Necrotizing enterocolitis (NEC) is an acquired intestinal disease seen primarily in preterm infants. It is a leading cause of morbidity and mortality in neonatal intensive care units. The exact cause is unknown but involves intestinal ischemia, enteral feeding, and pathogenic bacteria. Risk factors include prematurity, enteral feeding, and abnormal gut colonization. Clinically, NEC presents with abdominal signs and symptoms as well as systemic involvement. Treatment involves bowel rest, antibiotics, and surgery for perforation or necrosis. Despite management, NEC carries significant mortality and morbidities like short bowel syndrome.
Neonatal necrotizing enterocolitis
NEC is the most common life-threatening emergency of the gastrointestinal tract in the newborn period. The disease is characterized by various degrees of mucosal or transmural necrosis of the intestine. The cause of NEC remains unclear but is most likely multifactorial. The incidence of NEC is 1-5% of infants in neonatal intensive care units (NICUs). Both incidence and case fatality rates increase with decreasing birthweight and gestational age. Because very small, ill preterm infants are particularly susceptible to NEC, a rising incidence may reflect improved survival of this high-risk group of patients.
Clinical Manifestations
Infants with NEC have a variety of signs and symptoms and may have an insidious or sudden catastrophic onset (Table 96-1). The onset of NEC is usually in the 2nd or 3rd week of life but can be as late as 3 mo in VLBW infants. Age of onset is inversely related to gestational age. The 1st signs of impending disease may be nonspecific, including lethargy and temperature instability, or related to gastrointestinal pathology, such as abdominal distention and gastric retention. Obvious bloody stools are seen in 25% of patients. Because of nonspecific signs, sepsis may be suspected before NEC. The spectrum of illness is broad, ranging from mild disease with only guaiac-positive stools to severe illness with bowel perforation, peritonitis, systemic inflammatory response syndrome, shock, and death. Progression may be rapid, but it is unusual for the disease to progress from mild to severe after 72 hr.
Diagnosis
A very high index of suspicion in treating preterm at-risk infants is crucial. Plain abdominal radiographs are essential to make a diagnosis of NEC. The finding of pneumatosis intestinalis (air in the bowel wall) confirms the clinical suspicion of NEC and is diagnostic; 50-75% of patients have pneumatosis when treatment is started (Fig. 96-4). Portal venous gas is a sign of severe disease, and pneumoperitoneum indicates a perforation (Figs. 96-4 and 96-5). Hepatic ultrasonography may detect portal venous gas despite normal abdominal roentgenograms .
Neonatal necrotizing enterocolitis
NEC is the most common life-threatening emergency of the gastrointestinal tract in the newborn period. The disease is characterized by various degrees of mucosal or transmural necrosis of the intestine. The cause of NEC remains unclear but is most likely multifactorial. The incidence of NEC is 1-5% of infants in neonatal intensive care units (NICUs). Both incidence and case fatality rates increase with decreasing birthweight and gestational age. Because very small, ill preterm infants are particularly susceptible to NEC, a rising incidence may reflect improved survival of this high-risk group of patients.
Clinical Manifestations
Infants with NEC have a variety of signs and symptoms and may have an insidious or sudden catastrophic onset (Table 96-1). The onset of NEC is usually in the 2nd or 3rd week of life but can be as late as 3 mo in VLBW infants. Age of onset is inversely related to gestational age. The 1st signs of impending disease may be nonspecific, including lethargy and temperature instability, or related to gastrointestinal pathology, such as abdominal distention and gastric retention. Obvious bloody stools are seen in 25% of patients. Because of nonspecific signs, sepsis may be suspected before NEC. The spectrum of illness is broad, ranging from mild disease with only guaiac-positive stools to severe illness with bowel perforation, peritonitis, systemic inflammatory response syndrome, shock, and death. Progression may be rapid, but it is unusual for the disease to progress from mild to severe after 72 hr.
Diagnosis
A very high index of suspicion in treating preterm at-risk infants is crucial. Plain abdominal radiographs are essential to make a diagnosis of NEC. The finding of pneumatosis intestinalis (air in the bowel wall) confirms the clinical suspicion of NEC and is diagnostic; 50-75% of patients have pneumatosis when treatment is started (Fig. 96-4). Portal venous gas is a sign of severe disease, and pneumoperitoneum indicates a perforation (Figs. 96-4 and 96-5). Hepatic ultrasonography may detect portal venous gas despite normal abdominal roentgenograms .
POSTERIOR URETHRAL VALVES- Pediatric Surgery
• Dear viewers,
• Greetings from “ Surgical Educator”
• Today I have uploaded one more video in Pediatric Surgery/Pediatric Urology- “ Posterior Urethral Valves”
• Posterior Urethral Valves is the congenital cause for Bladder Outlet Obstruction, resulting in abnormal development of the kidneys as well as the bladder.
• In this video, I talked about the learning outcomes, introduction, etiopathogenesis, clinical features, investigations, differential diagnosis, treatment, follow-up and prognosis of “ Posterior Urethral Valves”
• I hope you will enjoy the video for its educational value.
• You can watch all my teaching videos in the following links
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video.
Necrotizing enterocolitis (NEC) is a life-threatening emergency of the gastrointestinal tract in the newborn period.
The most common gastrointestinal condition in premature neonates.
It is characterized by inflammation, ischemia, and permeability of the neonatal bowel wall to bacteria.
It is potentially life-threatening with significant associated morbidity.
The disease is characterized by various degrees of mucosal or transmural necrosis of the intestine.
POSTERIOR URETHRAL VALVES- Pediatric Surgery
• Dear viewers,
• Greetings from “ Surgical Educator”
• Today I have uploaded one more video in Pediatric Surgery/Pediatric Urology- “ Posterior Urethral Valves”
• Posterior Urethral Valves is the congenital cause for Bladder Outlet Obstruction, resulting in abnormal development of the kidneys as well as the bladder.
• In this video, I talked about the learning outcomes, introduction, etiopathogenesis, clinical features, investigations, differential diagnosis, treatment, follow-up and prognosis of “ Posterior Urethral Valves”
• I hope you will enjoy the video for its educational value.
• You can watch all my teaching videos in the following links
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video.
Necrotizing enterocolitis (NEC) is a life-threatening emergency of the gastrointestinal tract in the newborn period.
The most common gastrointestinal condition in premature neonates.
It is characterized by inflammation, ischemia, and permeability of the neonatal bowel wall to bacteria.
It is potentially life-threatening with significant associated morbidity.
The disease is characterized by various degrees of mucosal or transmural necrosis of the intestine.
Diagnosis of Inflammatory bowel disease have challenges including differentiating from Irritable bowel disease using noninvasive biomarkers. Fecal calprotectin is a novel fecal marker which meets the diagnostic & monitoring requirements for IBD.
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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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
2. Necrotizing Enterocolitis:
an acquired neonatal acute intestinal
necrosis of unknown etiology
NEC is neither a uniform nor a well-defined
disease entity
Acquired neonatal intestinal diseases (ANIDs)
Wider umbrella, includes different pathologies
affecting gastrointestinal tract in preterm and term
infants. Some which do lead to the common final
pathology of NEC and some which do not.
Includes:
NEC
SIP (isolated spontaneous intestinal perforation)
Viral enteritis of infancy
Cow’s milk protein allergy
3. Epidemiology
Incidence: 0.3-2.4 / 1000 live births
2-5 % of all NICU admissions
5-10 % of VLBW infants
Over 90 % of cases occur in preterm babies
About 10 % occur in term newborns: essentially
limited to those that have some underlying illness or
condition requiring NICU admission
Sex, race, geography, climate has no role in
determining the incidence of NEC
Prematurity is the single greatest risk factor
5. Risk factors influencing NEC prediposition
• Prematurity:
inflamatory propensity of the immature gut.
Decreases intestinal barrier function.
Decreased gut motility and abberent vascular regulation.
• Enteral feeding:
Aggressive advancement of feeding.
Non human milk feeding
• Abnormal bacterial colonization:
Prolonged emperical antibiotic therapy
Decreased commensal flora
Increased pathogenic bacteria
Maternal cocaine abuse – 2.5 times increases risk
6. Risk Factors: in Term Babies
Limited to those that have some underlying illness or
condition requiring NICU admission.
• Congenital Heart Disease
• Intrauterine growth restriction
• Polycythemia
• Hypoxic-ischemic events
• The mean gestational age of infants with NEC is 30 to 32
weeks, and the infants generally are weight appropriate
for gestational age.
• Postnatal age at onset is inversely related to birth weight
and gestational age with mean age at onset of 12 days
9. Microbiologic Flora and Infection
Several organisms have been accused, but non has been
proven to be causative:
– Enterobacteriaceae
– Enterobactersakazakii
– Coagulase-negative staphylococci: SIP
– Closrtidium perfringens
– Candida species: SIP
– Cytomegalovirus
– Torovirus
– HIV
– Mucormycosis
11. Clinical Presentation
• Course of the disease
Fulminant presentation
Slow, paroxysmal presentation
• The onset of NEC usually occurs in the 1st 2 weeks of
life (with a mean age at onset of 12 days) but can be as
late as 3 months of age in VLBW infants
12. • The 1st signs of impending disease may be
-Nonspecific including lethargy and temperature
instability or
-Related to gastrointestinal pathology such as
abdominal distention and gastric retention.
• Obvious bloody stools are seen in 25% of patients.
The spectrum of illness is broad and ranges from
-Mild disease with only guaiac-positive stools
to
-Severe illness with bowel perforation, peritonitis,
systemic inflammatory response syndrome, shock, and
death.
15. Laboratory features
• No lab test is specific for NEC
• The most common triad:
– Thrombocytopenia
– Persistent metabolic acidosis
– Severe refractory hyponatremia
Serial measurements of CRP – diagnostic and
prognostic
• ↑WBC, ↓WBC, ↓PMN
• Hyperkalemia
• Stool: reducing substances, occult blood
17. Radiology studies
• Abdominal X-ray:
•
•
•
•
•
Abnormal gas pattern, ileus
Bowel wall edema
Pneumatosis intestinalis
Fixed position loop
Intra hepatic-portal venous gas ( in the absence of
UVC)
• Pneumoperitonium - left lateral decubitus or crosstable lateral views
22. • Abdominal ultrasound:
– Thick-walled loops of bowel with hypomotility.
– Intraperitonealfluid is often present.
– Intramural gas can be identified in early-stage NEC
– In the presence of pneumatosisintestinalis, gas is
identified in the portal venous circulation within the
liver.
– Color Doppler US is more accurate than abdominal
radiography in depicting bowel necrosis in NEC.
23. • Differential diagnosis of NEC :
• Specific infections (systemic or intestinal)- Pneumonia,
Sepsis.
• Gastrointestinal obstruction, volvulus, malrotation,
• Isolated intestinal perforation.
• Severe Inherited Metabolic disorders. (e.g., galactosemia
with Escherichia coli sepsis)
• Feeding intolerance
• Severe allergic colitis
• Idiopathic focal intestinal perforation can occur
spontaneously or after the early use of postnatal steroids
and indomethacin.
24. • MODIFIED BELL’S STAGING OF NEC:
Based on:
1. Systemic Signs
2. Intestinal Signs
3. Radiological Signs
Classified into:
I. Suspected:
II. Definite :
A (Mildly ill) ,
B (Moderately ill)
III. Advanced:
A (Severely ill,bowel intact),
B (Severely ill,bowel perforated)
25.
26. • TREATMENT:
• Rapid initiation of therapy is required for suspected as well
as proven NEC cases.
• There is no definitive treatment for established NEC and,
therapy is directed at supportive care and preventing
further injury with
-Cessation of feeding,
-Nasogastric decompression, and
-Administration of intravenous fluids.
• Once blood has been drawn for culture, systemic
antibiotics (with broad coverage for gram-positive, gramnegative, and anaerobic organisms) should be started
immediately.
27. • TREATMENT: Contd..
• Umbilical catheters if present should be removed.
• Ventilation should be assisted as required.
• Intravascular volume replacement with crystalloid or blood
products.
• Cardiovascular support with volume and/or inotropes.
• Correction of hematologic, metabolic, and electrolyte
abnormalities.
• Careful attention to respiratory status, coagulation profile,
and acid-base and electrolyte balance are important.
28. • MONITORING:
• Sequential abdominal grith measuremet
• Sequential anteroposterior and cross-table lateral or lateral
decubitus abdominal x-rays to detect intestinal perforation;
• Serial determination of hematologic status,
• Serial determination of electrolyte status, and
• Serial determination of acid-base status.
29. • Indications for surgery :
• Absolute indications:
• Evidence of perforation on abdominal roentgenograms
(pneumoperitoneum) or
• Positive abdominal paracentesis (stool or organism on
Gram stain from peritoneal fluid).
•
•
•
•
•
Relative indications:
Failure of medical management,
Single fixed bowel loop on roentgenograms,
Abdominal wall erythema, or
A palpable mass.
30. • Ideally, surgery should be performed after
intestinal necrosis develops, but before
perforation and peritonitis occurs.
• Peritoneal drainage may be helpful for
patients with peritonitis who are too unstable
to undergo surgery. Peritoneal drainage is
more successful in patients with isolated
intestinal perforation.
31. Initial signs of possible NEC (bell’s stage I )
•NPO
•GI decompression- low constant sucton, replace output with electrolytes
•CBC with differentials, blood culture, CRP, S.Electrolytes
•Abdominal radiograph
•Begin antibiotics
Mild to Moderate (Bell’s stage II)
Advanced (Bell’s Stage III)
•Serial abdominal radiographs
•Serial abdominal radiographs
•Broad spectrum antibiotics for 7- 10 days •Broad spectrum antibiotics for 7- 10 days
•NPO for 5-10 days, parentaral nutrition •NPO for 10-14 days, parentaral nutrition
•Monitor electrolytes
•Monitor electrolytes
•Serial CBCs every 12h to 24h for 2-3 days
•Serial CBCs every 12h to 24h for 2-3 days
•Co-mangement with paediatric surgeon
•Hemodynamic support
•Monitor coagulation abnormalities and
correct
Indications for surgery
•Intestinal perforation
•Fixed adynamic loop – necrotic gut
•Signs suggestive of necrotic gut –persistent severe thrombocytopenia, severe
metabolic acidosis
32. • PROGNOSIS.:
• Medical management fails in about 20–40% of patients
with pneumatosis intestinalis at diagnosis; of these, 10–
30% die.
• Early postoperative complications : Wound infection,
dehiscence, and stomal problems (prolapse, necrosis).
• Later complications : Intestinal strictures develop at the site
of the necrotizing lesion in about 10% of surgically or
medically managed patients.
33. • PROGNOSIS….
• After massive intestinal resection,
-Complications from postoperative NEC include
short-bowel syndrome (malabsorption, growth failure,
malnutrition),
• Premature infants with NEC who require surgical
intervention or who have concomitant bacteremia are at
increased risk for adverse growth and neurodevelopmental
outcome.
• The overall mortality is 9% to 28% regardless of surgical or
medical intervention.
34. • PREVENTION:
• Always better than cure!
• Newborns exclusively breast-fed have a reduced risk of NEC.
• Early initiation of aggressive feeding may increase the risk of NEC
in VLBW infants.
• Gut stimulation protocol of minimal enteral feeds followed by
judicious volume advancement may decrease the risk.
• Probiotic preparations have also decreased the incidence of NEC.
. Induction of GI maturation.
• Incidence of NEC is significantly reduced after prenatal steroid
therapy.
• Alteration of the immunologic status of the intestine using
immunoglobulin A (IgA) and immunoglobulin G (IgG)
supplementation.