This document discusses preterm delivery and labor, including definitions, causes, risk factors, clinical features, investigations, and management. It begins with an overview of spontaneous preterm labor and preterm premature rupture of membranes. Key points include that infection is a major cause, cervical weakness can lead to ascending infection, and multiple pregnancies have an increased risk. Clinical assessment includes examination and testing fetal fibronectin and cervical length via ultrasound. Management aims to delay delivery and improve neonatal outcomes through treatments like corticosteroids and antibiotics.
Preterm labor is the labor that starts before the 37th completed week. In this presentation, we will discover causes, pathogenesis, diagnosis, clinical features, and management principles for preterm labor along with the most recent evidence.
Preterm labor is the labor that starts before the 37th completed week. In this presentation, we will discover causes, pathogenesis, diagnosis, clinical features, and management principles for preterm labor along with the most recent evidence.
Preterm labor is defined as the onset of labor before 37 weeks of gestation. It is a leading cause of neonatal morbidity and mortality, and can lead to long-term health problems for the baby. Risk factors for preterm labor include a history of preterm labor or delivery, multiple gestations, cervical incompetence, uterine anomalies, and infections.
Symptoms of preterm labor can include regular contractions, pelvic pressure or pain, backache, vaginal bleeding or discharge, and a change in vaginal discharge. If preterm labor is suspected, immediate medical attention is required. Treatment may include medications to stop or slow down labor, steroid injections to help speed up fetal lung development, and bed rest.
Prevention of preterm labor can be achieved through good prenatal care, including regular prenatal visits, proper nutrition, and management of underlying medical conditions. Avoiding certain risk factors, such as smoking and substance abuse, can also help reduce the risk of preterm labor.
In cases where preterm labor cannot be prevented, the goal is to delay delivery as long as possible to give the baby the best chance of survival and good health. This may involve hospitalization for bed rest, medication, and close monitoring of the mother and baby.
Preterm labor is a serious and potentially life-threatening complication of pregnancy, but with appropriate management and early intervention, the risk of morbidity and mortality can be minimized.
Preterm labor is defined as the onset of labor before 37 weeks of gestation. It is a leading cause of neonatal morbidity and mortality, and can lead to long-term health problems for the baby. Risk factors for preterm labor include a history of preterm labor or delivery, multiple gestations, cervical incompetence, uterine anomalies, and infections.
Symptoms of preterm labor can include regular contractions, pelvic pressure or pain, backache, vaginal bleeding or discharge, and a change in vaginal discharge. If preterm labor is suspected, immediate medical attention is required. Treatment may include medications to stop or slow down labor, steroid injections to help speed up fetal lung development, and bed rest.
Prevention of preterm labor can be achieved through good prenatal care, including regular prenatal visits, proper nutrition, and management of underlying medical conditions. Avoiding certain risk factors, such as smoking and substance abuse, can also help reduce the risk of preterm labor.
In cases where preterm labor cannot be prevented, the goal is to delay delivery as long as possible to give the baby the best chance of survival and good health. This may involve hospitalization for bed rest, medication, and close monitoring of the mother and baby.
Preterm labor is a serious and potentially life-threatening complication of pregnancy, but with appropriate management and early intervention, the risk of morbidity and mortality can be minimized.
10.2 Preterm labour and preterm rupture of the membranes.pdfChantal Settley
Define preterm labour and preterm rupture of the membranes.
Understand why these conditions are very important.
Understand the role of infection in causing preterm labour and preterm rupture of the membranes.
List which patients are at increased risk of these conditions.
Understand what preventive measures should be taken.
Diagnose preterm labour and preterm rupture of the membranes.
Manage these conditions.
Please find the power point on Management of Preterm labor. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Pre-labor rupture of membranes (PROM), previously known as premature rupture of membranes, is breakage of the amniotic sac before the onset of labor.
Women usually experience a painless gush or a steady leakage of fluid from the vagina.
If it occurs before 37 weeks it is known as PPROM (‘preterm’ prelabour rupture of membranes) otherwise it is known as term PROM.
Approach to patient with spinal cord lesions & diseases
Localize spinal cord lesions
Determining the Level of the Lesion in Myelopathy
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This is a comprehensive approach to a hypertensive patient presenting to the emergency department.
Discussing:-
- Hypertensive emergency
- Hypertensive Urgency
- Hypertensive Crisis
- Hypertensive encephalopathy and retinopathy
- Accelerated Hypertension
- Malignant hypertension
this is a complete discussion and an approach to a child with febrile seizure / convulsion.
It contains:-
Case scenario
Causes of Seizures in the setting of fever
Definition of Febrile Seizure
Age of Occurrence
Types of Febrile Convulsions
Risks of Recurrent Febrile Seizures
Risk For Developing Epilepsy After Febrile Seizures
Workup for Febrile Seizure
Red Flags in Febrile Seizures
Treatment
Prognosis
Approach to Syncope in Children (Pediatric Syncope).pptxJwan AlSofi
Approach to Syncope in Children (Pediatric Syncope), includes:-
Introduction
Differential diagnosis of syncope
Syncope vs vertigo vs Presyncope vs light-headedness.
Comparison of Clinical Features of Syncope and Seizures
Neurocardiogenic (Vasovagal) syncope
MECHANISMS and Causes of Syncope
Cardiac causes of syncope
Life-threatening causes of syncope
Red Flags in Evaluation of Patients With Syncope
Non-cardiac causes of loss of consciousness.
Noncardiac Causes of Syncope
Differentiating Features for Causes of Syncope
EVALUATION of syncope:- History, Examination,Treatment.
Summary
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
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
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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
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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
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.
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.
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.
2. LEARNING OBJECTIVES
• To understand the extent of the problem, its
causes and consequences.
• To be aware of the limitations of our current
understanding.
• To appreciate the problems and potential
complications associated with our current
management of preterm labour.
• To grasp the potential for improvements in our
management of preterm labour.
3. Case scenario
Rawshan is 26 years old pregnant lady
in her 31 weeks gestation presented to
labour room with history of colicky
abdominal pain of few hours duration, back
pain with thick vaginal discharge & good
fetal movement
4. Definitions
• In pregnancy, the gestational age of viability is 24wks.
• Currently, the ‘grey zone’ for viability is around 23 weeks.
o Occasional survivors are seen after delivery at 23 weeks, which has
become the ‘grey zone’ for viability.
• In pregnancy, term refers to the gestational period from 37+0 to 41+6 wks.
• Preterm labour (PTL) is the onset of labour before 37 weeks’ gestation.
o PTL are those that occur between 24+0 and 36+6 weeks gestation.
• Second trimester or late miscarriage occurs between 12 and 23 weeks
gestation.
o A more practical definition of late miscarriage is one occurring between
17 and 23 weeks.
5. Early births
Spontaneous deliveries:
the mother develops
spontaneous contractions or
membrane rupture earlier
than normal
spontaneous
preterm labour
(PTL)
preterm prelabour
rupture of
membranes
(PPROM)
Indicated deliveries :
delivery is felt to be in
the best interests of the
mother or baby
6. Categories
1. Spontaneous PTL 50%
2. PPROM 25%
3. Delivery for maternal or fetal indications 25%
Iatrogenic or medically-indicated deliveries
1. Pre-eclampsia
2. Maternal cardiac or renal conditions or malignancies .
3. Chorioamnionitis
4. APH
5. Fetal growth restriction (FGR)
7. According to etiology, outcome and recurrence
risk, it is divided into three gestational periods:
1) Extremely preterm births : 24+0 to 27+6 weeks.
2) very preterm births : 28+0 to 31+6 weeks.
3) Mildly preterm births : 32+0 to 36+6 weeks.
Classification of preterm births
8.
9. 1. Teenagers and women with advanced maternal age
(Parity 0 or >5)
2. Higher incidence of preterm deliveries in first
pregnancies.
3. Socioeconomic factors
4. Marital status
5. Genetic and environmental factors
6. Cigarette smoking, illegal substance (i.e. cocaine)
abuse, alcohol
7. Poor nutrition
8. Previous preterm
The risk of PTD
10.
11. Labour vs PTL
• Labour at term and prior to it share a common
pathway involving:
1. uterine contractility,
2. cervical effacement and dilatation
3. membrane rupture.
• At term, the activation of this pathway is
physiological.
• spontaneous preterm labor is an enigmatic
process that occurs when the normal labor
pathway is triggered through various pathologic
mechanisms.
• a variety of pathologies underlie labour remote
from term.
• It has been suggested by some authors that
preterm labour be considered a syndrome, in
order to emphasize its multifactorial nature.
12. Endocrinology and biochemistry of labour
1. During pregnancy the uterus undergoes marked
biochemical and physiological changes while
expanding to accommodate the growing fetus
and remaining quiescent.
2. The cervix remains rigid and closed to retain the
developing fetus within the uterus.
• Throughout pregnancy ‘pro-pregnancy’ factors
inhibit myometrial contractility.
• ‘pro-pregnancy’ factors :
1. progesterone,
2. relaxin,
3. (hCG)
4. prorelaxation prostaglandins (PGs), such as
prostacyclin
13. • The onset of labour involves the synchronization of myometrial
activity through greater expression of gap junctions that
connect myometrial cells.
• Increased myometrial activity results from the activation of a
‘cassette of contraction-associated proteins’ (CAPs), which
convert the myometrium from a quiescent to a contractile state
• CAPs include:
1. gap junction proteins,
2. oxytocin and prostanoid receptors,
3. enzymes for PG synthesis
4. cell signalling proteins.
• CAPs
1. Activate fetal membrane PG and cytokine production
2. Cervical remodelling and ripening.
14. • Progesterone maintains uterine quiescence
• Labour as an inflammatory process
• The roles of oxytocin and prostaglandins
17. Infection
• Infection of the fetal membranes, chorioamnionitis, is a major cause of
preterm birth particularly in deliveries before <32 weeks’ gestation.
• It is associated with a threefold increased risk of PTD with intact
membranes, and a fourfold increased risk with ruptured membranes.
• In most cases, infection ascends from the vagina, or transplacental or
introduced during invasive procedures.
• Overall, 33% of all pregnancies delivered after PPROM are
complicated by infection.
• The uterine cavity is normally sterile but the vagina contains
commensal bacteria.
• Depending on the bacterial load and cervical resistance, the
bacteria may ascend through the cervix and reach the fetal
membranes. This:
1. may activate the decidua, increase prostaglandin release and
trigger contractions.
2. Alternatively, it may weaken the membranes, leading to rupture.
18. • Abnormal vaginal flora, for example bacterial
vaginosis (BV), affects 16% of pregnant women and is
associated with PPROM and PTL, with a greater risk the
earlier in gestation <16 weeks is identified.
• Chorioamnionitis is associated with :
1. drives PTL,
2. fetal brain damage (periventricular leukomalacia (PVL)
and intraventricular haemorrhage (IVH)) ,
3. since intrauterine infection drives a fetal inflammatory
response, involving:
I. a proinflammatory cytokinaemia
II. morphologically, a vasculitis of the umbilical cord and/or the
vessels of the chorionic plate.
21. Multiple pregnancy and uterine distension
• Overall, 56% of multiple births deliver before 37 weeks and
10–15% before 32 weeks.
• The risk of PTD rises with fetal number, with triplets
delivering on average at 32 weeks and quadruplets delivering
at 28 weeks.
• Multiple pregnancies have an increased risk of pre-eclampsia,
FGR and other medical complications of pregnancy.
• Twins have a six to sevenfold increased risk of cerebral palsy.
• Polyhydramnios, the presence of too much amniotic fluid.
Severe polyhydramnios can be managed with amnio-drainage,
alternatively, indomethacin (NSAID), used as it reduces fetal
urine production.
22. Uterine müllerian anomalies
• Unrecognized but are estimated to occur in up to 4% of
women of reproductive age.
• Occur as a consequence of abnormal embryologic fusion and
canalization of the müllerian ducts and result in an
abnormally formed uterine cavity, range from an arcuate
uterus, results in minimal fundal cavity indentation, to
complete failure of fusion resulting in uterine didelphys.
• Associated with adverse pregnancy outcome in up to 25% of
women, including first and second trimester miscarriage,
PPROM, preterm birth, FGR, breech presentation and
caesarean section.
23.
24.
25.
26. Haemorrhage
• The presence of a subchorionic haematoma in early pregnancy
increases the risk of later PPROM, either through an effect of
thrombin on membrane strength or through the occurrence of
infection in the haematoma.
• Acute bleeding leads to the release thrombin that directly
stimulates myometrial contractions.
• Risk factors include pre-eclampsia and hypertension,
previous abruption, trauma, smoking, cocaine use,
multiple pregnancy, polyhydramnios, thrombophilias,
advanced maternal age and PPROM.
• When an abruption involves 50% or more of the placenta it is
frequently associated with fetal death.
30. History
- Dating of pregnancy / LMP
, early US
- Clinical presentation / risk factors:
1. Pain /uterine contraction
2. Vaginal loss
3. Pelvic pressure
4. low backache
5. Generally unwell, may be fever or urinary
symptoms
31. Examination
1. General examination:
• pulse, BP, temperature and state of hydration.
2. Abdominal examination:
• the presence of uterine tenderness, suggesting abruption or
chorioamnionitis.
3. Sterile Speculum examination:
• pooling of amniotic fluid,
• blood and/or abnormal discharge.
• Ask patient to cough/press over the fundus leaking liquor.
• A visual assessment of cervical dilatation
4. Vaginal examination:
• Digital exams should be limited, as they are known to stimulate
prostaglandin production and may introduce organisms into the
cervical canal.
• Repeat vaginal examination in 1–4 hours should be considered
essential in the absence of specialized tests. The interval between
assessments should be guided by the severity of the symptoms.
32. • Nevertheless, the diagnosis of preterm
labour remains notoriously difficult unless
contractions are accompanied by advanced
dilatation (>3 cm), ruptured membranes or
significant vaginal bleeding.
• Differential diagnosis of PTL:
1. Urinary tract infection
2. Gastroenteritis
3. Constipation
4. Red degeneration of fibroid
5. Placental abruption
33. Investigations
❖ Blood group & Rh
❖ Full Blood Count
❖ MSU / culture & sensitivity
❖ Cervicovaginal swab / microbiology
❖ Fetal fibronectin (fFN)
❖ TA/ TV US :
o Gestational age,
o cervical length
Cervical length measurement by TVU has been shown to improve
diagnostic accuracy.
A normal cervix measures approximately 35 mm in length .
Significant cervical shortening is often accompanied by dilatation and
funnelling of the membranes down the cervical canal .
o Amniotic fluid volume
o placental site
34. Fetal fibronectin (fFN)
• Testing the cervicovaginal fluid levels of fetal fibronectin
(fFN), a glycoprotein found in cervicovaginal fluid, amniotic
fluid, placental tissue and in the interface between the
chorion and decidua.
• It acts like ‘glue’ at the maternal–fetal interface and its
presence in cervicovaginal fluid between 22 and 36 weeks’
gestation has been shown to be a predictor of PTD.
Negative fFN test to be sent home.
Those with a positive fFN test can be admitted for tocolysis
and steroids for fetal lung maturation.
38. Treatment in symptomatic patient
o if cervix not dilated support
o if membrane ruptured contraction
wait & monitor
terminate
no contraction
39. Management of symptomatic PTL women
At tertiary center or intrauterine transfer
1. Communication and support:
• Ensure: Sympathy , pain relief, reassurance
2. Maternal corticosteroids:
• The most beneficial treatment in preterm labour is a course of
maternal steroids.
• a single course of maternal steroids (two injections 12–24 hours apart)
given between 28 and 34 weeks gestation and received within 7 days
of delivery.
• Maximum benefit from the injection is seen after 48 hours.
• Courses received less than 48 hours or more than 7 days before
delivery still lead to benefit, as may courses given between 24 and 28
weeks.
• They are not indicated below 24 weeks.
• Effects within 7 days of delivery: ↓RDS, ↓IVH, ↓necrotizing
enterocolitis, improve neonatal outcomes and lung function.
40. 3. Tocolytics:
• The sole reason for using tocolytics is to delay delivery
for 48-hour window to allow :
a course of steroids for fetal lung maturation to be
completed
to facilitate transfer of the undelivered mother to a unit
able to provide appropriate neonatal care.
In utero transfer.
• Tocolytics are only used for short pregnancy prolongation
(delay delivery) for about 48-hour.
• The first choice → CCB (nifedipine) or an OTR
antagonist (atosiban).
• However, recently PG inhibitors and CCB are most likely
the best therapy for PTD on the basis of delaying
delivery by 48 hours, neonatal mortality, neonatal (RDS)
and maternal side-effects.
41. Types of Tocolysis
1. Beta-sympathomimetics Beta-agonists (ritodrine, salbutamol and
terbutaline) are predominantly β2 adreno-receptor agonists),
which mediate myometrial relaxation by stimulating cyclic
adenyl monophospate (AMP) production.
2. Magnesium sulphate (muscle relaxant)
3. Non-steroidal anti-inflammatory drugs (Indomethacin for short
term use < 30 wks gestation)
4. Calcium channel blockers (Nifedipine)
5. Oxytocin receptor antagonists (OTR-A atosiban)
42.
43. 4. Antibiotics
- Given in case of :
1. Suspected or proved vaginal infection
2. ROM or established chorioamnionitis
10 days Erythromycin +/- Clindamycin or Metronidazole.
- The use of prophylactic antibiotics in uncomplicated
preterm labour before 37 weeks with intact membranes
did not confer any short-term neonatal benefit.
5. Pain killers
- Risk of placental retention / manual removal under anesthesia
6. Continuous (EFM).
• Because preterm infants have less reserve to tolerate the
stress of labour
7. Low threshold for CS (abnormal FHR Pattern, preterm
breech)
44. 8. Augment contractions
• After 24 weeks, if there is no evidence of acute maternal or
fetal compromise induction with milder prostaglandins +/-
conventional-dose oxytocin (precaution if history of uterine
surgery) can be considered as an alternative to a planned CS.
• If there is already clinical evidence of chorioamnionitis:
o Great care must be exercised.
o In these cases, delay in ending the pregnancy may lead to worsening
infection and consequent morbidity for both mother and baby.
o Augmenting labour may be the most appropriate management.
9. Emergency cervical cerclage
-Difficult if cervical dilatation >3 cm & effacement.
-Contraindicated:
1. Bleeding
2. Contractions
3. Infection
10. In utero transfer
47. 1. Early dating scan / accurate
2. Genital tract infection: Bacterial vaginosis
• early treatment of BV prior to 20 weeks gestation may lower the risk of late miscarriage
and early birth.
3. Asymptomatic bacteriuria:
• It carries an increased risk of preterm birth.
• Short courses of antibiotics based on culture sensitivities reduce the risk of
pyelonephritis and early delivery.
4. GBS genital colonization:
• Preterm infants are more susceptible to early-onset GBS infection, acquired during
passage through the birth canal.
• In women known to be at increased risk of early delivery, testing for GBS antenatally with
a combined low vaginal/rectal swab allows consideration of intrapartum prophylaxis.
• Attempts at antenatal eradication has repeatedly been shown to be of no benefit.
5. Fetal fibronectin : (at ≥ 22 weeks)
• Can only be undertaken after 23 weeks, as high levels may be physiological before then.
• In high-risk asymptomatic women:
o + test at 24 weeks gestation nearly half will deliver before 30 weeks gestation.
o - test the chance of such an early birth is less than 1 per cent with.
• This negative predictive value may be its main use, as interventions based upon positive
test results have not been shown to be helpful.
6. Tocolytics: no evidence of benefit from prophylactic or maintenance therapy with
conventional oral or intravenous tocolytics.
Management of high-risk asymptomatic women
48. 7. Progestational agents:
• Progesterone:
1. support of pregnancy through uterine quiescence.
2. it affects cervical ripening and mucous production.
3. have anti-inflammatory properties.
• It has a good safety profile when used in pregnancy.
• Using IM or intravaginal progesterone have shown some reductions in the incidence of
preterm birth.
8. Life style modification: may be helpful
• smoking cessation// sexual abstinence and/or psychological support: are no clearer.
9. Cervical length (TV/US):
• Cervical length can be accurately and repeatedly measured by TVUSS.
• In asymptomatic women with a short cervix, the risk of preterm delivery rises
dramatically with further decreases in length.
In the presence of a normal cervical length intervention can usually be deferred.
Short cervix at < 24 weeks can be managed by cervical cerclage.
When significant cervical shortening is found at or beyond 24 weeks:
1. women should be educated as to the signs and symptoms that should provoke
hospital attendance.
2. Prophylactic steroids should be considered.
3. vaginal progesterone reduces the risk of preterm delivery in cases where the cervix
is short.
10. Cerclage
Management of high-risk asymptomatic women, cont..
49. Elective cervical cerclage
• The procedure is usually performed at 12-14 wks
1. Elective cerclage may be advised solely based on a woman’s past
obstetric history.
• if history of 3 or more late miscarriage or very preterm deliveries.
2. In selective cerclage, surgery is based upon serial transvaginal ultrasound
measurements of cervical length.
• Cervical cerclage can be done under general or regional anaesthesia.
• Removed at:
1. 37 wks
2. if labour started at any time
3. If membrane ruptured
• McDonald’s technique , simple & quick (mersilene suture)
53. Case scenario
Manal is 34 years old lady, 29 weeks
twin gestation presented with history of
generalized mild abdominal pain & no
vaginal bleeding, , recurrent dampness,
decreased fetal movement, temperature =
37.2 0C
54. Differential diagnosis of watery vaginal discharge (gush of fluid)
1. ROM
2. Urine loss: incontinence and UTIs are both more common
in pregnancy
3. Vaginal infection
4. Leukorrhoea: the cervical glands often become overactive
during pregnancy
55. History of gush of
fluid
Dysuria,
frequency,
urgency &
incontinence
UTI
Whitish,
yellowish or
greenish
vaginal
discharge
± offensive
± itching
Vaginal
Infection
Colorless,
odourless
vaginal
discharge of
variable
amount &
not
associated
with pruritus
Leukorrhoea
Severe abd. Pain
, Fever,
tachycardia
Fetal
tachycardia
Offensive vag.
Discharge
Abdominal
tenderness
↑WBC & CRP
Chorioamnionitis
Recurrent dampness,
decreased fetal
movement
± pain
+
Sterile speculum
exam.
+
Investigation
ROM
56. Definitions
# PROM: It is the leakage of amniotic fluid beyond 37
weeks gestation, prior to the onset of labour (in
the absence of uterine contraction)
- Incidence: (8 %)
# PPROM: It is the leakage of amniotic fluid in the
absence of uterine activity in preterm pregnancy
(prior to 37 weeks)
- Incidence: (2 %)
57. • Latency Period: it is the time from membrane rupture until delivery
• from the onset of PPROM:
• 50% of women deliver within 1 week of PPROM.
• 75% within 2 weeks of PPROM.
• The earlier in pregnancy that PPROM occurs the shorter the
interval to delivery.
• Pregnancies complicated by PPROM prior to 23 weeks,
pulmonary hypoplasia may develop leading to an increased risk
of neonatal death.
• The presence of amniotic fluid greater than 2 cm on
ultrasound is associated with a lower incidence of
pulmonary hypoplasia.
58. Pathophysiology of PROM:
it is physiological condition:
- Apoptosis & Braxton Hicks contraction
- → ↑ stretching of the membranes
- → thinning focally & biochemical changes
- → membrane prolapse & rupture
61. History
• The most reliable diagnostic feature of PPROM from the history is the report of a
‘gush of fluid’ vaginally, usually followed by a more-or-less continuous dribble.
• The presence of any vaginal discharge should be ascertained.
• Fetal movements may be ↓ in strength or frequency after PPROM.
• occasionally uterine irritability or contractions may be reported.
Examiantion
1. General examination:
• Infection may lead to an increased pulse and temperature and a flushed appearance. .
2. Abdominal examination:
• may reveal a clinical suspicion of oligohydramnios
• uterine tenderness if chorioamnionitis is present.
3. Sterile Speculum examination:
• For definitive diagnosis of PPROM.
• It is done preferably after the patient has been resting supine for 20–30 minutes.
• A pool of amniotic fluid in the posterior vagina is diagnostic.
• Cough or fundal pressure leakage of liquor.
• It is also important at this point to visualize the cervix.
• Fluid may be seen trickling through the external os and dilatation can be assessed.
4. Vaginal examination:
• Digital vaginal examinations should be avoided if possible in PPROM,
as they are associated with a significant reduction in the latent interval before labour.
This reduction is most dramatic at the earliest gestations.
• Frequent vaginal examination should be avoided
62. • If a pregnant woman provides a clinical history highly
suspicious for PPROM, but diagnosis is not confirmed by initial
speculum exam, the woman can be placed in a semi-upright
position and reexamined after 1 hour to allow for vaginal
poring.
• As a last resort, if results are still equivocal, amniocentesis
with injection of indigo carmine dye may be performed.
• A tampon is placed and if any dye leaked from the cervix, a
blue staining would be noted on the tampon, confirming the
diagnosis of PPROM.
63. What investigations would be most helpful
and why?
1.Bed side tests:
* Nitrazine test:
o Amniotic fluid is alkaline, whereas the vaginal secretions are usually
acidic.
o An elevated pH turns a nitrazine stick black.
o Some units use nitrazine sticks to define the presence of amniotic
fluid.
o false positives occur with: blood, semen urine.
o However, the predictive value of a negative test is very high.
* Ferning test: microscopic dry smear of liquor
False positive: Cervical mucus
2.Genital tract swabs (specialized tests)
- HVS (high vaginal swab)
- Screening for GBS ( group B streptococcus)
Lower genital tract swabs are routinely taken, but cultures do not correlate
well with the risk of chorioamnionitis.
64. 3. Maternal well-being:
Conservative management includes intensive clinical surveillance for signs of
chorioamnionitis:
1. Regular recording of maternal temperature, heart rate or PR, blood pressure
2. serial white cell counts and C-reactive proteins as early markers of infection
4. Fetal well- being:
• Serial antepartum CTG is important after PPROM, as a gradually increasing
baseline heart rate or fetal tachycardia can be the first sign of intrauterine
infection.
5. US:
• Amniotic fluid volume, placental location, presentation & congenital
abnormality of the fetus, estimated fetal weight.
o Oligohydramnios offers supporting evidence for PPROM having occurred
butis not gold standard for the diagnosis.
o Normal or increased volume does not preclude the diagnosis.
• Unlike preterm labour, cervical length measurements do not have predictive
ability in PPROM.
6. Amniocentesis:
• A sample of amniotic fluid can be sent for Gram stain, microscopy and culture,
to establish whether there is an intrauterine infection (chorioamnionitis).
• There is, however, a risk of stimulating preterm labour by performing an
invasive test, and amniocentesis can be technically very difficult when there is
little amniotic fluid.
68. Treatment of PPROM
- It balances the risk of prematurity (if delivery is
encouraged) versus the risk of maternal and fetal
infection (if delivery is delayed) .
- Clinical management of PPROM is based on the
gestational age and mother-fetal condition :
1.Viability to 34 wks gestational age
2. 34 to 37 wks gestational age
69. PPROM before 34 weeks’ gestation
Conservative management in hospital is followed unless it is
contraindicated.
Conservative management include:
1. Hospital admission.
2. Close Fetal and maternal surveillance for Chorioamnionitis
/abruption/PTL/prolapse/non-reassuring fetal status ( either
with a nonstress test or biophysical profile).
3. Antenatal steroids –
i.m. betamethasone , 12 mg / 24 hours → 2 days Or
i.m. dexamethasone , 6 mg / 12 hours → 2 days
• There appears to be no increased risk of maternal infectious morbidity
from steroids administration.
• leukocytosis occurs after administration of steroid and may not be
representative of infection.
1. Viability to 34 wks gestational age
70. 1. Viability to 34 wks gestational age, cont..
4. Latency antibiotics.
• Administration of latency antibiotics:
1. improves neonatal outcomes.
2. ↓ RDS, NEC, neonatal sepsis, bronchopulmonary dysplasia, and pneumonia
3. ↑ latency interval.
4. Latency antibiotics along with antepartum steroids likely reduce perinatal
mortality.
• A typical antibiotic regimen includes 48 hours of intravenous ampicillin and
erythromycin, followed by 5 days of oral ampicillin and erythromycin.
• Ampicillin and amoxicillin cover GBS and provide gram-negative and some
anaerobic coverage.
• Erythromycin offers coverage of genital mycoplasma along with some coverage
of gram-positive cocci.
• Azithromycin, which has a better side effect profile than erythromycin, may be
used as an alternate macrolide.
• Amoxicillin-clavulanic acid should be avoided because of a possible increased
risk of NEC.
5. If there is cervical cerclage → removed
• PPROM at less than 23 weeks or greater than or equal to 32 weeks cerclage
should be removed immediately.
• For patients greater than or equal to 23 to less than 32 weeks cerclage should
either be removed immediately or after a 48-hr course of steroids.
71.
72. 6. Magnesium Administration
• For patients presenting with PPROM prior to 32 weeks, maternal administration
of magnesium sulfate may provide neuroprotective benefits for neonates.
• Pregnant women at risk for preterm delivery between 24 and 31 weeks because
of PPROM or advanced preterm labor who were randomized to magnesium
sulfate had a significantly lower risk of a child born with cerebral palsy.
• While protocols and dosing regimens may vary by center, administration of
magnesium sulfate for 24 hours, in the absence of maternal contraindications,
for patients presenting with PPROM prior to 32 weeks is a reasonable clinical
strategy.
• If a patient with PPROM is not at risk of imminent delivery 24 hours after
presentation, magnesium may be discontinued.
Induction of labour / at 34 weeks (if possible).
Immediate induction if ( contraindications for conservative management):
1. Chorioamnionitis.
2. Active labour
3. Non reassuring fetal heart tracing
4. Significant abruption
5. Cord prolapse
1. Viability to 34 wks gestational age, cont..
73. 2. 34 to 37 wks gestational age
PPROM greater than or equal to 34 weeks delivery is
recommended, because the fetal and maternal risks of
prolonging pregnancy outweigh fetal benefits of expectant
management.
• However, in remote locations without intensive neonatal care,
expectant management may be warranted up until 36 weeks.
PROM after 37 weeks’ gestation and labour has not already
begun Immediate induction of labour is advised by
oxytocin (iv) or PG vaginally or within 12 hours.
74. Chorioamnionitis:
It is an infection of chorion & amnion with an elevation
of temperature ≥ 38 ͦ C (> 100°F) with at least 2 of the
followings:
- Maternal PR ≥ 100 bpm
- FHR ≥ 160 bpm
- ↑CRP, ↑WBC
- Uterine tenderness
- Offensive vaginal discharge
75. - If chorioamnionitis is present, antibiotic (Ampicillin or
Erythromycin as prophylaxis ) & delivery are indicated
- If chorioamnionitis is not present antibiotic therapy
can significantly delay delivery
-Tocolysis is contraindicated due to the increased risk
of maternal and fetal infection in patients with PPROM.
In the majority of cases of PPROM there is time for
administration of corticosteroids and in utero transfer
before the onset of PTL.
- Amnio – infusion
76. Prediction of preterm delivery
• Past obstetric history
• Ultrasound measurement of cervical length
• Prevention of preterm delivery
1. Progesterone uterine quiescence and inhibit the production
of proinflammatory cytokines and PGs within the uterus
2. Cervical cerclage the cervix shortens (usually <25 mm) in
women with a history of cervical surgery or previous preterm
birth (ultrasound indicated cerclage); or when the cervix is
dilating in the absence of contractions (rescue cerclage).