This document defines neonatal hypoglycemia and provides classifications and risk factors. Neonatal hypoglycemia is defined as a blood glucose level below 35 mg/dL and can be mild (25-35 mg/dL) or severe (<25 mg/dL). It may cause neurological or autonomic symptoms. Risk factors include infants of diabetic mothers, prematurity, IUGR, and genetic metabolic disorders. Diagnosis involves blood glucose testing of at-risk infants. Treatment is intravenous glucose boluses or infusion, with monitoring until stable. Prevention focuses on early feeding of high-risk infants. Prognosis depends on severity and underlying cause.
Approach to Hypoglycemia in Children.pptxJwan AlSofi
Introduction
DEFINITION
Symptoms and Signs of Hypoglycemia
Sequelae of Hypoglycemia
Hormonal Signal
Regulation of serum glucose
Disorders of Hypoglycemia
Classification of Hypoglycemia in Infants and Children
DIAGNOSIS
EMERGENCY MANAGEMENT
Approach to Hypoglycemia in Children.pptxJwan AlSofi
Introduction
DEFINITION
Symptoms and Signs of Hypoglycemia
Sequelae of Hypoglycemia
Hormonal Signal
Regulation of serum glucose
Disorders of Hypoglycemia
Classification of Hypoglycemia in Infants and Children
DIAGNOSIS
EMERGENCY MANAGEMENT
Neonatal hypoglycemia and hyperglycemia Dr vijitha ASVijitha A S
Neonatal hypoglycemia and hyperglycemia BY Dr VIJITHA A S
Hypoglycemia is most common metabolic problem seen in newborns
No universally accepted definition ; Hypoglycemia cut off variable
A presentation to give suggestions that both mother and baby can benefit from, using our Forever Living Products.
The suggestions are guidelines only. We do not make any medical claims and would always advise Doctor or Midwife consultation first.
Neonatal hypoglycemia and hyperglycemia Dr vijitha ASVijitha A S
Neonatal hypoglycemia and hyperglycemia BY Dr VIJITHA A S
Hypoglycemia is most common metabolic problem seen in newborns
No universally accepted definition ; Hypoglycemia cut off variable
A presentation to give suggestions that both mother and baby can benefit from, using our Forever Living Products.
The suggestions are guidelines only. We do not make any medical claims and would always advise Doctor or Midwife consultation first.
Powerpoint Search Engine has collection of slides related to specific topics. Write the required keyword in the search box and it fetches you the related results.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
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- Prix Galien International Awards Ceremony
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2. defination
• The normal conc. Of blood glucose level in newborn
infant is 2-7mmol/l(35-120mg/dl
• In healthy term infants, serum glucose values are
rarely less than 35 mg/dL between 1 and 3 hr of life,
less than 40 mg/dL from 3 to 24 hr, and less than 45
mg/dlafter 24 hr
• Ablood glucose concentration below
2mmol/l(35mg/dl) is defind as neonatal
hypoglycemia
3. ….cont..
• Clinically hypoglycemia may also be defined as the
presence of neurologic (lethargy, coma, apnea,
seizures) or sympathomimetic (pallor, palpitations,
diaphoresis) manifestations that respond to
glucose,
• Mild hypoglycemia defind as blood glucose conc.
b/n1.5-2mmol/l(25-35mg/dl)
• Sever hypoglycemia is defind as blood glucose conc.
Below1.5mmol/l(25mg/dl)
4. CLASSIFICATION OF HYPOGLYCEMIA IN INFANTS AND
CHILDREN
1. NEONATAL TRANSIENT HYPOGLYCEMIA- Associated
with Inadequate Substrate or Immature Enzyme
Function in Otherwise Normal Neonates
2.Transient Neonatal Hyperinsulinism Present in:
Infant of diabetic mother,Small for gestational
age,Discordant twin,Birth asphyxia
6. WHICH INFANTS HAVE AN INCREASED RISK OF
HYPOGLYCAEMIA?
1.Hyperinsulinism like
• Infants of mothers with diabetes mellitus or gestational
diabetes
• infants with severe erythroblastosis fetalis,
• insulinomas,
• familial or sporadic hyperinsulinemia,
• Beckwith syndrome (an inherited disease that is
characterized by macroglossia, umbilical hernia,
hypoglycemia, abnormal enlargement of the viscera)
• panhypopituitarism
7. …Cont…
2.Increased metabolic demands: Hypoglycemia may
develop in very immature or severely ill infants as a
result of increased metabolic needs disproportionate to
substrate stores and the calories supplied like in
• low-birthweight infants with respiratory distress
syndrome
• perinatal asphyxia
• Polycythemia
• hypothermia,
• systemic infections
• infants in heart failure with cyanotic congenital heart
disease, are at increased risk.
8. …cont…
3.IUGR/prematurity: experienced intrauterine
malnutrition due to
• reduced hepatic glycogen stores and total body fat,
• impaired gluconeogenesis
• diminished free fatty acid oxidation
• low cortisol production rates
4. Genetic causes- primary metabolic defects, such as
Galactosemia,glycogen storage disease,fructose
intolerance etc.
9. Clinical manifastation
• Hypoglycaemia may produce NO CLINiCAL SIGNS
or present with non specific signs only.
• Often an infant has some signs of brain stimul
ation and other signs of brain depression at the
same time ,
• This makes the clinical diagnosis of hypoglycaemia
very variable difficult and unreliable.
10. …Cont…
• When present, the signs and symptom of
hypoglycaemia are:
1. DEPRESSION OF BRAIN FUNCTION. The infant may be
lethargic and hypotonic, feed poorly, have a weak cry,
apnoea, cyanosis or an absent Moro reflex.
2. OVERSTIMULATION OF BRAIN FUNCTION. The infant
may be jittery with a high pitched cry, a fixed stare and
fisting, have abnormal eye movements or convulsions.
3. EXCESSIVE SWEATING. This sign may not be present
especially in preterm infants
• cardiac arrest and failure also occur
11. Diagnosis of hyperglycemia
• The clinical diagnosis is difficult and often missed
.Therefore, it is essential that all infants at risk of
hypoglycaemia , and infants with clinical signs that
may be caused by hypoglycaemia, be screened with
reagent strips .
• Diagnosis of hypoglycemia by reagent strips should
be confirmed with alaboratory blood glucose
measurement.
12. Prevention of hypoglycemia
• The following steps must b e taken to prevent
hypoglycaemia:
1. Identify all infants at high risk of developing
hypoglycaemia.
2. Monitor the blood glucose concentration of these
infants with reagent strips so that afalling blood glucose
can be detected before hypoglycaemic levels are
reached.
3. Feed all infants as soon as possible after delivery,
espe cially preterm, underweight for gestational age
and wasted infants, as well as infants of diabetic
women.
13. …cont…
4. Whenever possible, milk feeds should b e given.
Both clear feeds orally and oral dextrose feeds
shouldn’t be used in newborn infants as they are
low in energy and may result in hypoglycaemia .
5. If milk feeds can not be given, then an intravenous
infusion of Neonatalyte should be comm
enced.Neonatalyte contains 10 % glucose.
6. Prevent hypothermia.
14. treatment
• When symptoms other than seizures are present, an
intravenous bolus of 200 mg/kg (2 mL/kg) of 10%
glucose is effective in elevating the blood glucose
concentration.
• In the presence of convulsions, 4 mL/kg of 10% glucose
as a bolus injection is indicated
• After initial therapy, a glucose infusion should be given
at 8 mg/kg/min
• If hypoglycemia recurs, the infusion rate and
concentration should be increased until 15-20% glucose
is used
15. …cont…
• if the infusion is inadquat to eleminate the
symptoms hyperinsulinemia is probably present
and diazoxide should be administered
• If the diazoxide is unsuccessful, octreotide may be
useful
• many infants with severe persistent
hyperinsulinemic hypoglycemia undergo subtotal
pancreatectomy
16. monitoring
• The serum glucose level should be measured every
2 hr after initiating therapy until several
determinations are above 40 mg/dL.
• Subsequently, levels should be measured every 4-6
hr and the treatment gradually reduced and finally
discontinued when the serum glucose value has
been in the normal range and the baby
asymptomatic for 24-48 hr.
• Treatment is usually necessary for a few days to a
week, rarely for several wks
17. prognosis
• The prognosis is good in asymptomatic patients
with hypoglycemia of short duration
• Symptomatic infants with hypoglycemia,
particularly
- low-birthweight infants,
-those with persistent hyperinsulinemic
hypoglycemia,
- and infants of diabetic mothers, have a poorer
prognosis for subsequent normal intellectual
development than asymptomatic infants do.
19. introduction
• Disorders of fluid and electrolyte balance are
among the commonest derangements encountered
in preterm and critically sick neonates
• The aim of fluid and electrolyte therapy is to ensure
a smooth transition from the aquatic in-utero
environment to the dry ex- utero environment
20. Changes in body water and solute after parturition
• After birth, there is efflux of fluid from the
intracellular fluid (ICF) to the extracellular fluid
(ECF) compartment.
• This increase in the ECF compartment floods the
neonatal kidneys eventually resulting in a salt and
water diuresis by 48-72 hours.
• Loss of this excess ECW results in physiological
weight loss in the first week of life.
21. …cont…
• Since the ECW compartment is larger in more
preterm neonates, the weight loss is greater in
preterm neonates.
• Failure to loose this ECF may be associated with
morbidities like patent ductus arteriosus (PDA),
necrotizing enterocolitis (NEC) and chronic lung
disease (CLD) in preterm neonates
22. Renal function
• Kidneys in the neonate have a limited capacity to
excrete both concentrated and dilute urine
• the neonatal kidney has a limited capacity both to
excrete and to conserve sodium.
• Therefore, sodium supplementation should be
started after ensuring initial diuresis(48-72hrs)
23. …cont…
• Sodium requirement ranges from 3-5 mEq/kg/day in
preterm neonates after the first week of life.
• Failure to provide this amount of sodium may be
associated with poor weight gain
• Very low birth weight infants on exclusive breast
feeding may need sodium supplementation in addition
to breast milk until 32-34 weeks corrected age
24. Fluid losses
1.sensible loss-kidneys and gastro-intestinal system
2.Insensible loss-evaporation from the skin(70%) and
respiratory tract(30%).
• The emphasis in fluid and electrolyte therapy
should be on prevention of excessive IWL rather
than replacement of increased IWL
25. Managment
Management of fluid in newborn depends on
gestational age and birth weight
1.Day 1: Term babies and babies with birth weight >
1500 grams. total fluid therapy would be 60
ml/kg/day of 10% dextrose
2.Day 1: Preterm baby with birth weight 1000-1500
grams.
26. …cont…
• the fluid requirement will be higher due to
increased IWL and increased weight loss .
• using caps, socks and plastic barriers under the
radiant warmer reduce the IWL
• Using this method we have found 80 ml/kg/day of
10% dextrose to be adequate on day 1 of life
27. …cont…
3. Day 2 -7: Term babies and babies with birth weight
>1500 grams.
• As the infant grows and receives enteral milk feeds,
the solute load presented to the kidneys increases
and the infant requires more fluid to excrete the
solute load.
• Water is also required for fecal losses and for
growth purposes.
28. …cont…
• The fluid requirements increase by 15-20 ml/kg/day
until a maximum of 150 ml/kg/day
• Sodium and potassium should be added after 48 h
of age and glucose infusion should be maintained at
4-6 mg/kg/min
29. …cont…
4.Day 2 –7: Preterm babies with birth weight 1000-
1500 grams
• As the skin matures in a preterm baby, the IWL
progressively decreases and becomes similar to
aterm baby by the end of the first week.
• Plastic barriers, caps and socks are used throughout
the first week in order to reduce IWL from the
immature skin.
30. …cont…
• Fluids need to be increased at 10-15 ml/kg/day
until a maximum of 150 ml/kg/day.
• Sodium and potassium should be added after 48
hours and glucose infusion should be maintained at
4-6 mg/kg/min
5.>Day 7: Term babies and babies with birth weight
>1500 grams Fluids should be given at 150-160
ml/kg/day
31. …cont…
6.Day 7: Preterm babies with birth weight 1000-1500
grams Fluids should be given at 150-160 ml/kg/day
• and sodium supplementation at 3-5 mEq/kg should
continue till 32-34 weeks corrected gestational age
32. Monitoring of fluid and electrolyte status
1.Body weight
2.Clinical examination-for any sign of dehydration.
• Infants with 10% (100 ml/kg) dehydration may
have sunken eyes and fontanel, cold and clammy
skin, poor skin turgor and oliguria
• Infants with 15% (150ml/kg) or more dehydration
would have signs of shock (hypotension,
tachycardia and weak pulses)
34. starting electrolytes in fluid therapy
• Sodium and potassium should be started in the IV
fluids after 48 hours, each in a dose of 2-3
meq/kg/day.
• Calcium may be used in a dose of 4 ml/kg/day (40
mg/kg/day) of calcium gluconate for the first 3 days
in certain high-risk situations
35. Referance
1. Nelson Textbook of Pediatrics (19th Edition)
2. Fluid and electrolyte management in term
and preterm neonates(AIIMS- NICU protocols
2008)
3.Internat
Editor's Notes
The physiological range for urine osmolality in neonates varies from a lower limit of 50 mmol/L to an upper limit of 600 mmol/L in preterms and 800 mmol/L in term infants2. An acceptable osmolality range of 300-400 mmol/L would correspond to a daily urine output of 2-3 ml/kg/hr.