Total parenteral nutrition (TPN) provides complete nutrition to patients intravenously when they cannot eat or absorb enough nutrients from food. It is used when the enteral route is unable to sustain sufficient caloric intake. TPN can be administered peripherally through arm veins for short term use or centrally through larger veins for longer term needs. While enteral nutrition is preferred when possible due to its benefits, TPN is important for patients who cannot or should not eat to prevent complications from malnutrition. Careful monitoring is needed with TPN to address nutrient needs and avoid potential complications.
Total enteral nutrition and total parenteral nutrition in critically ill pat...Prof. Mridul Panditrao
Prof. mridul panditrao, discusses intricate problems of starvation, the pathophysiological changes, Total enteral nutrition, total parenteral nutrition, various protocols etc...
Total enteral nutrition and total parenteral nutrition in critically ill pat...Prof. Mridul Panditrao
Prof. mridul panditrao, discusses intricate problems of starvation, the pathophysiological changes, Total enteral nutrition, total parenteral nutrition, various protocols etc...
In this presentation i have tried to explain in details about the Total Parenteral Nutrition (TPN) , what is it, who needs it, and how to prepare it and the necessary procedure with instructions. It is very useful for the individuals from Nutrition, Nursing, Pharmacists, and Medical background.
In this presentation i have tried to explain in details about the Total Parenteral Nutrition (TPN) , what is it, who needs it, and how to prepare it and the necessary procedure with instructions. It is very useful for the individuals from Nutrition, Nursing, Pharmacists, and Medical background.
Physical Therapy is an integral part of breast cancer rehabilitation. Those undergoing treatments for breast cancer often face surgery. Physical therapists can work with women to alleviate symptoms caused by surgical intervention or medical treatment for cancer. The Prospective Surveillance Model, or PSM, is a proactive approach to periodically examining patients and providing continued assessment during and after disease treatment, often in the absence of impairment.
Introduction to the peer review workshop for the PhD students of the Wageningen Graduate Schools. The goal is to explain peer review, entice PhD students to take part in the peer review process and give some tips on how to start with peer review.
this is a detailed presentation on the principles of surgical nutrition. the presentation started with surgical metabolism and epidemiology of malnutrition in surgical patients. Furthermore, the aetiology of malnutrition was discussed in surgical patients. Finally, the various types of nutritional support, enteral and parenteral, was discussed under indications, types, access, advantages, disadvantages, complications and monitoring.
Nutrition in Acute Pancreatitis (According to ESPEN guidelines 2002 and ACG g...Jibran Mohsin
This presentation compares the European Society of Parenteral & Enteral Nutrition (ESPEN) 2002 guidelines and American College of Gastroenterology (ACG) 2013 guidelines regarding nutrition in patients of acute pancreatitis
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
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disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
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AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
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Cardiac conduction defects can occur due to various causes.
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3. • It goes without saying that without food there
can be no life, that food is a basic human right
& that it is necessary for every doctor to pay
attention to the nutritional needs of their
patients.
• Nevertheless , approximately 1/3 rd of the
patients admitted to an acute hospital will
have evidence of PEM & 2/3 rd will leave the
hospital either malnourished or having lost
weight.
4. • Malnutrition has damaging effects on
psychological status, activity levels & appearance.
• Paradoxically, in the surgical patient a low body
fat content may sometimes viewed as an
advantage making technical aspects of surgery
easier.
• There is, however clear evidence that patients
with severe protein depletion have a significantly
greater incidence of postoperative complications
& prolonged hospital stay.
5. • Nutritional disorders in surgical practice have
two principal components.
• First – starvation can be initiated by the
effects of the disease, by restriction of oral
intake, or both.
Simple starvation leads to progressive loss of
body’s energy & protein reserves.
• Second – there are the metabolic effects of
stress/ inflammation
6. namely – increased catabolism & reduced
anabolism.
• In most surgical patients it results from a
combination of reduced food intake &
metabolic changes
7.
8. Nutrient requirements per day
Calories – 25 kcal/kg
• Proteins – 0.8-2kgs/day (mild/mod/sev stress
– 1,1.5,2g/kg/day)
• Carbohydrates –minimum – 75/100 g/day
• Fats – minimum requirement is 500 ml of 20%
lipid emulsion/week to prevent EFA deficiency.
9. • Water – 30/40 ml/kg/day + extra for any fluid
loss + 500 ml/day/degree Celsius rise in
temperature.
100 ml/kg for first 10 kg of wt. plus
50 ml/kg of wt. from 11-20 kg plus
Age ≤ 50 y.;20 ml/kg over 20 kg or
Age > 50 y.;15 ml/kg over 20 kg
13. Enteral Nutrition
• The enteral route is generally favored over the
parenteral one because it is the natural portal of
entry for exogenous nutrients.
• The enteral route obviates the need for intravascular
access with its attendant risk of infections and sepsis.
• The array of nutrients that can be administered via
the gastrointestinal tract is greater than what is
available for parenteral use, allowing for better
tailoring of nutrient intake.
14. More Advantages—
Enteral Nutrition
• Intake easily/accurately monitored
• Costs less than parenteral nutrition
• Supplies readily available
• Reduces risks associated with
disease state
• Preserves gut integrity
• Decreases likelihood of bacterial translocation
• Preserves immunologic function of gut
• Increased compliance with intake
15. Disadvantages—Enteral Nutrition
• GI, metabolic, and mechanical complications—
tube migration; contamination; tube obstruction;
• Labor-intensive assessment, administration, tube
patency and site care, monitoring
16. Parenteral nutrition
• Parenteral nutrition is the provision of all nutritional
requirements by means of the intravenous route and
without the use of gastrointestinal tract.
• Parenteral nutrition is used when the enteral route is
unable to provide or sustain sufficient caloric intake.
• About 5% of hospital admissions require TPN
17. Indications
• INDICATIONS
– Patient who can’t eat
– Patient who won’t eat
– Patient who shouldn’t eat
– Patient who can’t eat enough
“If the gut works, use it.”
18. Indications
• Those who do not eat: anorexia nervosa,
• Those who can not eat: esophageal
stenosis, prolonged ileus,
• Those who are not allowed to eat:
gastrointestinal fistula, inflammatory bowel
disease, radiation enteritis, GI chemo
toxicity, pancreatitis, tracheoesophageal
fistula, massive intestinal atresia.
19. Indications
• Those who are not eating enough: short
bowel syndrome, burns, sepsis
• Those who cant manage what they eat:
hepatic failure
• Others: renal failure, major surgeries.
20. General Conditions Suggesting
Initiation of Nutrition Support
▪ Poor nutritional status (oral intake <50% of
energy needs)
▪ Significant weight loss (>10%)
▪ Anticipated duration of artificial nutrition
longer than 7 days
▪ More than 7 days' inanition
▪ Serum albumin <3 g/dL in the absence of an
inflammatory state
21. The gut should always be the preferred route
for nutrient administration.
If you are going to start TPN, there needs to
be a reason why you cant use EN.
22. Routes for TPN
• Parenteral nutrition is administered through
either central or peripheral venous catheters.
• In the early days of parenteral nutrition, the
only energy source available was hypertonic
glucose which had to be given into a central
vein to avoid thrombophlebitis.
• In the second half of the last century, there
were a number of important developments
which led to usage of isotonic safe, non toxic
emulsions for TPN.
23. Peripheral TPN
• Peripheral veins cannot tolerate an osmolarity
of more than 750 mOsm/L (the equivalent of
12.5% dextrose)
• The fluid volume that can be tolerated limits
the caloric intake.
• Therefore, this route is used mainly for
supplementation or short-term feeding (<2
weeks).
24. PN: Peripheral Access
• Access can be achieved by means of a:
1) Dedicated catheter inserted into a peripheral
vein and maneuvered into central venous
system (peripheral inserted central venous
catheter PICC line).
2) Conventional short cannula in the wrist veins.
25. Peripherally inserted central catheters
(PICCs)
• Introduced via the basilic vein,
• Can be used both in the inpatient setting and also for
longer-term outpatient therapy.
• PICC line in the outpatient setting has a lifetime of 4 to 6
weeks
– Benefits
• Access to central vein
• Can accommodate hypertonic fluids
• Lower risk of phlebitis than PPN
• Easier to insert than central line
26.
27.
28. PPN Solution
1. Typically delivers 1400-2500 kcals/day
2. Carbohydrate: Dextrose (glucose)
3. Protein: AAs
4. Lipid: IV lipid emulsion
a. Concentrated source of kcals
b. Isotonic
c. Administered every day to protect
vein
29. Central TPN
• Central venous catheters are the main route of TPN
administration.
• The catheter should be a single-lumen catheter, used
only for TPN.
• Multiple-lumen catheters and multiple-purpose
single-lumen catheters have higher infection rates .
30. • The preferred entry of location is the
subclavian vein, which provides a stable site,
good patient acceptability, and lower infection
rates than either the internal jugular or
femoral routes.
• Most intensive care physicians and
anesthetists favor jugular veins as it is
technically easier.
31. Subcutaneously tunneled central catheters (Hickman)
• The catheter of these
devices can be inserted into
the vein percutaneously
(e.g., the subclavian, internal
jugular, or femoral) and then
tunneled to the final skin
exit site
• Subcutaneous tract forms a
barrier to bacterial
encroachment and
colonization
• Tunneled catheters are
desirable when frequent
access is required
32. Implanted Venous Access Device
(portacath)
• Portacath is completely
subcutaneous
• It is accessed by
percutaneous insertion
of a special low-profile
needle (Huber needle)
• Which passes through
the self-sealing
diaphragm of the device
into the chamber.
35. Energy Expenditure and Caloric
Requirements
• Basal energy expenditure (BEE)—also called basal
metabolic rate (BMR)—the energy expenditure on
awakening from a 12-hour fast measured in a
thermoneutral environment (25°C).
• Thermogenic effect of food—also called specific
dynamic action—the energy expenditure after the
ingestion of food. After a meal, energy expenditure
may increase 5% to 10%
36. • Resting energy expenditure (REE)—the energy
expenditure while resting in the supine
position with eyes open. Includes the
thermogenic effect of food if performed
within a few hours of a meal or during
continuous infusions of nutrients such as
during continuous TPN administration. About
10% greater than BEE.
• Sleeping energy expenditure (SEE)—the
energy expenditure during sleep; it is usually
10% to 15% lower than REE.
37. • Activity energy expenditure (AEE)—the energy
expended during physical activity. During
maximum exercise it can be 6- to 10-fold
greater than the BEE.
• Environmental temperature—energy
expenditure increases to warm patients
placed in a cold environment. Warming occurs
through shivering and increased metabolism
of brown fat (neonates).
38. • Fever—Fever increases metabolic rate 10%
per °C (or 7% per °F).
• Total energy expenditure (TEE)—total energy
expended over 24 hours: the sum of energy
expended during periods of sleep, resting, and
activity.
39. Energy requirement in adults
• 1.Basal energy expenditure (BEE)
• Harris-Benedict equation
• Males: eBEE (kcal/day) =
66 + (13.7 • W) + (5 • H) - (6.8 • A)
• Females: eBEE (kcal/day) =
655 + (9.6 • W) + (1.7 • H) - (4.7 • A)
*W=kg. (actual or usual wt.), H=cm.,A=yr.
40. • eREE = eBEE • stress factor
• eTEE = eREE • activity factor
• Total energy expenditure (TEE)
TEE= BEE x AF x SF kcal/day
• eBEE, estimated basal energy expenditure; W,
weight (kg); H, height (cm); A, age (years); eREE,
estimated resting energy expenditure; eTEE,
estimated total energy expenditure.
41. 2.Activity Factor (AF)
- with respiratory supports = 0.7-0.9
- bed rest = 1.2
- ambulatory = 1.3
3.Stress Factor (SF)=Metabolic Factor e.g.
Fever 1+0.13/1 c
Mild infection 1.0-1.2
Moderate infection 1.2-1.4
Minor operation 1.2
Moderate operation 1.2-1.4
Skeletal trauma 1.35
Major sepsis 1.4-1.6
Peritonitis 1.05-1.25
Cancer 1.0-1.25
Soft tissue trauma 1.0-1.3
Weight gain 1.1
Burns ; 10-30% BSA 1.5
; 30-50% BSA 1.75
; > 50% BSA 2.0
Energy requirement in adults
46. Proteins
• Protein (or amino acids, the building blocks of
proteins) is the functional and structural
component of the body, so fulfilling patient’s
caloric needs with non-protein calories (fat
and glucose) is essential.
47. Protein Requirements
• Tissue synthesis
• Constitutes of hair, skin, nails, tendon, bones,
ligaments, major organs, muscle
• Precursors of neurotransmitters
• Major part of antibodies, enzymes, transports
of ions and substrates in blood
• Initiators of muscle contraction
49. Amino acid solutions –
• Ex: 10% amino acids solution
• Content – 100g/L
• Nitrogen content – 15.34g/L
• Calorie – 400 kcal/L
• Osm – 965 mOsm/L
• The concentration of amino acids should be
reduced in patients suffering from hepatic &
renal failure.
50. Carbohydrate
• Primary source of energy for normal healthy
person
• Principle energy substrate for brain, which
utilizes 130-140 g of glucose per day
• All CHO are absorbed in the form of glucose
• Reduces ketone production
• Facilitates storage of TG in fat tissue
• Preserve body protein ( gluconeogenesis)
•
51. provides the obligatory needs of the substrate ,
thus reducing gluconeogenesis and sparing
endogenous protein.
1 gm of glucose gives 4 Kcals.
• Most stable patients tolerate rates of 4-5 mg.kg-1.Min-
1, but insulin resistance in critically ill patients may
lead to hyperglycemia even at these rates, so insulin
should be incorporated acc. to blood sugar levels
52. Route
• Glucose in 5% solution can be safely
administered via a peripheral vein, but higher
concentrations require a central venous line.
• 20, 25, or even 50 % solutions are needed to
administer meaningful amounts of energy to
most patients for proper volume
administration
53. Lipids
• Source of energy
• Carriers of fat-soluble vitamins
• Precursors of eicosanoids, modulate immune
function
• Substrate for fat formation in adipose tissue
High energy content in
a low volume:
9 kcal/g lipids
54. Lipids, cont.
e. Helps minimize hyperglycemia
f. Helps prevent respiratory acidosis (in respiratory
failure)
g. Need at least 10% of kcals from lipid to prevent EFA,
which are the building blocks for many of the
hormones involved in the inflammatory process as
well as the hormones regulating other body
functions.
h. Excessive lipid administration may suppress immune
fx.
i. Often hung separately
j. Admixtures (3:1) becoming more common
k. Potential source of vit. K: potential problem if
anticoagulants used
55. • Fat mobilization is a major response to stress
and infection.
• Triacylglycerol are an important fuel source in
those conditions, even when glucose
availability is adequate.
• Need to be restricted in patients with
hypertriglyceridemia.
56. • Fat emulsions can be safely administered via
peripheral veins, provide essential fatty acids, and
are concentrated energy sources for fluid-
restricted patients.
• Ideally, energy from fat should not exceed 40% of
the total (usually 20-30%).
• Though lipids have a calorific value of 9Kcal/g, the
value in lipid emulsions is 10Kcal/g due to the
contents of glycerol and phospholipids
61. Electrolytes
Suggested
electrolytes in adults
(per L)
Conditions that require
alteration of amount
provided
Na 60-150 mEq
K 40-120 mEq
Cl 60-120 mEq
PO4 10-30 mM
-Renal failure,
GI loss, Traumatic brain injury
-Renal failure, GI loss,
Metabolic acidosis, Refeeding
-Renal failure, GI loss, Acid-
base status
-Renal function, Refeeding,
Bone disease, Hypercalcemia,
Rapid healing,Hepatic failure
62. Vitamins
• Vitamin requirements
- Vitamin requirements during PN therapy are
uncertain because they are not based on balance
studies.
- The requirements for an adult TPN:
FDA 2003 (increase in vitamin B1, B6,
C and folic acid and include 150 μg of
vitamin K)
63. Vitamins in PN
Vitamin Amount
Thiamine B1
Riboflavin B2
Pyridoxine B6
Cyanocobalamin B12
Niacin
Folic acid
Pantothenic acid
Biotin
Ascorbic acid
Vit. A
Vit. D
Vit. E
Vit. K
6 mg (3)
3.6 mg
6 mg (4)
5 μg
40 mg
600 μg (400)
15 mg
60 μg
200 mg (100)
3300 IU
5 μg
10 IU
150 μg
64. Trace Elements
• Prosthetic groups of enzymes
• Routine addition of zinc, copper, selenium,
chromium, and manganese recommended
• Addition of molybdenum probable
Vitamin and trace element levels should be
monitored periodically during long-term PN
administration
65. Requirement of Trace element in PN
Trace elements
Trace elements
Requirement/day (adult)
Zn (mg)
Cr (μg)
Cu (mg)
Mn (μg)
Fe (mg)
I (μg/kg)
Mo (μg)
Se (μg)
2.5-4.0
10-15
0.3-0.5
60-100
1.0-2.0
1.0-2.0
20-130
20-40
66. Trace Elements
Trace Elements Comments
Zn
Cu
Cr
Mn
Mo
-Increase dose with catabolic
state, intestinal loss
12.2 mg/L small bowel fluid loss
17.1 mg/kg stool/ileostomy
-Reduce or hold dose with biliary
disease
-Increase to 20 μg with intestinal
losses, reduce in renal disease
-Reduce dose with biliary disease
-Reduce dose with biliary disease
67. TPN Administration
A. Rate
1. Start slowly, especially w/dextrose. Allows
blood to adapt to increased glucose/osmolality
2. Infusion pump is used to ensure proper rate.
3. Start slowly
(1 L 1st day; 2 L 2nd day)
Example: Start at 40ml/hr x 24hr. Then progress to
80ml/hr x 24h (equivalent to increasing TPN by 1
liter per day), etc. until goal rate has been reached
or patient intolerance is noted.
68. a. If rate is increased too quickly, hyperglycemia may result
b. Monitor tolerance: electrolytes, blood glucose,
triglycerides, ammonia, etc.
4. Introduce lipids gradually to avoid adverse reactions (fever,
chills, backache, chest pain, allergic reactions, palpitations,
rapid breathing, wheezing, cyanosis, nausea, and
unpleasant taste in the mouth)
5. When pt. is taken off TPN, rate must be tapered off
gradually to prevent hypoglycemia.
6. PPN doesn’t need to be tapered off (uses more dilute
solution w/less dextrose)
69. B. Cyclic Infusion
1. TPN infused at a constant rate for only <24
hours/day (e.g. 12-14hr overnight)
2. Allows more freedom/normal daytime activity
3. Can be used to reverse fatty liver resulting from
continuous infusion
(Chronically high insulin levels may inhibit fat mobilization
fatty liver)
4. Fewer kcals may be necessary to maintain N
balance (body fat better mobilized for energy)
5. Requires higher infusion rate: not all patients can
tolerate it.
70. Why should we do monitoring?
It helps us in -
• Detection of Efficacy of therapy
• Complication detection and prevention
• Clinical condition evaluation
• Clinical outcome determination
81. Substrate intolerance
• Hypoglycemia
– Abrupt discontinuation of PN can lead to
rebound hypoglycemia
– Excessive or erroneous insulin
administration
– Pts. requiring large doses of insulin have
a greater risk for rebound hypoglycemia
82. Substrate intolerance
• TX -Initiation of a 10% dextrose
infusion
-Administer 50% dextrose
-Stopping any source of insulin
administration
83. Substrate intolerance
• Prevention
– 10% dextrose should be infused for 1 or 2 hrs
following PN discontinuation avoid a possible
rebound hypoglycemia
– Infusion 1 to 2 hrs taper down in susceptible
pts.
– Obtaining a capillary blood glucose conc. 30
min. to 1 hr after the PN solution is
discontinuation will help identify rebound
hypoglycemia
84. Substrate intolerance
• Refeeding syndrome
– Refers to the metabolic and physiological shifts
of fluid, E’lytes and minerals e.g. P, Mg, K
– Occurs in malnourished pts. during rapid
nutritional replacement
– Risk factor; starvation, alcoholism, anorexia,
morbid obesity with massive wt. loss
• Symptoms - Generalized fatique, lethargy
muscle weakness, edema, cardiac arrhythmia,
and hemolysis
85. Substrate intolerance
• Prevention;
– start low and go slow
– Gradual provision of calories over 3 to 5
days
– Thaimine replacement
– E’lytes replacement: K, Mg, P
86. Substrate intolerance
• Hyperlipidemia
– Serum triglyceride > 220 mg/dL
– Risk;neonate , very low birth wt, sepsis
– Tx – Stop or limit the lipid content in TPN
87. Substrate intolerance
• Essential fatty acid deficiency (EFAD)
– Only two fatty acids are known to be essential for humans:
alpha-linolenic acid (an omega-3 fatty acid) and linoleic
acid (an omega-6 fatty acid)
– Scaly dermatitis, alopecia, anemia, fatty liver,
hepatomegaly, thrombocytopenia
88. Substrate intolerance
• Prevention;
– 1-2% of daily energy requirement should be
derived from linoleic acid
– 0.5% of energy from linolenic acid
– Approximately; twice weekly of
- 500 ml of 10% fat emulsion
- 250 ml of 20% fat emulsion
– Alternately; 500 ml of a 20% fat emulsion
once a week
89. Substrate intolerance
• Azotemia (azot, "nitrogen" + -emia, "blood
condition") & Hyperammonemia
– Excessive protein intake
– Increased BUN
– Pts. With hepatic or renal disease are
prone to developing azotemia
– Osmotic diuresis, dehydration, coma
– Tx- decrease/stop protein in PN
90. Substrate intolerance
• Hepatobiliary complications
– Disorders of the liver and biliary system
are common in pts. receiving, long term
PN
– Types of Hepatobiliary disoders
- Steatosis
- Acalculus cholecystitis
*disorders may coexist
91. Substrate Intolerance
• Steatosis-Hepatic Fat
– Steatosis is the condition of hepatic fat
accumulation
– Predominant in adults and is generally benign
– Most pts. are asymptomic
– Steatosis is a complication of overfeeding
– Dextrose Dose related
– Excessive glycogen deposition in liver which
can progress to severe dysfunction
92. Acalculous Cholecystitis
• The absence of lipids in the proximal small
bowel prevents cholecystokinin-mediated
contraction of the gallbladder.
• Bile stasis
• Acalculous cholecystitis
96. Mucosal Atrophy
• The absence of bulk nutrients in
the bowel produces atrophy and
disruption of the bowel mucosa.
• These changes can predispose to
translocation of enteric pathogens
across the bowel mucosa and
subsequent septicemia.
• Because TPN is usually
accompanied by bowel rest, one of
the indirect complications of TPN is
bacterial translocation and sepsis of
bowel origin.
• Glutamine-supplemented TPN may
help reduce the risk of this
complication.
97. Metabolic Bone Disease
• Patients administered TPN over prolonged periods
have decreased bone mineral density (BMD)
• Patients at greatest risk are postmenopausal women,
patients with long-standing malnutrition or
malabsorption (e.g., Crohn's disease), those with
preexisting liver disease, or patients receiving
steroids
• TPN-associated deficiency states, such as calcium,
magnesium, copper, boron or silicon, have been
suggested to play a role.
• Use of bisphosphonates which prevents osteoclast-
mediated bone resorption is being tried
98. Infectious complications
• Sepsis is a serious complication in PN
• Cause;
– Catheter contamination ; PVC > Silicone
rubber, exit site infection/cellulitis
– Infections are uncommon during the first 72 hours
after insertion but then increase in incidence
– Staphylococcus epidermis,
Staphylococcus aureus, Candida
albicans, Bacteria gram negative
99. Infectious complications
• Diagnostic criteria;
– Fever >38.5 c or rise in temp. of >1 c
– Increased White blood count
– catheter site induration, erythema or
purulent discharge
– A positive blood culture
– Exclusion of other potential sources of
infection.
100. Infectious complications
• Indication to remove the catheters
1. Pts.-Septic shock
2. Persistent pyrexia with positive blood
cultures after 48 hrs. of appropriate
antibiotics
3. fungemia
101. Infectious complications
• Prevention;
– Aseptic techniques; catheters access, dressing
– Amino acid/glucose infusion giving sets and
extensions can be left 48-72 hrs. in-between
changing.
– Lipid sets should be changed every 24 hrs.
– PN solution should be changed every 24 hrs
– Nurses should be taught about the signs of
catheter related sepsis
104. How much feed should we give?
• Overfeeding is
– useless - upper limit to amounts of protein and
energy that can be used
– dangerous
• hyperglycaemia and increased infection
• uraemia
• hypercarbia and failure to wean
• hyperlipidaemia
• hepatic steatosis
105. HOME PARENTERAL NUTRITION
• Patients who are unable to eat and absorb adequate
nutrients for maintenance over the long term may be
candidates for home parenteral nutrition e.g. extensive
Crohn's disease, mesenteric infarction, or severe abdominal
trauma.
• patients must be able to master the techniques associated
with this support system, be motivated, and have adequate
social support at home.
106. HOME PARENTERAL NUTRITION
• A patient who is judged to be a candidate for home
parenteral nutrition requires an indwelling Silastic
catheter designed for long-term permanent use.
• The nutrient solutions are prepared weekly and
delivered to the patient's home.
• The patient sets up the infusion system and
attaches the catheter to the delivery tubing in the
evening for infusion over the next 12-16 h. The
intravenous nutrition is terminated by the patient
the next morning.