Lecture given during Port said fifth neonatology conference, 23-24 October 2014 by Dr.Osama Arafa Abd EL Hameed M. B.,B.CH - M.Sc Pediatrics - Ph. D. Consultant Pediatrician & Neonatologist Head of Pediatrics Department - Port-Fouad Hospital
This presentation is aimed at giving the basic information of a neonate classification on basis of gestational age and the birth weight. Prematurity has been discussed in details. I have also included the growth charts that can be used for growth monitoring in term as well as preterm babies.
** This presentation is available in a video lecture format at my youtube channel - NeonatoHub. Do watch it for further understanding of the topic & subscribe to the channel.
History of pediatric nursing from prehistoric time to modern era. Why a pediatric nurse must know about the history of Pediatrics? Father of Pediatrics.
This presentation is aimed at giving the basic information of a neonate classification on basis of gestational age and the birth weight. Prematurity has been discussed in details. I have also included the growth charts that can be used for growth monitoring in term as well as preterm babies.
** This presentation is available in a video lecture format at my youtube channel - NeonatoHub. Do watch it for further understanding of the topic & subscribe to the channel.
History of pediatric nursing from prehistoric time to modern era. Why a pediatric nurse must know about the history of Pediatrics? Father of Pediatrics.
A 100 years ago, when neonatal intensive care units (NICUs) started to be well established, the race never stopped trying to add new regimens to improve neonatal survival. On the other hand, long term sequelae of medications used at NICUs were usually not sufficiently studied and left mostly unnoticed for many years by neonatologists. Here we are trying to understand & & shed the light on some of these sequelae in a trial avoid those sequelae while working on NICU candidates.
Lecture given at the 6th Conference for Nile Basin Pediatrics 2-5 December 2015, Hurgada, Egypt
One of lectures presented in our Port said fifth neonatology conference 23-24 October 2014, presented by prof Olfat Fawzy, M.D, M.Sc.,Professor of Endocrinology Al Azhar university
Trophic feeding, by dr Amal Ahmed Khalil ,Port Said University, mohamed osama hussein
Trophic feeding is the practice of feeding small volume of enteral feeds in order to stimulate the development of the immature gastrointestinal tract of the preterm infant. This practice has also been termed as minimal enteral nutrition (MEN).
Basic concepts in neonatal ventilation - Safe ventilation of neonatemohamed osama hussein
Lecture by by dr Muhammad Ezzat Abdel-Shafy MB.BCh, M.Sc Pediatrics Neonatology Sp. , Benha Children Hospital, provided during our Doctors neonatology workshop, 20th of January 2017
By Prof. ATEF DONIA Professor of Pediatrics Al Azhar University
The role of reactive oxygen species (ROS) in pathogenesis of common disorders of the preterm infant.
The unique susceptibility of premature infants to oxidative stress. Potential for therapeutic interventions using enzymatic and/or non-enzymatic antioxidants
Definition of High-risk Neonate: Any baby exposed to any condition that make the survival rate of the neonate at danger.
Factors that contribute to have a High-risk Neonate:
A) High-risk pregnancies: e.g.: Toxemias
B) Medical illness of the mother: e.g.: Diabetes Mellitus
C) Complications of labor: e.g.: Premature Rupture Of Membrane (PROM), Obstructed labor, or Caesarian Section (C.S).D) Neonatal factors: e.g.: Neonatal asphyxia
INTRODUCTION
A newborn, regardless of gestational age or birth weight, who has a greater than average chance of morbidity or mortality because of conditions or circumstances superimposed on the normal course of events associated with birth and the adjustment to extra uterine existence.
FACTORS – TO DEFINE HIGH RISK NEWBORN
DEMOGRAPHIC SOCIAL FACTORS:
Maternal age <16 or >40, unmarried, physical stress, socio-economic status.
PAST MEDICAL HISTORY:
Diabetes Mellitus, genetic disorder, hypertension
PREVIOUS PREGNANCY:
Intrauterine death, neonatal death, IUGR, congenital malformations.
PRESENT PREGNANCY:
Vaginal bleeding, PROM, multiple gestation, pre-eclampsia, abnormal USG findings.
LABOR: AND DELIVERY:
Obstructed labor, fetal distress, forceps delivery, meconium stained liquor.
NEONATE:
Birth weight <2000 or >4000, gestation <37 or >42.
DEFINITIONS
Low birth weight: Live born baby weighing 2500 gram or less at birth. (VLBW: <1500 gm, ELBW: 000 gm).
Preterm: When the infant is born before term i.e. before 38 weeks of gestation.
Premature: When the baby is born before 37 weeks of gestation.
Full term: When the infant is born between 38-42 weeks of gestation.
Post term: When the baby is born after 42 weeks of gestation.
HYPOTHERMIA
DEFINITION
It is a condition characterized by lowering of body temperature than 36℃.
TYPES OF HYPOTHERMIA
It can be classified according to causes and according to severity.
CLASSIFICATION BASED ON CAUSE:
Primary Hypothermia:
Seen immediately after delivery.
Normal term baby delivered into a warm environment may drop its rectal temperature by 1 – 2℃ shortly after birth and may not achieve a normal stable body temperature until the age of 4 – 8 hours.
In low birth weight baby, the decrease of body temperature may be much greater and more rapid unless special precautions are taken immediately after birth. (Loss at least 0.25℃./min).
Secondary Hypothermia:
This occurs due to factors other than those immediately associated with delivery.
Important contributory factors are: e.g. acute infection especially septicaemia.
CLASSIFICATION BASED ON SEVERITY:
According to severity:
Mild Hypothermia: <36℃.
Moderate Hypothermia: <35.5℃.
Severe Hypothermia: <35℃.
CLINICAL FEATURES
Decrease in body temperature measurement.
Cold skin on trunk and extremities.
Poor feeding in the form of poor suckling
Shallow respiration
Cyanosis
Decrease activity, e.g. weak cry.
FOUR MODALITIES OF HEAT LOSS IN NEONATES
Evaporation: Heat loss that resulted form expenditure of internal thermal energy to convert liquid on an exposed surface to gases, e.g. amniotic fluid, sweat.
Prevention: Carefully dry the neonates after delivery or after bathing.
Radiation: It occurred from body surface to relatively distant objects that are cooler than skin temperature.
Conduction: Heat loss occurred from direct contact between body surface and cooler solid object.
Prevention: Keep the baby out of drafts and close end of heat shield in in
Neonatal and Pediatric Critical Care - Mostafa QalavandWang Lang
Neonatal and pediatric critical care is markedly different from adult critical care because of the physiologic and hemodynamic dissimilarities between immature and adult animals. Clinicians are often wary of treating these patients because of their small size and the presumptive limitations in diagnostic and therapeutic interventions. Nevertheless, we have the ability to treat these young animals aggressively. In doing so, however, we must be cognizant of the unique distinctions among pediatric patients with regard to normal physiologic variables that affect physical examination findings and diagnostic test results.
By dr Rabab Hashem, MRCPCH, pediatrician at El Nasr hospital Port said.
Cranial sonography is the most widely used neuroimaging procedure in premature infants. US helps in assessing the neurologic status of the child, since clinical examination and symptoms are often nonspecific. It gives information about immediate and long term prognosis.
jaundice in neonate, by Dr Nagwa Rizk, pediatric department, Nursing college, Port said University, Port said. Presented in the NICU nursing workshop, organized by Nursing syndicate in Suez canal & Sinai in cooperation with Port said university college of nursing & Port said neonatology society, December,2014 Port said
Care of neonate, by Dr Mona Abo zid, pediatric department Nursing college, Port said University, Port said. Presented in the NICU nursing workshop, organized by Nursing syndicate in Suez canal & Sinai in cooperation with Port said university college of nursing & Port said neonatology society, December,2014 Port said
Neonatal mechanical ventilation by dr Osama Hussein, president of Port said neonatology society. Presented in the NICU nursing workshop, organized by Nursing syndicate in Suez canal & Sinai in cooperation with Port said university college of nursing & Port said neonatology society, December,2014 Port said
Neonatal resuscitation, by Dr Osama Hussein, president of Port said neonatology society. Presented in the NICU nursing workshop, organized by Nursing syndicate in Suez canal & Sinai in cooperation with Port said university college of nursing & Port said neonatology society, December,2014 Port said
Normal newborn needs, by Dr Rehab Hany, pediatric department, Nursing college, Port said University, Port said. Presented in the NICU nursing workshop, organized by Nursing syndicate in Suez canal & Sinai in cooperation with Port said university college of nursing & Port said neonatology society, December,2014 Port said
Normal newborn care, by Dr Amal Khalil, Dean of Nursing college, Port said University, Port said. Presented in the NICU nursing workshop, organized by Nursing syndicate in Suez canal & Sinai in cooperation with Port said university college of nursing & Port said neonatology society, December,2014 Port said
One of lectures presented in our Port said fifth neonatology conference, 23-24 October 2014 by Prof Mohamed El Sawy, Prof in Pediatric department , faculty of medicine, Ain Shams university
One of lectures given during our Port said fifth neonatology conference, 23-24 October 2014 given by dr Dr El Sayed Khalaf MD Pediatrics,Consultant Pediatric and Neonatology
Hypoxic ischemic insult, by prof Ayman Galhom, ass prof neurosurgery, Suez ca...mohamed osama hussein
A lecture given by dr Ayman Galhom, assistant professor neurosurgery, Suez canal university, during Port said fourth neonatology conference, at 24-25 October, 2013. This lecture was a discussion of the pathophysiology & management of hypoxic ischaemic insult to an infant in PICU
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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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
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.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
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
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.
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
1. High-Risk Neonate
&
neurodevlopmental outcome
By
Dr.Osama Arafa Abd EL Hameed
M. B.,B.CH - M.Sc Pediatrics - Ph. D.
Consultant
Pediatrician & Neonatologist
Head of Pediatrics Department - Port-
Fouad Hospital
2.
3.
4. GOALS
• Perinatal prevention
• Resuscitation and stabilization
• Evaluate and manage
• Monitoring and therapeutic
modalities
• Family centered care
5. Predisposing factors
• Pregnancy between the age of 15-19yrs
• Elderly women
• Wrong dates
• Multiple pregnancy
• Fetal anomalies
• Hereditary
6. Introduction:
Definition of High-risk Neonate:
Any baby exposed to any condition that
make the survival rate of the neonate at
danger.
Factors that contribute to have a High-risk
Neonate:
A) High-risk pregnancies: e.g.: Toxemias
B) Medical illness of the mother: e.g.:
Diabetes Mellitus
7. C) Complications of labor: e.g.:
Premature Rupture Of Membrane (PROM),
Obstructed labor, or Caesarian Section (C.S).
D) Neonatal factors: e.g.: Neonatal
asphyxia
8. Classification of High Risk
Newborns
• Gestational Age
– Preterm
– (Late Preterm)
– Term
– Postterm
• Gestational Age &
Birth Weight
– SGA
– AGA
– LGA
9. Some Definitions:
- Low Birth Weight Infant:
Is any live born baby weighing 2500 gram or
less at birth. (VLBW: <1500 gm, ELBW:<1000
gm).
- Preterm:
When the infant is born before term. i.e.:
before 38 weeks of gestation.
- Premature:
When the infant is born before 37weeks of
gestation.
10. - Full term:
When the infant is born
between 38 – 42 weeks of gestation.
- Post term:
When the infant is born
after 42 weeks of gestation.
11. Identification of some High-risk
Neonates:
The previous conditions often will result in:
Premature birth, Low birth weight infants, or
infants suffering from: Hypothermia,
Hyperthermia, Hypoglycemia, Infant of Diabetic
Mother (IDM), Neonatal Sepsis,
Hyperbilirubinemia, and Respiratory Distress
Syndrome (RDS).
18. Definition:
It is a condition characterized by
lowering of body temperature than 36°C.
Types of Hypothermia:
It could be classified according to:
Causes and according to Severity.
19. I) According to Causes:
1- Primary Hypothermia: (immediately
associated with delivery)
In which the normal term infant delivered into a
warm environment may drop its rectal temperature
by 1 – 2°C shortly after birth and may not achieve a
normal stable body temperature until the age of 4 – 8
hours.
In low birth weight infants, the decrease of body
temperature may be much greater and more rapid
unless special precautions are taken immediately
after birth. (loss at least 0.25 °C/ min.) (careful
dryness).
20. Situations which contribute to develop
Primary Hypothermia:
e.g.: Low birth weight infants.
2- Secondary Hypothermia:
This occurs due to factors other than
those immediately associated with
delivery.
Important contributory factors are:
e.g.: Acute infection especially
Septicemia.
21. II) According to Severity:
(1) Mild Hypothermia:
When the
infant’s body temperature is less than 36°C.
(2) Moderate Hypothermia:
When
the infant’s body temperature is less than
35.5°C.
(3) Severe Hypothermia:
When the
infant’s body temperature is less than 35°C.
22. *) Clinical Picture:
1- Decrease in body temperature
measurement.
2- Cold skin on trunk and extremities.
3- Poor feeding in the form of poor
suckling.
4- Shallow respiration.
5- Cyanosis.
6- Decrease activity, e.g.: Weak crying.
23. The Four modalities by which the
infant lost his/ her body temperature:
1- Evaporation:
Heat loss that resulted from
expenditure of internal thermal energy to
convert liquid on an exposed surface to
gases, e.g.: amniotic fluid, sweat.
Prevention:
Carefully dry the infant
after delivery or after bathing.
24. 2- Conduction:
Heat loss occurred from
direct contact between body surface
and cooler solid object.
Prevention:
Warm all objects before
the infant comes into contact with
them.
25. 3- Convection:
Heat loss is resulted from
exposure of an infant to direct source of
air draft.
Prevention:
· Keep infant out of drafts.
· Close one end of heat shield in
incubator to reduce velocity of air.
26. 4- Radiation:
It occurred from body
surface to relatively distant objects that
are cooler than skin temperature.
29. *) General management:
1- Infant should be warmed quickly by wrapping
in a warm towel.
2- Uses extra clothes or blankets to keep the
baby warm.
3- If the infant is in incubator, increase the
incubator’s temperature.
4- Use hot water bottle (its temperature 50 °C).
5- Food given or even intravenous solution
should be warm.
6- Avoid exposure to direct source of air drafts.
7- Check body temperature frequently.
8- Give antibiotic if infection is present.
31. Definition:
It is a condition
characterized by an elevation in body
temperature more than 38°C.
Causes:
1- Disturbance in Heat Regulating Center
caused by intracranial hemorrhage, or
intracranial edema.
2- Incubator temperature is set too high.
3- Dehydrating fever
32. *) Management :
1) Undress the infant. If at home; keep light
cloths, cover that containing light sheet, Or only a
diaper if the infant is inside an incubator.
2) Reduction of incubator temperature.
3) Provide Tepid sponge bath.
4) If available; fill the water mattress with tape
water, and keep it in contact with the infant’s skin.
5) Increase fluid intake in the form of 5cc of
Glucose 5% between feeds to prevent dehydration.
34. Ideally, neonatal hypoglycemia would be defined as the
blood glucose concentration at which intervention
should be initiated to avoid significant morbidity,
especially neurologic sequelae.
However, this definition remains elusive because the
blood glucose level and duration of hypoglycemia
associated with poor neurodevelopmental
outcome has not been established.
Neonatal hypoglycemia, defined as a plasma glucose
level of less than 30 mg/dL (1.65 mmol/L) in the first 24
hours of life and less than 45 mg/dL (2.5 mmol/L)
thereafter
35. Definition:
Neonatal hypoglycemia is usually defined as
a serum glucose value of < 40-45 mg/dl.
For the preterm infant a value of < 30 mg/dl is
considered abnormal (hypoglycemia).
36. N.B.: The normal plasma glucose
concentration in the neonate is
approximately 60 to 80 percent of the
maternal venous glucose level, or
nearly between 70 – 80 mg/dl in
neonates of normoglycemic mothers. A
steady-state level occurs by
approximately three hours after birth.
37. *) Neonates at risk for developing
hypoglycemia:
1- The main cause may become maternal
malnutrition during pregnancy which leads to fetal
malnutrition and of course a low birth weight.
2- Those infants whom are Small for
gestational age infants (SGA), that manifested
by decrease in their birth weight and
subcutaneous fat and hepatic glycogen.
3- Those infants’ of diabetic mothers (IDM) or
those named as large for gestational age
(LGA).
38. 4- Those whom placentas were abnormal,
e. g.: placenta previa .
5- Those whom their mothers had toxemia
during pregnancy, e. g.: eclampsia or pre-eclampsia
induction of labor preterm
infant.
6- Those very ill or stressed neonates whom
their metabolic needs were increased due to
hypothermia, infection, respiratory distress
syndrome, or cardiac failure.
39. Pathophysiology:
The fetus receives glucose from the mother
continuously across the placenta. As soon as the cord is cut,
within 2 hours the normal neonate’s blood glucose level falls
from 70 – 80 mg/dl to 50 mg/dl. At this time, hepatic glucose is
released into the blood and the serum glucose level returns to
its normal level at birth (70 – 80 mg/dl). So, after birth the
neonate must kept well nourished because of the newly
acquired stressors as; abrupt transition from warm intrauterine
environment to a relatively cold extra-uterine one,
beginning the respiratory cycles by the neonate own
self, muscular activity, and suckling effort to prevent
carbohydrates storage consumption and the neonate become
at risk for developing hypoglycemia.
41. 7- Hypothermia.
8- Irregular respiratory pattern (Apnea).
9- Irritability.
10- High pitched cry followed by weak cry.
11- poor reflexes, especially sucking reflex.
42. Management of the Neonate at Risk:
Prevention:
first of all, providing a warm environment.
Early enteral feeding is the single
most important preventive measure.
If enteral feeding is to be started,
breast or artificial milk should be used
if the infant is able to tolerate nipple or
naso-gastric tube feeding.
43. These infants should have glucose values
monitored until they are taking full feedings
and have three normal pre-feeding readings
above 40-45 mg/dl. Care must be taken to
ensure that breast-feeding mothers are
providing an adequate intake.
If the infant at risk for hypoglycemia is unable
to tolerate nipple or tube feeding,
maintenance IV therapy with 10% glucose
should be initiated and glucose levels
monitored.
44. Management of the Neonate with
Hypoglycemia:
Infants who develop hypoglycemia should
immediately be given 2cc/kg of 10% dextrose
over 5 minutes, repeated as needed.
45. A continuous infusion of 10% glucose at a
rate of 8-10 mg/kg/min should be started to
keep glucose values normal (NOTE: 10
mg/kg/min of 10%dextrose = 144cc/kg/day).
Frequent bedside glucose monitoring is
necessary.
When feedings are tolerated and
frequent bedside glucose monitoring
values are normal, the infusion can be
tapered gradually.
48. Introduction:
Good control of maternal
diabetes is the key factor in determining fetal
outcome. Recent data indicates that perinatal
morbidity and mortality rates in the offspring of
women with diabetes mellitus have improved
with dietary management and insulin therapy.
Infants of diabetic mothers are large plump
with plethora faces resembling patients
receiving cortisone.
50. Pathophysiology:
Maternal hyperglycemia fetal
hyperglycemia (because the placental barrier passes from
70 – 75% of maternal glucose level to the fetus) fetal
hyperinsulinemia which in turn increased glycogen
synthesis and storage in the liver and increased fat
synthesis weight and size of all infants organs
except the brain (Macrocosmic infant). Sudden placental
separation and cord clamping interrupts the transplacental
glucose supply to the newly born infant without a similar
effect on the hyperinsuilinemia (Pancreatic Hyperplasia),
this leads to hypoglycemia during the first 2 hours after
birth.
51. Specific Disorders frequently encountered
in Infants of Diabetic Mothers (IDM):
*) Hypoglycemia.
*) Hypocalcemia.
*) Hypomagnesemia.
*) Cardio-respiratory disorders.
*) Hyperbilirubinemia (Unconjugated)
*) Birth injuries
*) Congenital malformations
52. Management:
I) For the mother:
Through good antenatal
care for proper control of maternal
diabetes.
53. II) For an infant:
All IDMs should receive
continuous observation and intensive care.
Serum glucose levels should be checked at birth and
at half an hour, 1, 2, 4, 8, 12, 24, 36 and 48 hours of
age:
- If clinically well and normoglycemic; oral or
gavage feeding should be started and continued
within 2 hours intervals.
- If hypoglycemic; give 2 – 4 ml/kg of 10%
dextrose over 5 minutes, repeated as needed. A
continuous infusion of 10% glucose at a rate of 8-10
mg/kg/min. Start enteral feeding as soon as possible.
Give Corticosteroids in persistent hypoglycemia.
54. Treatment of other complications
should also start; oxygen therapy
for RDS, calcium gluconate 10%
for hypocalcemia, phototherapy
for hyperbilirubinemia……………..
etc.
57. Introduction:
The newborn infant is
uniquely susceptible to acquire infection,
whether bacterial, viral or fungal. Bacterial
sepsis and meningitis continue to be major
causes of morbidity and mortality in the
newborn. The mortality rate due to sepsis
ranges from 20% to as high as 80% among
neonates. Surviving infants can have
significant neurologic squeal because of CNS
involvement.
58. Definition:
Neonatal sepsis is a disease of
neonates (who are younger than one
month) in which they are clinically ill and
have a positive blood culture.
59. Risk Factors:
I) Maternal risk factors:
- e.g.: Premature rupture of
membrane.
II) Neonatal risk factors:
- e.g.: Prematurity (less immunologic
ability to resist infection + more liable
to penetrate their defensive barriers).
60. Bacteria can reach the fetus or newborn and cause
infection in one of the following ways:
• Bacteria can pass through the maternal blood through
placenta as rubella, toxoplasma, and syphilis.
• Bacteria from the vagina or cervix can enter the
uterus, as groups B streptococci.
• The newborn may be come contract with bacteria as it
passes through the birth canal as gram negative
organisms.
• The newborn may come in contact with bacteria in its
environment after birth (Coagulate positive or negative
staphylococci.)
• When a susceptible host acquires the pathogenic
organism, and the organism proliferates and
overcomes the host defense, infection results.
61. Classification of neonatal sepsis:
Neonatal sepsis may be categorized as
early or late onset .
Newborns with early-onset infection
present within 24 hours till 72 hours. Early-onset
sepsis is associated with acquisition
of microorganisms from the mother during
pregnancy (transplacental infection),
or during labor (an ascending infection
from the cervix).
62. Late-onset sepsis; occurs beyond the
first 72 hours of life (most common
after the 3rd day till the 7th day after
birth) and is acquired from the care
giving environment (Nosocomial
infection).
63. Clinical presentation of neonatal
sepsis:
Physical findings may be nonspecific and
are often subtle.
e.g.: apnea , Jaundice , Hypothermia ,
Bulging or full fontanel , Seizures ,
hypotonia
64. Laboratory indicators of sepsis
include:
- Total leukocytic count (WBC count)
- C – reactive Protein (CRP)
- Erythrocyte Sedimentation Rate
(ESR)
- Cultures:
65. Management of Sepsis:
- Prevention: through proper application
to infection control practices.
- Early onset sepsis; give intrapartum
antimicrobial prophylaxis (IAP) to the
mother.
66. - Neonates with clinically suspected
sepsis:
*) Culture should be obtained first.
*) The recommended antibiotics are ampicilin and
gentamicin.
*) Third generation cephalosporins (Cefotaxime) may
replace gentamicin if meningitis is clinically suspected or if
gram-negative rods are dominant in the unit.
- Late onset neonatal sepsis:
Vancomycin in combination with either gentamicin or
cephalosporins should be considered in penicillin
resistant cases.
Note: Administer all medications IV.
68. Prevention
1- Demonstrate the effect of hand washing upon
the prevention of the noscomical infections.
2 -Standard precautions should be applied in the
nursery for infection prevention.
3- Instillation of antibiotics into newborn’s eye 1-2
hours after birth is done to prevent the infection.
4- Skin car should be done using worm water and
may use mild soup for removal of blood or
meconium and avoid the removal of vernix
caseosa.
5- Cord care should be cared out regularly using
alcohol or an antimicrobial agent.
69. Curative
• Encourage breast feeding from the mother.
• Adequate fluid and caloric intake should be
administered by gavage feeding or intravenous
fluid as ordered.
• Extra-measure for hypothermia or hyperthermia
that may take place to the newborn.
• Administering medications as doctor order.
• Follow the isolation precautions.
• Monitoring intravenous infusion rate and
antibiotics are the nurse responsibility.
70. • Administer the medication in the prescribed
dose, route, and time within hour after it is
prepared to avoid the loss of drug stability.
• Care must be taken in suctioning secretions
from the newborn as it may be infected.
• . Isolation procedures are implemented
according to the isolation protocols of the
hospital.
• Observe for the complication e.g. meningitis
and septic shock.
• Encourage in-service programs and
continuing education of nurses regarding the
infection control precautions.
72. Grade I HIE:
- Alternating periods of lethargy and
irritability, hyper-alertness and jitteriness.
- Poor feeding.
- Exaggerated and/or a spontaneous Moro
reflex.
- Increased heart rate and dilated pupil.
- No seizure activity.
- Symptoms resolved in 24 hours.
73. Grade II HIE:
- Lethargy.
- Poor feeding, depressed gag reflex.
- Hypotonia.
- Low heart rate and papillary constriction.
- 50-70% of infants display seizures,
usually in the first 24 hours after birth.
- Oliguria.
79. Definition:
Hyperbilirubinemia is an
elevation in the neonatal serum bilirubin
characterized by JAUNDICE, which is
defined as “yellowish discoloration of skin
and mucous membranes”. In the neonate
clinical jaundice is diagnosed if the total
serum bilirubin is ≥ 7 mg/dl.
80. N.B.:
The normal adult range of Total
Serum Bilirubin is 0.2 – 1 mg/dl (Direct:
0 – 0.2 mg/dl and Indirect: 0.2 – 0.8
mg/dl).
81. Pathophysiology: = Neonatal Bile Pigment
Metabolism.
Destruction of RBCs
Hemoglobin Salts
Water
Heme globin
(protein portion reused by
the body).
+ O2
Biliverdin
82. +
more O2
Unconjugated Bilirubin
+
Plasma protein
Liver
Which released from plasma protein inside the liver and
connected with Glucuronic acid and Glucuronyl Transferese
Enzyme (in the presence of normal Ph, O2, and normal body
temperature) to become Conjugated Bilirubin , that has 3
pathways:
Bile duct Kidney Gastrointestinal
tract
To digest fat. (Urobilin Urobilinogen) (Stercobilin
Stercobilinogen)
to obtain normal color of urine. to obtain normal
color of stool.
83.
84.
85.
86. The following are possible causes of
hyperbilirubinemia in the newly born
infants:
1. Over production of bilirubin.
2. Under excretion of bilirubin.
3. Combined over production and
under excretion.
4. Physiological jaundice.
5. Breast milk associated jaundice.
87. Complication:
The most common
complication of hyperbilirubinemia is Kernicterus
(Bilirubin Encephalopathy), which usually
occurs when the unconjugated serum bilirubin level
exceeds than 20 mg/dl. In small, sick preterm
infants, even a bilirubin level in a low range may
cause Kernicterus.
88. Clinical Presentation:
Kernicterus progresses through 4 stages:
Stage I: Poor Moro reflex, poor feeding, vomiting,
high-pitched cry, decreased tone and lethargy.
Stage II: Spasticity, seizures, fever. Neonatal
mortality is high at this stage (80%).
Stage III: A symptomatic (Spasticity decreases
and all remaining clinical signs and symptoms may
disappear).
Stage IV: Appears after the neonatal period.
Long-term sequelae can include: spasticity
quadriplegia, deafness and mental retardation (for
the 20%).
90. •Phototherapy:
Nursing care for those infants receiving
Phototherapy:
1. Cover the infant’s eyes and genital
organs.
2. The infant must be turned frequently
to expose all body surface areas to the
light.
3. Serum bilirubin level /4 – 12 hours.
4. Each shift, eyes are checked for
evidence of discharge or excessive
pressure on the lids and eye care should
be done using warm water, then apply eye
drops or ointment.
91. 5. Eye cover should be removed during
feeding, and this opportunity is taken to
provide visual and sensory stimuli.
6. Avoid oily lubricants or lotion on the
infant’s exposed skin, because this can act
as a barrier that prevent penetration of light
through the skin.
7. Increase feeds in volume and calories.
Add 20% additional fluid volume to
compensate for insensible and intestinal
water loss.
8. Intake and output chart.
92. • Blood exchange transfusion
Carry out this technique Beside the
Crash Cart.
95. Common Neonatal Respiratory
disorders:
· Respiratory distress syndrome (RDS)
= Hyaline membrane disease (HMD).
· Transient tachypnea of the newborn
(TTN).
· Meconium aspiration syndrome
(MAS).
· Apnea.
96. A) Respiratory distress syndrome
(RDS) = Hyaline membrane disease
(HMD).
Definition:
Respiratory distress
syndrome is A low level or absence of
surfactant system.
98. Clinical Presentation:
Grade I: (Mild distress): Rapid respiratory rate
(tachypnea >60 breaths per minute) + nasal flaring
(alae nasai).
Grade II: (Moderate distress): GI +
intercostals and substernal retractions.
Grade III: (Severe distress): GI + GII +
expiratory grunting.
Grade IV: (Advanced distress): GI + GII + GIII
+ central cyanosis and disturbed consciousness.
99. Management of RDS:
A) General:
* Basic support including thermal
regulation and parentral nutrition and
medications (antibiotics).
* Oxygen administration, preferably
heated and humidified
B) Specific:
Surfactant replacement therapy
through ET tube.
100. B) Transient Tachypnea of the
Newborn (TTN).
Definition:
TTN is a benign disease of near-term
or term infants who display respiratory
distress shortly after delivery. It occurs when
the infant fails to clear the airway of lung fluid
or mucus or has excess fluid in the lungs, this
limit the amount of alveolar surface available
for gas exchange, leading to respiratory rate
and depth to better use of the surface
available.
101.
102. Risk factors:
· Secondary to hypothermia.
· Infant born by Cesarean section, in
which the thoracic cavity is not squeezed by
the force of vaginal pressure, so that less
lung fluid is expelled than normally happen.
103. Clinical presentation:
* The infant is usually near-term or term.
* Exhibits tachypnea (> 80 breaths/min)
shortly after delivery.
* The infant may also display mild grunting,
nasal flaring, intercostals retraction, and
cyanosis.
* Spontaneous improvement of the neonate,
which considered as the most important
marker of TTN.
104. Management of TTN:
- Oxygenation.
- Fluid restriction.
- Start feeding as tachypnea improves.
Outcome and prognosis:
·Peaks intensity reached at 36 hours of infant’s life.
·The disease is self-limited (respiratory symptoms
improve as intrapulmonary fluid is naturally
absorbed or artificially mobilized using diuresis).
·No risk of recurrence or further pulmonary
dysfunction.
105. C) Meconium Aspiration Syndrome
(MAS).
Definition:
This respiratory disorder is
caused by meconium aspiration by the fetus
in utero or by the newborn during labor and
delivery. MAS is often a sign that the neonate
has suffered asphyxia before or during birth.
The mortality rate can be as high as 50% and
survivors may suffer long-term sequelae
related to neurological damage.
106. Causes and Pathophysiology:
1. Fetalis hypoxia; e.g. cord prolapse that
comes around the neck of the fetus many
days before delivery.
2. Babies born breech presentation.
In both cases; intrauterine hypoxia Or breech
presentation vagal nerve stimulation
relaxation of the sphincter
muscle
releasing of the first stool (meconium) in the
intrauterine life and becomes mixed with the
amniotic fluid, with the first breath the baby
can inhale meconium.
107. Dangerous of MAS:
The aspirated meconium can cause
airway obstruction clinical
manifestations of RDS, and an
intense inflammatory reaction.
108. Management of MAS:
*) Suctioning of the oropharynx by
obstetricians before delivery of the shoulders.
*) Immediate insertion of an ET tube and
tracheal suctioning before ambu bagging
(Maintain a neutral thermal environment).
*) Gastric lavage, and emptying of the stomach
contents to avoid further aspiration.
109. *) Postural drainage and chest vibration
followed by frequent suctioning.
*) Pulmonary toilet to remove residual
meconuim if intubated.
*) Antibiotic coverage (Ampicillin &
Gentamicin).
*) Oxygenation ( maintain a high saturation
> 95%)
*) Mechanical ventilation to avoid
hypercapnia & respiratory acidosis.
110. D) Apnea.
Definition:
Apnea is the cessation of respiration
accompanied by bradycardia and/or cyanosis for
more than 20 second.
Types:
1- Pathological apnea:
Apnea within 24 hours of
delivery is usually pathological in origin.
2- Physiological apnea:
Apnea developing
after the first three days of life and not associated
with other pathologies, may be classified as apnea
of prematurity.
111. Management of apnea:
· Monitor at-risk neonates of less than 32
weeks of gestation.
Begin with tactile stimulation ; gentle
shaking or prick the sole of the foot often
stimulate the infant to breath again.
112. · If no response to tactile stimulation, bag
and mask ventilation should be used
during the spell.
· Provide CPAP or ventilatory support
in recurrent and prolonged apnea.
· Pharmacological therapy:
- Theophylline.
Treat the cause, if identified, e.g., Sepsis,
Hypoglycemia, Anemia ………….. etc.
114. Monitoring the neonatal brain
Can we do more?
More direct monitoring parameters are needed:
• Stable and recognizable parameters
• Bedside monitoring possible for extended periods of time
115. Monitoring the brain
• Near Infrared Spectroscopy (NIRS)
• 1 or 2 channel EEG: aEEG
116. Near Infrared Spectroscopy (NIRS)
• Monitoring technique for cerebral oxygenation and
haemodynamics
• Based on absorption of near-infrared light by
oxygenated [O2Hb] and deoxygenated Hb [HHb]
• Absorption-changes in NIR-light (D ODs) can be
converted in changes of [DO2Hb] and [DHHb]
• Regional (mixed) cerebral O2-saturation: rScO2
117.
118. Reproducibility is good when used for
trend monitoring
Menke et al, Biol Neon 2003
Fronto-parietal
position
(r= 0.88,
p <0.01)
rScO2-Right (%)
rScO2-Left (%)
Lemmers et al, Pediatr Res, 2009
121. Continuous
Background patterns
Burst Suppression
Discontinuous
Cont. Low Voltage Flat Trace
= 10 min
Thanks to
LdeVries/MToet
122. Has cerebral monitoring add any
additional value in clinical care for the
neonate in N.I.C.U
123. Brain monitoring in clinical practice
non invasive monitoring
Preterm infants <32 wks
Term infants after hypoxic
ischemic events
Preterm infants <32 wks for 72 h
Neonates after perinatal asphyxia
124. Brain monitoring in clinical practice
• Arterial saturation
(pulse oxymetry)
• Arterial blood
pressure
• Heart rate
• Cerebral oxygenation
by NIRS (rScO2)
• aEEG
125. Monitoring the neonatal brain
• aEEG and NIRS in clinical practice
• Relation with other clinical conditions
• Blood pressure
• Patent ductus arteriosus
• Autoregulatory ability
• (Mechanical) ventilation
• Surgery
127. Limits of normal blood pressure in neonates
• Not well defined
• Mostly used definition MABP (mmHg)<GA (wks)
• Hypotension is related with brain damage
• Hypotension is not directly related to outcome
(Dammann 2002; Limperopoulos 2007)
• Recent papers show good outcome when accepting
lower limits for MABP (Dempsey 2013)
128. Dopamine
5μg/kg/min
$
*
$ p<0.05 vs controls;
* p<0.05 vs before
dopa
N=38
Bonestroo et al, Pediatrics 2011
$
N=39
132. Conclusion
aEEG should be continued for at least 48 hrs to be able
to detect late onset seizure after HI
133. Suggestion
• Brain monitoring by NIRS and aEEG
could be a useful approach to judge the
need of blood pressure support in
infants with low blood pressures
135. Hemodynamically important
PDA
• Ductal steal phenomenon in cerebral arteries
is a risk factor for cerebral damage in the
preterm infant (Perlman 1981)
136. PDA surgery after failure medication
*
GA 26.7 ±1.8 wks
PNA 7 days [4-39]
surger
y
p<0.05 vs pre-clip
137. Suggestions
• Monitoring of rScO2 during surgical ductal closure
can prevent surgery-related brain damage
• Cerebral oxygenation should play a role in the
ultimate decision to close of a hemodynamically
important ductus arteriosus
142. Suggestions
• Monitoring MABP and rScO2 can, within certain limits,
identify infants with absence of autoregulatory ability
• Identification of absence of autoregulatory ability may
help to prevent brain damage
144. Suggestion
• Brain monitoring during (artificial)
ventilation can help to prevent
hypo/hyper perfusion and
hyper/hypoxemia and so brain damage
145. Relat ion br ain monit or ing
Hypotension
Patent ductus arteriosus
Autoregulatory ability
(Mechanical) ventilation
Surgery
146. Neonatal cardiac surgery
Low cerebral saturations (<35%-45% )
related with adverse outcome
Toet et al Exp Brain Res 2009
Phelps et al 2009
Sood et al J Thorac Cardiovasc surg 2013
147.
148. Conclusions
• The current results of these studies in
neonates strongly suggest that SaO2 does not
always reflect oxygenation of the neonatal
brain.
• Thus monitoring of cerebral oxygenation by
NIRS and brain function by aEEg in addition to
SaO2 and blood pressure, can help to prevent
brain damage but also prevent unnecessary
treatment.
149. • The number of infants with (minor)
neurodevelopmental problems is high in infants
undergoing surgical procedures in neonatal period
So
• Neurodevelopmental delay needs to be investigated
in relation to brain injury :
• brain monitoring
• (pre-existing) riskfactors
• brain injury by neuro-imaging
• longterm follow-up
• larger cohorts
• collaboration between disciplines in hospitals and
multi-center
Preterm &lt; 37 wksSGA – below 10th percentile
Late preterm 34.0 – 36.6 wksAGA – Between 10th & 90th percentile
Term 37-42 wksLGA - &gt; 90th percentile
Post term &gt;42 wksIUGR – pregnancy circumstances that contribute to growth restriction. May be maternal, placental or fetal.
Gestational age and birth weight are criteria used to measure neonatal maturity and mortality risks. As weight and gestation increase, neonatal mortality risks decrease.
Relation in the clinical situation of PDA and the cerebral hemodynamics
Relation in the clinical situation of PDA and the cerebral hemodynamics
Relation in the clinical situation of PDA and the cerebral hemodynamics
Broekhuyzen; a term
Asfyxie door onder onbekende oorzaak; maar meteen post portum zeer ernstig bloeddruk problemen ondanks maximale inotropie en veel vulling.( geen sepsis)
Bij kopje hypotensie zakte de bloeddruk nog dieper en ( mean &lt;20) en werd er snel op de hand gevuld waarna herstel aEEG
Broekhuyzen
Broekhuyzen
Relation in the clinical situation of PDA and the cerebral hemodynamics
Relation in the clinical situation of PDA and the cerebral hemodynamics
Autoregulation is the ability to keep the organ blood flow constant despite fluctuations in perfusion pressure. It is accomplished by regulation of the arterial tone so that low perfusion pressure results in vasodilation and high perfusion results in vasoconstriction. On the systemic level, organs such as the brain, heart and adrenals are vital and autoregulation maintains normal organ blood flow when systemic blood flow is low, while non-vital organs (e.g. skin and kidney) vasoconstrict to direct the circulating blood to the vital organs.
Cerebral autoregulation has limited capacity and is thought to be particularly fragile in the immature brain (Greisen 2005). Pressure passive flow is a state where the blood flow follows blood pressure. It is hypothesized that the fluctuations in flow that this entails is a potential cause of cerebral haemorrhages in premature infants. It is a problem that, at the current state, the identification of the threshold blood pressure below which cerebral blood flow begins to fall is not possible (Cayabyab et al 2009).
confirm
Relation in the clinical situation of PDA and the cerebral hemodynamics
Relation in the clinical situation of PDA and the cerebral hemodynamics