Venous Thromboembolism (VTE) refers to deep vein thrombosis (DVT) and pulmonary embolism (PE). Pregnancy is a risk factor for VTE due to physiological changes in the coagulation system that promote clotting. The risk is highest in the first trimester through 6 weeks postpartum. Management involves risk assessment, diagnosis, anticoagulation therapy like heparin, prevention through prophylaxis for high risk women, and consideration of risk factors when stopping treatment.
Sickle cell anemia is an autosome linked recessive trait that can be transmitted from parents to the offspring when
both the partners are carrier for the gene (or heterozygous). The disease is controlled by a single pair of allele, HbA
and HbS. Out of the three possible genotypes only homozygous individuals for HbS (HbS, HbS) show the diseased phenotype. The ability to predict the clinical course of SCD during pregnancy is difficult. It is mandatory to follow up the patient closely from the very beginning i.e. from preconception to antenatal till labor. SCD is associated with both maternal and fetal complications and is associated with an increased incidence of perinatal mortality, premature
labor, fetal growth restriction and acute painful crises during pregnancy.
Seizures during pregnancy can cause: Slowing of the fetal heart rate. Decreased oxygen to the fetus. Fetal injury, premature separation of the placenta from the uterus (placental abruption) or miscarriage due to trauma, such as a fall, during a seizure
Sickle cell anemia is an autosome linked recessive trait that can be transmitted from parents to the offspring when
both the partners are carrier for the gene (or heterozygous). The disease is controlled by a single pair of allele, HbA
and HbS. Out of the three possible genotypes only homozygous individuals for HbS (HbS, HbS) show the diseased phenotype. The ability to predict the clinical course of SCD during pregnancy is difficult. It is mandatory to follow up the patient closely from the very beginning i.e. from preconception to antenatal till labor. SCD is associated with both maternal and fetal complications and is associated with an increased incidence of perinatal mortality, premature
labor, fetal growth restriction and acute painful crises during pregnancy.
Seizures during pregnancy can cause: Slowing of the fetal heart rate. Decreased oxygen to the fetus. Fetal injury, premature separation of the placenta from the uterus (placental abruption) or miscarriage due to trauma, such as a fall, during a seizure
Thromboprophylaxis in pregnancy and puerperiumManju Puri
This presentation is about thromboprophylaxis in pregnancy and puerperium and describes the risk assessment , indications, drugs to be used, when to start, for how long to continue.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
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
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.
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.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
- 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
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.
3. Introduction
One of the many early physiological adaptations of
pregnancy involves changes in the coagulation system,
which promote coagulation and impair fibrinolysis. The
physiological goal is to prepare for the haemostatic
challenge of delivery. A ‘side effect’ of this change is an
increased risk of thrombosis. All pregnant women are
therefore at risk of thrombosis, compared with non-
pregnant women. This risk is manifest from early in the
first trimester until 4−6 weeks post partum.
5. PHYSIOLOGICAL CHANGES IN THE
COAGULATION SYSTEM DURING PREGNANCY
These changes, which may not completely return to baseline until more than 8 weeks post partum, begin at
conception.
6. RISK FACTORS FOR VTE IN PREGNANCY
In some women the risks are increased further
because they have one or more additional risk
factors.
So pregnant women should have a risk assessment
for VTE to include the risk factor as listed.
This risk is not static and should be reconsidered in
any case.
A careful hx should be taken from the woman of
any prior or family hx of thromboembolic events.
8. Clinical Presentation
Type Signs and Symptoms
Pulmonary embolism • Dyspnea
• Palpitations
• Pleuritic chest pain
• Hemoptysis
• Cyanosis/hypoxia in massive PE
• Tachycardia
• Tachypnea
• Hypotension
• Collapse
• +/- symptoms or signs of DVT
Deep vein thrombosis • DVT in pregnancy usually proximal
• Unilateral leg pain/tenderness
• Swelling in an extremity
• Increase calf/thigh circumference
• Increased temperature
• Prominent superficial veins
• Pitting edema
9. Differential Diagnosis
• DVT: swelling and lower leg discomfort are
not unusual in a normal pregnancy. Other
possibilities include muscle strain, a ruptured
Baker’s cyst, cellulitis, superficial
thrombophlebitis, ruptured plantaris tendon
and trauma.
• PE: potentially extensive but specifically rule
out chest infection and an intra-abdominal
bleed (look for abdominal signs, shoulder tip
pain from diaphragmatic irritation and a low
JVP).
10.
11.
12.
13.
14. Management
Massive life treatening PE
• Management by an experienced multidisciplinary team
involving senior obstetrician,physicians and radiologist
for collapsed,shock patient.
• An urgent portable echocardiogram should be
arranged within one hour presentation.
• Immediate thrombolysis should be considered when
massive PE is confirmed or extensive circumstance
occur.
• IV unfractionated heparin.
15. General points
• In a woman with a past history of VTE or with a known inherited
thrombophilia, it is best to refer her prior to a planned pregnancy
for optimum prophylaxis throughout the pregnancy.
• Medical anticoagulation is the treatment of choice for acute VTE.
Subsequently, surgical interventions may be considered
• Anticoagulation is by far the most common treatment option.
Heparin is the most frequently used drug, being non-toxic to the
fetus (it does not cross the placental barrier). However, its main
disadvantages are that it has to be parentally administered and, in
the long-term, may give rise to heparin-induced osteoporosis and
thrombocytopenia. In some patients, it can also provoke a painful,
localized allergic reaction on administration.
• Warfarin is the other treatment option in the postnatal patient but
it must be avoided antenatally, as it is teratogenic and can also
cause placental abruption and fetal/neonatal hemorrhage.
• In clinically suspected DVT or PE, treatment with unfractionated
heparin or LMWH should be given until the diagnosis is excluded.
16. Initiating treatment
There are several different types of heparin to choose from:
• LMWH: this is the drug of choice. It has been shown to be
more effective than unfractionated heparin with lower
mortality and fewer hemorrhagic complications in the
initial treatment of DVT in non-pregnant subjects.
• Intravenous unfractionated heparin: this is an extensively
used drug in the acute management of VTE, particularly
massive PE with cardiovascular compromise
• Subcutaneous unfractionated heparin: this has been shown
to be as effective as the intravenous form.
• Additionally, the leg should be elevated and a graduated
elastic compression stocking applied to reduce edema.
Mobilization with graduated elastic compression stockings
should be encouraged.
17. Maintenance therapy
Pregnancy
• Heparins are the maintenance treatment of choice.
• Subcutaneous LMWH appears to have advantages over aPTT-
monitored unfractionated heparin in the maintenance treatment of
VTE in pregnancy. Women should be taught to self-inject and can then
be managed as outpatients until delivery.
• If unfractionated heparin is used, monitor the platelet count at least
every other day for the first 14 days or until treatment is stopped
(whichever comes first).
• Seek specialist advice if the patient develops heparin-induced
thrombocytopenia or a heparin allergy and requires continuing
anticoagulant therapy. She should be managed with the heparinoid,
danaparoid sodium or fondaparinux, under specialist supervision.
18. Labour
• When the patient thinks she is going into labour, she should stop injecting and get
in touch with the delivery ward staff that will manage the anticoagulation
throughout labour and immediately post-delivery. Alternatively, planned elective
induction of labour or caesarean section at least 12 hours after prophylactic-dose
LMWH or 24 hours after therapeutic-dose LMWH can be considered. As these
patients are at high risk of hemorrhage, they will be managed with intravenous
unfractionated heparin throughout this time. Regional anaesthetic or analgesic
techniques should not be undertaken until at least 24 hours after the last dose of
therapeutic LMWH.
Postpartum
• Depending on the patient's individual circumstances, she may be managed with
ongoing heparin treatment or warfarin postpartum. If she opts for warfarin, this
needs to be avoided until at least day three postpartum with an INR check at day
two of warfarin treatment: aim for an INR between 2 and 3. Continue heparin
treatment until there have been two successive readings of an INR >2. Although
these drugs are detectable in breast milk, all are safe for use during breast-feeding
because warfarin metabolites are inactive and heparin is not absorbed through the
gastrointestinal tract.
• Postnatal review for women who develop VTE during pregnancy or the puerperium
should, whenever possible, be at an obstetric medicine clinic or a joint obstetric
hematology clinic.
19. Stopping treatment
• In theory, therapy should be continued for six
months as would be the case for non-pregnant
patients. However, the postpartum state is a
period of physiological fluctuation of coagulation
factors. Therefore, current advice is to continue
therapy for at least 6-12 weeks postpartum or
until at least three months of therapy have been
completed. At that point, the patient should be
assessed for the presence of ongoing risk factors
for a VTE prior to making the decision to stop
anticoagulation therapy.
20. Prevention: prophylaxis
Guidance from the Royal College of Obstetricians and Gynecologists’
suggests:Antenatally
• Regardless of their VTE risk, dehydration and immobilization of the patient should be avoided
throughout pregnancy.
• Women at high risk of VTE in pregnancy should be offered pre-pregnancy counseling and a
prospective management plan for thromboprophylaxis in pregnancy. Those who become
pregnant before receiving such counseling should be referred to a nominated expert early in
pregnancy.
• All women with previous VTE should receive postpartum prophylaxis, as this is the time of
highest risk.
• In addition, women whose original VTE was unprovoked, idiopathic or related to estrogen, or
who have other risk factors, a family history of VTE in a first-degree relative or a documented
thrombophilia require LMWH antenatally and for six weeks postpartum.
• Women with recurrent VTE may already be on warfarin. They should be advised to stop
warfarin and change to LMWH as soon as pregnancy is confirmed, ideally within two weeks
of the missed period and before the sixth week of pregnancy. Women not on warfarin should
be advised to start LMWH as soon as they have a positive pregnancy test.
• Women with asymptomatic inherited or acquired thrombophilia only, may be managed with
close surveillance antenatally and be considered for LMWH for at least seven days
postpartum. Exceptions are women with antithrombin deficiency, those with more than one
thrombophilic defect (including homozygosity for factor V Leiden) or those with additional
risk factors where antenatal prophylaxis should be considered.
21. Intrapartum
• Women taking LMWH should be advised that, if they bleed
vaginally or contractions begin, they should not inject any further
doses. They should be assessed in hospital and further doses be
prescribed by medical staff.
Postpartum
• All women with obesity (BMI greater than 40 kg/m2) should be
considered for prophylactic LMWH for seven days after delivery.
Other postnatal risks include prolonged labour, immobility,
infection, hemorrhage and blood transfusion.
• All women who have had an emergency Caesarean section should
be considered for LMWH for seven days after delivery. All women
who have had an elective caesarean section who have one or more
additional risk factors should be considered for LMWH for seven
days after delivery.
• In addition, properly applied graduated compression stockings are
recommended for women travelling long-distance for more than
four hours, women who are still outpatients but have prior VTE
(usually combined with LMWH), women who are hospitalized and
have a contra-indication to LMWH and those who are hospitalized
post-caesarean section (combined with LMWH) and considered to
be at particularly high risk of VTE.