1) The document discusses the management of pre-eclampsia and eclampsia. It outlines goals of treatment, definitions, assessments, and principles of management including controlling blood pressure, preventing seizures with magnesium sulfate, fluid management, and timing of delivery.
2) Magnesium sulfate is the primary treatment for preventing and controlling seizures, with protocols for loading doses and maintenance doses as well as monitoring for toxicity.
3) Management involves strict fluid balance, blood pressure control with antihypertensive medications, fetal monitoring, and timely delivery once the mother is stabilized. Close monitoring is needed after delivery to watch for recurrence of seizures.
Please find the power point on Puerperal sepsis. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Pregnancy induced hypertension introduction
Classification of pregnancy induced hypertension
Preeclampsia -
Definition
Criteria for diagnosis of preeclampsia,
Epidemiology of preeclampsia,
Risk factors of preeclampsia,
Pathogenesis of preeclampsia,
Pathophysiology of preeclampsia,
Course of preeclampsia,
Complications of preeclampsia,
What is HELLP ?
Management of preeclampsia at home, at hospital, during labour, during puerperium,
Management of acute fulminant preeclampsia
INTRODUCTION
DEFINITION
TYPES
CAUSES
MANAGEMENT-Management of 3rd stage bleeding
Actual management
MANAGEMENT OF 3RD STAGE BLEEDING
Steps of management
1. Placental site bleeding-
To palpate the fundus and massage the uterus to make it hard. The massage is to be done by placing four fingers behind the uterus and thumb in front.
To start crystalloid solution (NS or RL) with oxytocin (1L with 20 units) at 60 drops per minute and to arrange for blood transfusion if necessary.
Oxytocin 10 unit IM or methergine 0.2 mg is given intravenously.
To catheterize the bladder.
To give antibiotics (Ampicillin 2gm and Metronidazole 500mg IV)
2. Management of traumatic bleed
The uterovaginal canal is to be explored under general anesthesia after the placenta is expelled and haemostatic sutures are placed on the offending sites.
STEPS OF MANUAL REMOVAL OF PLACENTA
The patient is placed in lithotomy position. With all aseptic measures, the bladder is catheterized.
One hand is introduced into the uterus in cone shaped manner following the cord. While introducing the hand, the labia are separated by the fingers at the other hand.
Counter pressure on the uterine fundus is applied by the hand placed over the abdomens. The abdominal hand should steady the fundus and guide the movement of the fingers inside the uterine cavity till the placenta is completely separated.
Please find the power point on Puerperal sepsis. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Pregnancy induced hypertension introduction
Classification of pregnancy induced hypertension
Preeclampsia -
Definition
Criteria for diagnosis of preeclampsia,
Epidemiology of preeclampsia,
Risk factors of preeclampsia,
Pathogenesis of preeclampsia,
Pathophysiology of preeclampsia,
Course of preeclampsia,
Complications of preeclampsia,
What is HELLP ?
Management of preeclampsia at home, at hospital, during labour, during puerperium,
Management of acute fulminant preeclampsia
INTRODUCTION
DEFINITION
TYPES
CAUSES
MANAGEMENT-Management of 3rd stage bleeding
Actual management
MANAGEMENT OF 3RD STAGE BLEEDING
Steps of management
1. Placental site bleeding-
To palpate the fundus and massage the uterus to make it hard. The massage is to be done by placing four fingers behind the uterus and thumb in front.
To start crystalloid solution (NS or RL) with oxytocin (1L with 20 units) at 60 drops per minute and to arrange for blood transfusion if necessary.
Oxytocin 10 unit IM or methergine 0.2 mg is given intravenously.
To catheterize the bladder.
To give antibiotics (Ampicillin 2gm and Metronidazole 500mg IV)
2. Management of traumatic bleed
The uterovaginal canal is to be explored under general anesthesia after the placenta is expelled and haemostatic sutures are placed on the offending sites.
STEPS OF MANUAL REMOVAL OF PLACENTA
The patient is placed in lithotomy position. With all aseptic measures, the bladder is catheterized.
One hand is introduced into the uterus in cone shaped manner following the cord. While introducing the hand, the labia are separated by the fingers at the other hand.
Counter pressure on the uterine fundus is applied by the hand placed over the abdomens. The abdominal hand should steady the fundus and guide the movement of the fingers inside the uterine cavity till the placenta is completely separated.
Obstetric emergency which can kill instantly !! - PPH presenting to ED, so what is the role of Emergency Dept ? The most basic presentation of Obstetric emergency and how to tackle it? Being an emergency physician, obstetrics is always challenging! Keep yourself updated with Obstetric emergency.
Miscarriage is pregnancy loss before 22 weeks’ gestation based on the LMP or if gestation age is unknown, it is the loss of an embryo or a fetus of less than 500g.
Evaluation and options in Managing Subfertile CoupleEddie Lim
Subfertility - Failure to conceive within 12 months of
regular sexual intercourse without any form
of contraception.
Woman older than 35 years -- have not
conceived during a 6-month period of trying.
Endometrial hyperplasia - irregular proliferation of the endometrial glands with an increase in the gland to stroma ratio when compared with proliferative endometrium
Endometrial Ca - most common gynaecological maglinancy in the western country, endometrial hyperplasia as the precursor
Incidence of endometrial hyperplasia 3 folds higher than endometrial Ca
Fourth most common cancer in women in Peninsular Malaysia
Abnormal uterine bleeding can occur when a woman experiences a change in menstrual loss, or the degree of loss or vaginal bleeding pattern differs from that experienced by the age-matched general female population
AUB is not restricted to menstrual bleeding that is abnormally heavy, but includes bleeding that is abnormal in TIMING
Hypertensive Disorders in Pregnancy (HDP) represented 15.4% of total numbers of maternal death- the 4th main cause after obstetric embolism, PPH and other medical non HDP conditions
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
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
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.
Follow us on: Pinterest
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
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stock
Telegram: bmksupplier
signal: +85264872720
threema: TUD4A6YC
You can contact me on Telegram or Threema
Communicate promptly and reply
Free of customs clearance, Double Clearance 100% pass delivery to USA, Canada, Spain, Germany, Netherland, Poland, Italy, Sweden, UK, Czech Republic, Australia, Mexico, Russia, Ukraine, Kazakhstan.Door to door service
Hot Selling Organic intermediates
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
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. GOALS
1. Adequate treatment of hypertension
2. To identify, diagnose and manage PE
3. Management of eclampsia patient
3. CLASSIFICATION
Classification Characteristics
1) Pregnancy-induced HPT @ Gestational HPT
PIH HPT only
PE HPT + proteinuria
Eclampsia
2) Chronic HPT HPT < 20 weeks @ before
pregnancy
3) Chronic HPT with superimposed PE/Eclampsia
4) Unclassified HPT HPT >20 weeks with no
BP recorded before 20
weeks
Based on ISSHP 2001 (International Society for Study of Hypertension in
Pregnancy)
4. DEFINITION – PRE-ECLAMPSIA
A multisystem disorder
Develops after 20 weeks of gestation
With
Hypertension ≥ 140/ 90 (2x readings 4 - 6 hours apart with
rest in between)
Systolic BP ≥ 30mmHg @
Diastolic BP ≥ 15 mmHg
- from the antenatal booking BP
Proteinuria Urine dipstick for protein : ≥ 2+
24 hour urine albumin ≥ 300 mg
5. WHY IS PE IMPORTANT?
Maternal Complications Hypertension
Risk of Cerebrovascular accident e.g. stroke
Pulmonary oedema
Renal failure
Liver failure
DIVC
Placenta abruptio
Eclampsia (Risk of aspiration pnuemonia)
Fetal Complications Prematurity
IUGR
IUD
Acute fetal distress
6. ASSESSMENT OF SEVERE PE
History including symptoms of impending eclampsia
Headache
Blurring of vision
Epigastric pain
Examination including
BP & PR
Reflexes (Brisk)
7. Investigations
If suspected UTI : UFEME + Urine C&S
Blood Urine
1) FBC (esp. platelet)
2) BUSE
3) Se Creatinine & Uric
acid
4) LFT
5) PT/APTT
6) Group & Save (GSH)
1) Urine albumin/protein (dipstick or
UFEME)
*24h urine collection – usually done if urine
albumin + or 2+ (not needed if clear cut PE)
8. Observation
MATERNAL FETAL
- SYMPTOM
- BP, PR
- REFLEXES + CLONUS
- URINE PROTEIN
- URINE OUTPUT
-CTG
-ULTRASOUND
-DOPPLER (IF INDICATED)
Designate one to one midwifery care
Transfer to Labour Ward when stable
9. Control BP (anti-hypertensives)
Prevent seizures (MgSO4)
Fluid management
Maternal and fetal monitoring
Decide on mode & timing of delivery
PRINCIPLES OF MANAGEMENT
10. 1. CONTROL BP
Acute hypertensive crisis
Systolic BP ≥ 180 mmHg
Diastolic BP ≥ 110 mmHg
Mean arterial pressure ≥ 125mmHg
Persistent hypertension
BP ≥ 160/100 mm Hg
Acute HPT crisis Persistent HPT
IV labetalol
IV hydralazine
IV GTN
T. Labetalol
T. Methyldopa
T. Nifedipine
11. Avoid too rapid fall in BP
Continuous FHR monitoring
TARGET BP…
SBP < 150, DBP 80-100 mmHG
If end organ damage, aim for 140/90 mmHg
12. CLINIC SETTING – PE
Hypertension + proteinuria – refer to Dr. in MCH stat @
refer directly to SGH (do not wait for an appointment)
Any proteinuria with hypertension should be referred
irregardless of whether the patient has UTI or not
If urine FEME shows UTI picture – there can be a proteinuria of 1+
or 2+. Do not assume proteinuria of 3+ to 4+ is due to UTI.
13. 2. PREVENT SEIZURE/ ECLAMPSIA
Seizures usually occurring in women with PIH/PE not
due to other causes (e.g. epilepsy, brain tumour)
Any seizures occurring in pregnancy is usually treated
as eclampsia until proven otherwise
Antenatally 38%
Intrapartum 18%
Postpartum 44% (especially the first 24 hours)
14. MANAGEMENT FOR ECLAMPSIA ??
Do not leave patient alone
Call for HELP
DR ABC—left lateral position, if supine, turn the patient’s
head to the side
Airway (e.g. guedel mouthpiece, prevent tongue biting)
Breathing
Circulation
Obtain IV access (2x, large bore (14-16G))
Control seizure – Mg SO4
Control HPT
Deliver once stable
15. Seizures are usually self limiting
MGSO4 is the ANTICONVULSANT of choice
Both in controlling as well as in preventing seizure
IV diazepam is NOT the drug of choice unless MgSO4 is not
available.
Avoid poly-pharmacy to treat seizures, as this
increases the risk of respiratory arrest
16. Protocol
Loading dose of MGSO4 (4 gm over 10-15 minutes)
8 mls of MgSO4 dilute in 12 mls of N/S (20 cc syringe)
Followed by maintenance dose of 1 gm/hr
50 mls (10 ampoules) in 500 mls N/S @ Hartmann’s solution
Give at 21 mls/hr (1g/hour)
Usually continued for 24 hours after delivery or after the last
convulsion (not 24 hours after starting MgSO4)
Important : Rapid/bolus injection of MgSO4 can cause
cardiorespiratory arrest! Be careful!
17. If no IV access, can administer MgSO4 through deep
intramuscular route:
Loading dose : IM MgSO4 5g (10ml) in each buttock (10g total) @
IV 4g over 10-15min
Maintenance : IM MgSO4 5g every 4 hourly
Extremely painful, risk of gluteal abscess
Addition of 1ml of 1% xylocaine to the solution may help to
reduce the pain at the injection site
18. 3. MONITORING WHEN ON MGSO4
Hourly monitoring
Patellar Reflexes should be present
Earliest sign if toxicity develops
Respiratory Rate >12-16 bpm
Urine Output > 30 mls/h (@ 100mls/4 hours)
Ensure MgSO4 is excreted through the kidneys
MgSO4 does not cause renal impairment/failure
Oxygen saturation
19. MANAGEMENT OF MGSO4 TOXICITY
Urine output <100ml/4hr @ <30mls/hr
May challenge with 250cc of Hartman solution
If no clinical signs of magnesium toxicity, reduce rate
to 0.5gm/hrs
Absent patellar reflexes
Stop MgSO4 infusion
May resume if patellar reflexes return
20. Respiratory depression
Stop MgSO4 infusion
Give oxygen and monitor closely
Respiratory arrest / Cardiac arrest
Resuscitate---CPR, intubate and ventilate immediately
Stop MgSO4 infusion stat
ANTIDOTE : IV Calcium gluconate
10% Calcium Gluconate 10ml IV over 3-5 minutes
21. MANAGEMENT OF RECURRENT SEIZURES
Seizures continue or recur
Give a 2nd bolus dose of MgSO4
Over 10 to 15 minutes
2g if < 70kg and 4g if > 70kg
Check deep tendon reflex & RR before repeating dose
22. What if seizures continues despite further bolus dose of
MgSO4?
Options include: DIAZEPAM (10mg) or
THIOPENTONE (50mg IV)
Intubation then becomes necessary in such women to
protect the airway and ensure adequate oxygenation.
FURTHER SEIZURES SHOULD BE MANAGED BY
INTERMITTENT POSITIVE PRESSURE VENTILATION AND
MUSCLE RELAXATION (anaesthetist)
CT Scan Brain to assess for intracerebral bleeding
23. 4.MANAGEMENT OF FLUID BALANCE
BEWARE: Iatrogenic fluid overload in PE/ eclampsia
Due to damage endothelial linings of the capillary - 3rd space fluid
loss
Can cause pulmonary edema
Strict I/O chart
Maintain crystallloid fluid (N/S & Hartman)
Total fluid/day : 80 mls/H (1ml/kg/H)
Includes all fluid given (e.g IVD, IV drugs)
Diuretics--only if confirmed pulmonary oedema
Selective CVP use
24. 5. DELIVERY
Delivery is decided based on:
Patient’s condition (Clinical/Biochemical)
Gestational age
In severe pre-eclampsia or eclampsia, the definitive
treatment is delivery
However, it is inappropriate to delivery an unstable
mother even if there is fetal distress.
25. If delivery to be delayed and gestation less than 34
weeks
IM Dexamethasone 6mg 12 hours apart for 48 hours or 12
mg bd for 1 day
Close monitoring
Either IOL @ Caesarean section depending on situation
Avoid ergometrine in 3rd stage
26. High dependency care for the first 24 to 48 hours after
delivery
One-to-one care
Anti-hypertensive reduce in a step-wise fashion
Close attention to fluid balance
Contraception and spacing
Future pregnancy plan- early booking & aspirin
Post delivery care
27. Maintain vigilance as majority of eclamptic seizures
occur after delivery
Reduce anti-hypertensive medications as indicated
Repeat Investigations (FBC, clotting screen, liver function
test, urea and electrolytes) 6-12 hrly if indicated
29. Comprising of Haemolysis, Elevated liver enzymes and Low
platelets syndrome (4 to 12 % of severe pre eclampsia patients)
Hypertension not always a clinical feature.
Can present with vague symptoms of nausea ,vomiting,
epigastric pain & right upper quadrant pain, because of this
there is delay in diagnosis.
Management of HELLP as for severe pre eclampsia is to
evaluate,stabilize and deliver