Malnutrition is common in critically ill ICU patients and can lead to organ dysfunction and poor outcomes. Enteral nutrition is preferred over parenteral nutrition due to lower risks of infection and other complications. Early initiation of enteral feeding within 48 hours for stable patients is recommended. Formulas are tailored to patient needs and disease states. Monitoring for complications like hyperglycemia, liver issues, and electrolyte imbalances is important during nutrition support. Overall goals are to prevent further malnutrition while avoiding overfeeding and its risks.
In the changing scenario of pharmacy practice in India, for successful practice of
Hospital Pharmacy, the students are required to learn various skills like drug distribution,
drug dispensing, manufacturing of parenteral preparations, drug information, patient
counselling, and therapeutic drug monitoring for improved patient care
In the changing scenario of pharmacy practice in India, for successful practice of
Hospital Pharmacy, the students are required to learn various skills like drug distribution,
drug dispensing, manufacturing of parenteral preparations, drug information, patient
counselling, and therapeutic drug monitoring for improved patient care
Appropriate and safe assessment and administration of fuid therapy and nutritional support is of key importance in good surgical practice. It is imperative that the preoperative nutritional state of the patient and the impact of any surgical intervention are taken into account when considering nutritional requirements and the mode of nutrient delivery.
comprehensive presentation on 2D echo use in ICu set up. helpful in finding causes of shock and also in monitoring of fluid status in critically ill patients.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
1. NUTRITION IN ICU
Dr. Nisheeth M. Patel
M. D (Medicine), FCCCM
Consultant Physician & Intensivist
2. Introduction:
• Malnutrition is a disorder in body composition in
which inadequate macronutrient (protein,
carbohydrate, and fat) or micronutrient (vitamins,
minerals, and trace elements) intake results in
decreased body mass, reduced organ mass, and most
important, decreased organ function.
• Malnutrition is most frequently associated with a
risk for immune dysfunction-related infection,
wound healing/fascial dehiscence, and breakdown
of surgical anastomoses, it can affect virtually all
organ systems when severe.
3. Effects of Malnutrition
• Skeletal muscle wasting
• Decreased myocardial mass
• Diastolic cardiac dysfunction
• Decreased sensitivity to inotropic agent
• Respiratory insufficiency
• Need for prolonged mechanical ventilation
• Renal cortical atrophy
• loss of gastrointestinal absorptive/barrier
functions.
4. • Malnutrition becomes particularly important in
critically ill patients, in whom the combination
of bed rest and catabolic illnesses
▫ Sepsis
▫ Multiple trauma
▫ Burns, pancreatitis
▫ Acute respiratory distress syndrome (ARDS)
• Hasten the malnutrition, loss of lean body mass,
and organ system dysfunction.
5. Starvation versus Stress Metabolism
• Starvation is a clinical situation that develops
whenever nutrient supply is inadequate to meet
nutrient demand.
• Stress metabolism is a generalized response
whereby energy and substrate are mobilized to
support inflammation, immune function, and
tissue repair. It occurs in response to a variety of
stimuli such as sepsis, multiple trauma, burns,
pancreatitis, bone marrow transplantation, and
major surgery.
7. Carbohydrate Metabolism in Critical
Illness:
• Carbohydrate metabolism in critical illness is
characterized clinically by hyperglycemia, often
described as being due to “insulin resistance”
based on increased blood glucose levels in the
presence of high circulating levels of insulin.
• Cellular glucose uptake and oxidation in the
critically ill are increased
• Hyperglycemia is associated with increased
glucose production, decreased insulin-mediated
glucose uptake, and increased non–insulin-
mediated glucose uptake.
8. Fat Metabolism in Critical Illness
• Marked increase in lipolytic activity in adipose
tissue as a result of catecholamine-mediated
stimulation of β2-receptors; cytokines may also
participate in this process
• Increased oxidation of fatty acids of all chain lengths
and decreased plasma levels of medium- and long-
chain essential fatty acids relative to the quantities
of oleic acid
• Hypertriglyceridemia is common in critically ill
patients results from the combination of increased
hepatic triglyceride production and decreased
clearance
• Ketonemia is common in starvation, whereas
ketogenesis is decreased in stress metabolism.
9. Protein Metabolism in Critical Illness:
• Protein synthesis is increased in the stressed state
relative to that seen in starvation.
• Protein breakdown is markedly increased in
comparison to the synthetic rate, thereby resulting
in net protein catabolism and a rapid decrease in
lean body mass
• Amino acids mobilized from skeletal muscle are
redistributed to other areas of the body to support
immune function, wound healing, and tissue repair,
as well as for the hepatic synthesis of acute-phase
proteins, presumably in an attempt to enhance
survival.
10. Indications for Nutrition Support
• Nutrition support should be considered once
hemorrhage has been controlled, devitalized tissue
débrided, fractures stabilized, and the patient
resuscitated from shock.
• There are suggestions in the literature that early
enteral feeding, within 24 to 72 hours of admission,
may help decrease post burn and post injury hyper
metabolism and reduce infectious complications.
• Initiated in any patient who is malnourished on
admission to the intensive care unit (ICU), for any
patient who is likely to become malnourished during
a long and complicated ICU stay, and for any patient
who has not eaten for 5 to 7 days.
11. Goals of Nutrition Support
• The goals of nutrition support in a critically ill
patient are to minimize the effects of starvation to
provide appropriate doses of macronutrients and
micronutrients, to minimize complications of
nutrition support, and to improve outcomes.
• To provide sufficient calories to meet the energy
requirements of the hyper metabolic state while
avoiding the complications associated with
overfeeding.
• Provide sufficient protein to attain nitrogen balance
or minimize the nitrogen deficit, provide electrolytes
to maintain normal levels while taking into account
excessive losses or impaired excretion, and provide
appropriate vitamins and trace elements with
consideration of disease-specific requirements.
12. BEE, basal energy expenditure; IDC, indirect calorimetry; RDA, recommended
dietary allowance; REE, resting energy expenditure.
Nutrient General Recommendation
Total calories
25-30 kcal/kg/day
OR
BEE × 1.2-2.0
OR
REE by IDC
Glucose
5 g/kg/day
OR
20 kcal/kg/day
OR
60-70% of calories
Fat
15-40% of calories
OR
Less than 1 g/kg/day
Amino acids or protein 1.2-2.0 g/kg/day
Trace elements and vitamins RDA
Electrolytes Maintain normal levels
13. Route and Timing of Administration
• Nutrition support can be delivered
▫ Enterally (via the gastrointestinal tract)
▫ Parenterally (via the intravenous route)
14. Total Parental Nutrition
Advantages Disadvantages
• Does not require an intact or
functioning gastrointestinal
tract
• Convenient to use
• Prescribed nutrients will be
administered
• These nutrients will appear in
the bloodstream.
• Cost
• Procedure (central venous
catheter)-related
complications
• Increased likelihood of
metabolic complications,
including hyperglycemia
• Increased risk of infectious
complications.
15. Enteral Nutrition:
Advantages Disadvantages
• Less expensive
• More physiologic
• Less metabolic complications
such as electrolyte
abnormalities and
hyperglycemia
• Stimulates gut function
• Preserves mucosal integrity
and barrier function
• Requirement for an intact and
functioning gastrointestinal
tract
• Procedure (feeding tube
placement)-related
complications
• Pulmonary aspiration
• Malabsorption
• Feeding intolerance (pain,
vomiting, bloating, diarrhea)
• Inability to deliver the entire
nutrient prescription.
16. • Less costly and associated with fewer metabolic
complications and a lower incidence of infection,
the enteral route continues to be the
recommended route for nutrition support.
• Some percentage of critically ill patients, enteral
nutrition is either contraindicated or not
tolerated, and parental nutrition remains a
viable option
• In TPN overfeeding should be avoided and
hyperglycemia should be controlled.
17. Timing for Initiating feeding
• Enteral nutrition started early (within 24 to 72
hours of admission ) is associated with less gut
permeability, release of inflammatory cytokines, and
reduced systemic endotoxemia.
• In patients who are hemodynamically stable, it is
recommended that enteral nutrition be started
within 48 hours of admission
• In a recent RCT, it had been observed that Early
parenteral nutrition, even when used to supplement
enteral nutrition, may be harmful and should be
avoided unless the patient is chronically
malnourished.
18. Types of nutrition formulas
• Parenteral nutrition is most commonly
administered as a three-in-one solution of dextrose,
lipid, and amino acids.
• TPN order forms typically allow the physician to
order “standard” or custom solutions, fluid-
restricted solutions, and in some cases, disease-
specific solutions such as renal failure or hepatic
failure solutions.
• Enteral formulas are usually premixed with a fixed
nonprotein calorie-to-nitrogen ratio, and the needs
of a specific patient are generally met by changing
the formula.
• Protein and carbohydrate supplements can be added
at the bedside to alter premixed formulas.
19. • High-protein formulas contain more than 45 g
protein per 1000 kcal and are designed for
patients with increased protein needs, such as
patients with catabolic illness.
• Calorie-dense formulas are designed for patients
in whom fluid restriction is required. They are
generally relatively low in protein and not ideal
for a stressed patient.
20. Organ-Specific Enteral Formulas
• Pulmonary failure formulas:
• acute respiratory failure associated with chronic
lung disease.
• At least 50% of calories as fat:
▫ Reduce CO2 production
▫ Decrease the work of breathing relative to high-
carbohydrate formulas.
• Avoiding overfeeding is more important in
reducing ventilatory demand.
21. Hepatic failure formulas
• Contain high concentrations of branched-chain
amino acids and reduced concentrations of
aromatic amino acids.
• Although these solutions have been shown to
correct the abnormal amino acid profile
characteristic of patients with liver failure.
• Hepatic failure formulas should be reserved for
the rare encephalopathic patient who is
refractory to lactulose and luminal antibiotics.
22. Renal Failure Formulas
• Renal failure formulas have reduced
concentrations of electrolytes and decreased
protein content to minimize nitrogenous waste
in patients with renal failure.
• Patients with acute renal failure frequently have
associated catabolic illness and as a result need
more protein rather than less.
• Although these formulas may be useful in
patients with electrolyte abnormalities not yet
being dialyzed.
• Inappropriate for patients with catabolic illness
who are undergoing dialysis and particularly
CRRT.
23. • Immunomodulating enteral formulas are
supplemented with various combinations of specific
nutrients, arginine, ω-3 polyunsaturated fatty acids,
nucleotides, glutamine, and antioxidants aimed at
improving immune function and reducing
inflammation in critically ill patients.
• Guidelines for the PANST in the Adult Critically Ill
Patient, published jointly by the SSCCM and ASPEN
recommend the use of an immunomodulating
enteral formula supplemented with fish oil and
antioxidants for patients with acute lung
injury/ARDS.
• Further, these guidelines recommend enteral
formulas supplemented with arginine for patients
with major surgery, burns, and trauma, but
emphasize that such formulas may be harmful in
severe sepsis.
24. Nutrition Assessment
• Anthropometric measurements such as triceps
skinfold thickness (SFT), midarm circumference
(MAC), and arm muscle area, which is derived from
SFT and MAC, can be used to estimate fat mass and
lean body mass.
• These measurements are not practical for
nutritional monitoring in a recumbent, critically ill
patient.
• Visceral protein levels have long been used in
nutritional assessment and monitoring and can be
useful in the appropriate clinical setting.
25. • Albumin, Transferrin, retinol binding protein,
transthyretin can be used for assessment for
nutritional status.
• However, visceral protein levels are affected by a
variety of non-nutritional factors, they are not
recommended for the monitoring of nutritional
status in critically ill patients.
• Nitrogen balance is the nutritional parameter
most consistently associated with improved
outcomes, and nitrogen balance studies are used
routinely to monitor nutrition support. Ideally,
positive nitrogen balance is the goal.
26. • Numerous techniques for assessment and
monitoring of energy balance
▫ Continuous whole-body calorimetry
▫ Doubly labeled water technique
▫ Nuclear magnetic resonance spectroscopy
using 31P
• No method is ideal.
• Though potentially useful, these methods are
either cumbersome, expensive, or impractical for
use in critically ill patients.
• Overall, assessing the nutrition in critically ill
patients is challenging and for accurate
methods, trials are still going on.
27. Complications of Enteral Nutrition
Support
• Mechanical and technical complications of
enteral nutrition include:
▫ Feeding tube misplacement
▫ Gastrointestinal perforation
▫ Sinusitis
▫ Otitis media
▫ Ulceration of the nasal septum
▫ Obstruction of the feeding tube
28. • Aspiration pneumonia is the major infectious
complication of enteral nutrition.
• Bolus feeding carries a higher risk of aspiration
than continuous feeding does.
• Gastrointestinal complications:
▫ Abdominal distention
▫ Nausea
▫ Vomiting
▫ Diarrhea
▫ Constipation
29. Complications of Parenteral Nutrition
Support
• Mechanical and technical complications are related
to central venous catheter placement and include
pneumothorax, arterial injury, hemothorax,
hydrothorax, cardiac arrhythmia, and cardiac
perforation with tamponade.
• Catheter infection and catheter-associated
bloodstream infection are the major infectious
complications of parenteral nutrition.
• Most common infecting organisms are coagulase-
negative staphylococci, Staphylococcus aureus,
and Candida species
30. Metabolic Complications
• Common metabolic complications of nutrition
support include
▫ Hyperglycemia
▫ Hepatobiliary complications
▫ Disturbances in water and electrolyte balance
▫ Acid-base abnormalities.
• Though more common in patients receiving
parenteral nutrition, metabolic complications
can occur with either form of nutrition support.
31. Hyperglycemia
• Frequently in critically ill patients receiving
nutrition support
• Most common in diabetic patients and those with
catabolic illness.
• Complications related to hyperglycemia include:
▫ Infection
▫ Hyperosmolarity
▫ Osmotic diuresis.
• The first step in the control of blood sugar is
avoidance of overfeeding
• Currently, most practitioners aim for blood glucose
levels below 150 to 180 mg/dL.
32. Hepatobiliary complications
• Hepatic steatosis (Intrahepatic and extrahepatic
cholestasis)
• Hepatic steatosis may develop after 7 to 21 days of
parenteral nutrition and is characterized initially by
elevated transaminases.
• Usually asymptomatic, fatty infiltration can, in severe
cases, be accompanied by hepatomegaly and right upper
quadrant abdominal pain.
• Cholestasis occurs later in the course of parenteral
nutrition and is characterized by elevations in bilirubin
and alkaline phosphatase.
• Cholelithiasis has been linked to long-term TPN use.
• Management of hepatobiliary complications is aimed at
prevention. Overfeeding should be avoided.
33. Electrolyte disturbance & Acid Base
disorder
• Hypernatremia or hyponatremia can be managed by
increasing or decreasing free water.
• Refeeding syndrome, serum levels of these
intracellular electrolytes fall precipitously, with
hypophosphatemia resulting in hemolysis,
rhabdomyolysis, and heart failure with hypokalemia and
hypomagnesemia leading to cardiac arrhythmias.
• Serum levels of intracellular electrolytes should be
corrected before and, in particular, 24 hours after the
institution of nutrition support.
• Hyperkalemia and hypomagnesemia may lead to
weakness and cardiac arrhythmia
34. • Hyperphosphatemia may result in hypotension,
hypocalcemia, and metastatic calcification.
• Hyperphosphatemia is often treated with oral
phosphate binders such as calcium carbonate.
• Metabolic acidosis related to nutrition support is
most commonly due to excess chloride
administration and resultant renal bicarbonate
losses.
• Also occur as a result of thiamine deficiency with
resultant lactic acidosis.