnormalities and ataxia). If left untreated, it can progress to the
amnestic-confabulatory syndrome called Korsakoff. The therapeutic benefit of thiamin has been
demonstrated in alcoholic patients even without severe Wernicke-Korsakoff encephalopathy.

● Mainly thiamine
8- What are the caloric demands of this patient? (make calculation with best predictive equation in
hepatic patients)
● 35–40 kcal/kg/day is adequate for adults with cirrhosis If the px is in ICU = give 25
gr/kg/day
● 1gr /kg/day of Proteins
○ If catabolic à 1.2 gr/kg/day of proteins
● During encephalopathy a REDUCE protein intake during 48hrs give LACTULOSE
○ Lactulose = 0.8 gr/kg/day for TWO days, then increase proteins to 1g/kg/day
○ Aromatic amino acids (AAA) found in proteins, cross BHE and act like false
neurotransmitters
■ Aromatic = tirocine, aromatic
○ Give more Branch-Chain-AA (BCAA) are anabolic and don’t cross the BHE
■ Leucine, valine, isoleucine
● Reduce SALT intake when there’s ASCITES/edema
● Give CARNITINE to encephalopathy Px

Height: 1.56
Ideal BMI=21.5
Ideal weight=BMIi*h2=_ 52.32___
Adjusted weight=52.32 + (116-52.32)*0.4=__77.8__
Adjusted weight*25=_1945___ kcal
Adjusted weight*35=__2723__ kcal
Ideal weight*40=__3112__ kcal
Carbs:
45-60%*25=_ 875.25-1167__ kcal/4= __ 218.81-291.75_ gr
45-60%*35=__1222.35-1633.8__ kcal/4= _305.6-408.45__ gr
45-60%*40=__ 1400.4-1867.2__ kcal/4= _350.1-466.8__ gr
Proteins:
10-30%*25=_ 194.5-583.5__ kcal/4= _48.62-145.87__ gr
10-30%*35=_ 272.3-816.9__ kcal/4= _ 68.05-204.22__ gr
10-30%*40=_ 311.2-933.6__ kcal/4= __ 77.8-233.4_ gr
Well: 1.2 g/kg/day= _93.36__
Stressed: 1.5 g/kg/day=_116.7__
Medically refractory HE: 0.8 g/kg/day + 0.25 g/kg/day of BCAA=_62.24 + 19.45=81.69__
Fat:
25-30%*25=_486.25-583.5__ kcal/9=_54-64.83__ gr
25-30%*35=_ 680.75-816.9__ kcal/9=_75.63-90.76__ gr
25-30%*40=_778-933.6__ kcal/9=_86.44-103.7__ gr

● Adjusted weight formula not ideal because we would be underfeeding the px

● Indirect calorimetry

●
● Aromatic amino acids: we give BCAA amino acids

9- What are the protein demands of this patient? Which specific amino-acids are indicated?
● 35–40 kcal/kg/day is adequate for adults with cirrhosis
○ If the px is in ICU = give 25 gr/kg/day
● 1gr /kg/day of Proteins
○ If cataboic à 1.2 gr/kg/day of proteins
● During encephalopathy a REDUCE protein intake during 48hrs give LACTULOSE
○ Lactulose = 0.8 gr/kg/day for TWO days, then increase proteins to 1g/kg/day
○ Aromatic amino acids (AAA) found in proteins, cross BHE and act like false
neurotransmitters
■ Aromatic = tirocine, aromatic
○ Give more Branch-Chain-AA (BCAA) are anabolic and don’t cross the BHE
■ Leucine, valine, isoleucine
● Reduce SALT intake when there’s ASCITES/edema
● Give CARNITINE to encephalopathy patients
10- Is fluid intake restriction indicated?
● Yes, because the patient has mild hyponatremia.
● Chronic hyponatremia, associated with higher morbidity and mortality, is prevalent in patients
with ascites. It is typically a hypervolemic hyponatremia, and in most patients fluid restriction
does not need to be considered until hyponatremia is severe. Fluid restriction should be
considered when sodium levels decrease to less than 130 mEq/L. Fluid restriction of 1 to 1.5 L
fluid/day once serum sodium declines to less than 120 to 125 mEq/L is considered standard
practice
● Cirrhotic patients usually become ascitic → suggestions for restriction of sodium, fluid and other
substrates depending on comorbid conditions like renal failure or diabetes mellitus.
● In cirrhotic patients, the free water clearance is dramatically reduced (usually below 1 ml/min)
equivalent to intake of only 1.5 liters of fluid/day before fluid accumulation arises, causing a
dilutional hyponatremia (serum sodium < 130 mmol)
● ASCITES → Edema → higher intra abdominal pressure = respiratory distress

11- Name micronutrient deficiencies.

● Patients with cirrhosis may present deficiencies in water- soluble vitamins, particularly thiamine,
and lipid soluble vitamins such as vitamin D
● Zinc and vitamin A supplements by improving dysgeusia may indirectly improve food intake and
nutritional state
● Zinc and selenium deficiency have been observed in patients with alcoholic as well as
non-alcoholic liver disease
● B complex, calcium, zinc, Mg
● Some of the most common deficiencies include: vitamin A, iodine, iron, zinc, and folate.
● In cirrhotic patients, micronutrients should be administered to treat confirmed or clinically
suspected deficiency.

12- Why do we use carnitine in hepatic failure treatment?

ALC is an endogenous molecule synthesized in mitochondria by the enzyme ALC transferase and is the
predominant acylcarnitine in normal tissues. Acylcarnitine is the fatty acid–bound form of L-carnitine,
which has an important role in the transport of long-chain fatty acids into mitochondria and in their
b-oxidation. Serum acylcarnitine is mainly composed of short-chain fatty acid L-carnitine, especially
ALC.
 ● Fatigue is frequently reported in hepatic encephalopathy (HE) and may be related to
hyperammonemia. Acetyl-L-carnitine (ALC) offers neuroprotective benefits and improves
mitochondrial energetics and function.
● It was shown that L-carnitine has a protective effect against ammonia-evoked encephalopathy in
cirrhotic patients and acetyl-L-carnitine (ALC) administration improved neurologic symptoms
and plasma variables in selected cirrhotic patients with hepatic coma.
● ALC treatment reduces fatigue in the elderly and in centenarians
● Whether the medication works by improving blood ammonia levels or whether it works centrally
perhaps by decreasing brain ammonia uptake remains unclear.
Carnitine increases FFA inside mitochondria → Energy available → strength, mental status. Reduces
inflammation → reduce catabolism.
● 40 mg/kg/day

● Reduce inflammation → reduce catabolism

13- Why do we use fiber and probiotics in hepatic failure?

● The gut-liver axis provides for an interaction between bacterial components like
lipopolysaccharide and hepatic receptors (Toll-like receptors). Dysbiosis and altered intestinal
permeability may modulate this interaction and therefore result in hepatic disorders or worsening
of hepatic disorders. Administration of health-promoting microbial strains may help ameliorate
these harmful interactions and hepatic disorders.
○ The effect is believed to be modulated by changes in gut microbiota: an increase in
non-urease-producing bacteria like lactobacilli and a concomitant reduction in urease
producers like Escherichia coli and Staphylococcus aureus.
● Fiber helps your liver work at an optimal level.
● Probiotics are able to decrease the permeability of the intestinal wall, and decrease bacterial
translocation and endotoxemia in animal models as well as in clinical studies, which is extremely
important in the prevention of complications of liver cirrhosis and infection after liver
transplantation. Probiotics could limit oxidative and inflammatory liver damage and, in some
situations, improve the histological state, and thus non-alcoholic steatohepatitis could be
considered as another possible indication.
● Probiotics can improve not only the health of our gut but liver health, as well. Increased
awareness of the importance of the microbes that live in our gut has spurred a great deal of
research on the microbiome and fueled a booming probiotics industry.
 ● Short chain fatty acids feed 60% of GI
○ Reduce inflammation → butyrate
■ Reduce risk of fatty liver/stress in pancreas (reduces pancreatic insufficiency)
○ Reduce fibrosis
■ Reduced risk of cirrhosis
● Bacteria gives us 10% of energy that we need daily
Increased insulin sensitivity due to reduced pancreatic insufficiency

● EPA anti inflammatory action, fiber combined w/probiotics and omega 3 it is quicker and
better
● Give probiotics with regular basis → for 3-6 months
REFERENCES
● Arthur I. Cederbaum. (1999) Effects of alcohol on hepatic mitochondrial function and
DNA. Gastroenterology. vol 117 (1), P265-269.
DOI:https://doi.org/10.1016/S0016-5085(99)70578-0
● Nassir, Fatiha, and Jamal A Ibdah. (2014) “Role of mitochondria in alcoholic liver
disease.” World journal of gastroenterology vol. 20,9: 2136-42.
doi:10.3748/wjg.v20.i9.2136
● Jan B. Hoek, Alan Cahill, And John G. Pastorino (2002). Alcohol and Mitochondria: A
Dysfunctional Relationship. Gastroenterology.122(7): 2049–2063. doi:
10.1053/gast.2002.33613
● Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman;
2002. Section 30.5, Ethanol Alters Energy Metabolism in the Liver.
https://www.ncbi.nlm.nih.gov/books/NBK22524/
 Clinical case. Pancreatitis.
57 year old female presented with sudden acute onset of bilateral upper quadrant abdominal pain,
nausea, vomiting, and fever. Initial elevated amylase and lipase suggested acute pancreatitis.
Over the first 6 hours of hospitalization she developed respiratory distress and hypoxemia
requiring mechanical ventilation. Her BMI is 35, her temperature is 39 °C, BP 180/70, heart rate
135. Her abdomen is distended and bowel sounds are hypoactive but present, she has lower
extremities with mild edema.
Labs: WBC 21, Hb 10.5, Hcrt 32.8, BUN 55, Creatinine 2.5, K3.4, Na 155, glucose 186, albumin
2.8, LDH 400, calcium 7.5. A CT scan revealed an enlarged edematous pancreas with
inflammatory changes of the gland and free fluid in the lesser sac. An abdominal ultrasound
revealed a prominent common bile duct with choledocholithiasis.

1- What are the main causes associated with acute pancreatitis? Is obesity a risk factor?
● obstruction of the common bile duct by stones and alcohol abuse are the most frequent
causes of acute pancreatitis
● Endoscopic retrograde cholangiopancreatography (ERCP) is a potential cause of acute
pancreatitis
● Certain medications.
● Hypercalcaemia
○ Risk factors
■ Excessive alcohol consumption
■ Cigarette smoking
■ Obesity
■ Family history of pancreatitis.

Inflammation → insulin resistance → pancreatic disease

Main causes
- Women: gallstones
- Men: alcohol
Obesity is a risk factor because its a chronic inflammation, the fatty livers lead to inflammation
2- Chronic pancreatitis might lead to which diseases?
● The primary complications include abdominal pain, diabetes mellitus, exocrine
pancreatic insufficiency, metabolic bone disease, and pancreatic cancer. Additional
anatomic complications can include pseudocysts, splanchnic venous thrombosis, and
duodenal or biliary obstruction

DM, kidney failure, cancer, malabsorption, osteoporosis

3- What are the Ranson criteria? Does she has any of them?
● Ranson criteria are used to predict the severity and mortality of acute pancreatitis. Five
parameters are assessed on admission, and the other six are assessed at 48 hours
post-admission

● 5 ranson criteria
Age, WBC, LDH, BUN, calcium → severity and prognosis of the patient → 40% risk
4- What is the Bisap score of the patient?

● 3 = severe pancreatic disease

Severity
When there is a lot of fluid along your lungs you can't breathe correctly, you check the presence
of fluid → in X ray you see edema → Respiratory distress

5- Perform the subjective global assessment

● Weight change: BMI 35 (class II obesity) → no weight changes informed.
● Dietary Intake → no information about dietary intake
● Gastrointestinal symptoms → Nausea and Vomiting
● Functional capacity → No information was given.
● Physical findings → She has lower extremities with mild edema (+1pt )
● Disease and its relation to nutritional requirements → Severe acute pancreatitis /
Coledocholithiasis; Metabolic demand: High

→ Overall SGA: C: severely malnourished

Feed the patient as soon as possible.
6- Does she need nutrition therapy? Why? (remember the benefits of a nutritional
therapy)
● She does need nutrition therapy:
○ Acute Pancreatitis causes a massive systemic inflammatory response, increasing
risk for deterioration of nutritional status, septic morbidity, organ failure, and
prolonged hospitalization.
○ Patients with pancreatitis are at high risk of malnutrition
○ Nutritional support is one of the cornerstones of management because of the high
catabolic state present in pancreatitis.

7- Does she has other co morbidities? Why is the calcium low?

● Class II obesity (BMI 35 )
● Metabolic Syndrome

Hypocalcemia
● Exact mechanism of hypocalcemia in acute pancreatitis is unknown. Several mechanisms
proposed for hypocalcemia seen in early phase are autodigestion of mesenteric fat by
pancreatic enzymes and release of free fatty acids, which form calcium salts.
● Pancreatitis can be associated with tetany and hypocalcemia. It is caused primarily by
precipitation of calcium soaps in the abdominal cavity, but glucagon-stimulated
calcitonin release and decreased PTH secretion may play a role.
● When the pancreas is damaged, free fatty acids are generated by the action of pancreatic
lipase. Insoluble calcium salts are present in the pancreas, and the free fatty acids avidly
chelate the salts, resulting in calcium deposition in the retroperitoneum. In addition,
hypoalbuminemia may be a part of the clinical picture, resulting in a reduction in total
serum calcium. In patients with concomitant alcohol abuse, a poor nutritional intake of
calcium and vitamin D, as well as accompanying hypomagnesemia, may predispose these
patients to hypocalcemia
FFA attach to Calcium
Hypoalbuminemia (correct the formula of Ca because it's higher but it's attached to something
else) → Calcium is transported by albumin and there’s Hypoalbuminemia, calcium is low.

8- What would be your first nutritional approach in severe pancreatitis? (Fasting,

enteral, parenteral) Why?
Nutritional status must be evaluated. In most patients, an oral soft or solid diet can be beneficial
if tolerated. When oral feeding is not tolerated for a few days, Enteral Nutrition feeding through
a nasogastric or nasojejunal feeding tube should be attempted within the first 72hrs. of
administration. Parenteral Nutrition should be minimized for its risks of infection and other
complications. Only if enteral route is not available or tolerated, PN may be considered.
 ● Start early nutritional support with Enteral Nutrition
○ Enteral nutrition can be used in the presence of:fistulae, ascites, pseudo cysts
○ To prevent pancreas auto-digestion, which leads to the release of
pro-inflammatory mediators
○ Continuous infusion
○ Nasogastric access is adequate, post pyloric access is not needed
○ Peptidic formula with MCT is better tolerated

● Parenteral Nutrition is indicated when enteral nutrition is contraindicated or not tolerated

○ Add lipids in bag if TG<400 and no history of dyslipidemia
○ Add glutamine 0.3 gr/kg
○ Energy 25-30 kcal/kg
○ Protein demand 1.2 – 1.5 gr/kg
Enteral → avoid translocation (septic complications) and severity of the problem

9- How could internal access be achieved? (gastric, jejunal, veins)

● NG appears to be the best current initial approach to enteral feeding, bc NJ requires
endoscopy or radiology, although more proximal feeding increases pancreatic stimulation
and more severe pancreatitis. Lately NJ EN has been preferred over NG EN or duodenal
feeding believed to increase chances of aspiration pneumonitis and stimulating pancreatic
secretion. In this specific patient we prefer NG because of the bronchoaspiration risk
She has a bronchoaspiration risk so feed the jejunum

10- What formula should be used?

● Peptidic formula with medium chain triglycerides. Semi Elemental or elemental formula.
Polimeric also can be used if the elemental/semi-elemental are not available.

11- Which immune modulators can be given to favor the outcome of the patient?
● Duodenal infusion of the amino acid glutamine has shown the expression of the major
cytoprotective enzyme, heme-oxygenase-1 (HO-1). HO-1 is an important enzyme for
immune homeostasis and exerts anti-inflammatory effects in animal models of intestinal
inflammation. Medium chain triglycerides have been shown to exert anti-inflammatory
effects in animal models of inflammatory bowel disease. Also omega 3 to reduce
inflammation
○ Glycyrrhizin is a therapeutic agent which demonstrates reduction in serum
levels of CCL2 (C–C motif chemokine ligand 2), amylase and lipase activity
through inhibition of the recruitment of inflammatory cells into pancreas. b.
○ Sivelestat demonstrated strong anti-inflammatory potential; it interfered with
regulatory mechanisms of immune cells, and demonstrating its action through
 reduced expression of lipase, amylase, IL-1β, TNF-α and NF-αB; its
administration increased antioxidant power and IL-4 serum level
○ Flavocoxid reduced levels of TNF-α, serum levels of prostaglandin E2 (PGE2)
and leukotriene B4 (LTB4), and reduced histological damage. It influenced
neutrophil and macrophage action via cyclooxygenase-2 (COX-2) and
5-lipoxygenase (5-LOX) blockade
○ Rofecoxib and Lisinopril demonstrated reduced levels of CCL2, CCL3, TNF-α,
IL-6, influencing macrophage infiltration via COX-2 pathway inhibition

Glutamine increases Heat Shock proteins (“chaperonas”), anti-inflammatory and W3

Heat shock proteins (chaperonas) checked how we create and pack the proteins.
In pancreatitis → heat shock proteins are reduced → there’s a burst of enzymes and lysosomes
inside cells. → necrosis caused by autodigestion
NF- KB → responsible of nuclear attraction

To solve pancreatic pedo, you give Glutamine that gives the aa to create a la chaperona.
Glutamine helps to synthesize Heat shock proteins
12- How should we monitor the patient’s enteral tolerance?
● We know the patient does not tolerate enteral nutrition if there is vomit, abdominal
bloating, diarrhea or pain. These symptoms should stop if the nutrition is held. We need
to start nutrition in small amounts → Minimal enteral nutrition
● Parameters: food chart, fluid balance, weight/BMI, temperature/pulse/respiration, bowels,
capillary blood glucose, medications, nausea and vomiting, feeding tube position, feeding
tube insertion site, tube integrity, general clinic condition, oral health. Biochemistry
monitoring: sodium, urea, creatinine, potassium, phosphate, magnesium, corrected
calcium, glucose, liver function tests, c-reactive protein, albumin, zinc, copper, selenium,
folate, B12, vitamin D
Pain (blood P, pulse, fever, saturation down), nausea, diarrhea, vomiting, bloating
Increased Heart Rate

13-Do complications as pseudocyst formation, pancreatic ascites or pancreatic

fistulas preclude enteral nutrition?
● No, Pancreatic ascites is a somewhat rare entity that results from a pancreatic duct injury,
leading to persistent leakage of pancreatic secretions into the peritoneum. The severity of
this condition varies widely and is often dependent on the location and degree of ductal
injury and any infection in the fluid. While mild cases of pancreatic ascites resolve
spontaneously, persistent pancreatic ascites and infection are associated with significant
morbidity and mortality. This activity illustrates the evaluation and treatment of
pancreatic ascites and reviews the role of the interprofessional team in managing those
with this condition.
“Jump the pancreas and feed the gut” → MORE BENEFITS

14- Which pharmacological treatment is recommended in case of steatorrhea?

● In patients with pancreatic deficiency the oral administration of pancreatin (replacement
of pancreatic enzymes) improves steatorrhea and clothes symptoms associated with
indigestion
○ Enzyme supplementation with lipase and pancreatin
Not Long chain fatty acids, give pancreatic enzymes
.
15- When would you be forced to give parenteral nutrition?
● PN is indicated in patients undergoing minimally invasive necrosectomy who do not
tolerate EN or who are unable to tolerate targeted nutritional requirements, or if there
exist contraindications for EN.
 ● Complications of severe AP, which may occur and represent a contraindication for EN,
include bowel obstruction, abdominal compartment syndrome, prolonged paralytic ileus
and mesenteric ischemia
○ Patients with necrotic pancreatitis won't tolerate PN for too long (tops 5 days)
● Parenteral Nutrition should be minimized for its risks of infection and other
complications. Only if enteral route is not available or tolerated, PN may be considered.
● Parenteral Nutrition is indicated when enteral nutrition is contraindicated or not tolerated
○ Add lipids in bag if TG<400 and no history of dyslipidemia
○ Add glutamine 0.3 gr/kg
○ Energy 25-30 kcal/kg
○ Protein demand 1.2 – 1.5 gr/kg
Don’t tolerate, necrotic pancreatitis

16-Which nutrient is contraindicated in parenteral nutrition in case of

Hypertriglyceridemia?
● IV fat emulsions
● Lipids

Bibliography
1- Krause and Mahan’s Food & The Nutrition Care Process. 15TH EDITION. Chapter 28:
Medical nutrition therapy for hepatobiliary and pancreatic disorders.
2- Marianna Arvanitakis, Johann Ockenga, Mihailo Bezmarevic, Luca Gianotti, Zeljko Krznaric,
Dileep N. Lobo, Christian Lo€ser, Christian Madl, Remy Meier, Mary Phillips, Henrik Højgaard
Rasmussen, Jeanin E. Van Hooft, Stephan C. Bischoff. ESPEN guideline on clinical nutrition in
acute and chronic pancreatitis. Clinical Nutrition 39 (2020) 612e631
3- Gao W, Yang H-X, Ma C-E (2015) The Value of BISAP Score for Predicting Mortality and
Severity in Acute Pancreatitis: A Systematic Review and Meta- Analysis. PLoS ONE 10(6):
e0130412. doi:10.1371/journal.pone.0130412
4- Guo-Jun Wang (2009) Acute pancreatitis: Etiology and common pathogenesis. World J
Gastroenterol. 2009 Mar 28; 15(12): 1427–1430. doi: 10.3748/wjg.15.1427
5- Mitchell L. Ramsey. (2017) Complications of Chronic Pancreatitis. NCBI. doi:
10.1007/s10620-017-4518-x

Surgical fistulae
- Adhesion rupture
- Intestinal resection in IBD or cancer
- Surgery in pancreatitis
- Urgent surgery
- Surgery in radiated abdomen
All of this ones have something in common: theres some trauma, stress and Inflammation

Spontaneous fistulae
- Radiation
- Inflammatory bowel disease
- Diverticular disease
- Appendicitis
- Intestinal ischemia
- Duodenal ulcer perforation
- Pancreas cancer, gynecologic cancers
- Intraabdominal abscess

Associated complications
- Sepsis
- Electrolytic unbalance
- Hemorrhage
- Pain
- Expenses
- Death

Diagnose
- Abdominal pain, fever WBC, material exit 24-48 hrs after cellulitis
- Oral blue methylene (verifies)
- Image (obstruction, abscess)
- Fistulogram → Gold Standard → X ray with a marker

Nutritional intervention
- Parenteral nutrition
- Spontaneous Closure 4-6 weeks
Factors that favor or not the closure
- Oral esophagus, duodenal, jejunum
- Well nourished
- No sepsis
- Cause: appendicitis, diverticulitis or Cx
- Small output, without abscess
- Gastric, ileum
- Undernourished
- With sepsis
- Cause: IBD, cancer, radiation
- Abscess distal obstruction, active disease

Enteral nutrition

Parental Nutrition
 - Distal access nos possible
- Pancreatic fistulae
- High output
- Drainage not collected adequately
- Outpit increases with enteral nutrition

Specific nutrients
- Output content (electrolytes)
- Cu, Zn (for GAP functions) (12-17 mg per Liter from the output), b12 IV (or IM)
- Ocreotide? Reduce output

Know what and from where your patient is loosing