This document discusses obstetric shock, its causes, signs, stages, and management. Shock is a life-threatening medical emergency characterized by inadequate tissue perfusion and oxygenation. The major causes of obstetric shock are hemorrhage, sepsis, cardiogenic issues, neurogenic issues, and anaphylaxis. Untreated shock progresses through compensated, decompensated, and irreversible stages. Initial management focuses on airway, breathing, circulation, oxygenation, intravenous fluids, blood transfusion, and identifying and treating the underlying cause. Prompt recognition and treatment of obstetric shock can improve maternal and fetal outcomes.
This topic contains definition, meaning, classification, pathophysiology, clinical menifestations, metabolic and general changes, management of obstetrical shock
Cord prolapse is a frightening and life-threatening event that occurs in labor. Rapid identification and immediate appropriate response may well save the life of a neonate. Therefore, clinicians should be knowledgeable in its recognition and management.
When fetal head is delivered, but shoulders are stuck and cannot be delivered it is known as shoulder dystocia.
The anterior shoulder becomes trapped behind on the symphysis pubis, whilst the posterior shoulder may be in the hollow of the sacrum or high above the sacral promontory.
This topic contains definition, meaning, classification, pathophysiology, clinical menifestations, metabolic and general changes, management of obstetrical shock
Cord prolapse is a frightening and life-threatening event that occurs in labor. Rapid identification and immediate appropriate response may well save the life of a neonate. Therefore, clinicians should be knowledgeable in its recognition and management.
When fetal head is delivered, but shoulders are stuck and cannot be delivered it is known as shoulder dystocia.
The anterior shoulder becomes trapped behind on the symphysis pubis, whilst the posterior shoulder may be in the hollow of the sacrum or high above the sacral promontory.
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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.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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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.
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.
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Obstetrical shock
1. Prof. M.C.Bansal
MBBS,MS,MICOG,FICOG
Professor OBGY
Ex-Principal & Controller
Jhalawar Medical College &
Hospital
Mahatma Gandhi Medical
College, Jaipur.
2. Shock is a critical condition and a life
threatening medical emergency.
Shock results from acute , generalised
, inadequate perfusion of tissues; below that
needed to deliver the oxygen and nutrients for
normal function.
Prompt recognition and management can
improve maternal and fetal outcome in
obstetrical shock.
4. Untreated shock progresses through three stages.
Stage1 Compensated --Fall in BP and cardiac
output is compensated by adjustment of
homeostatic mechanism, if cause removed –iv
fluid therapy it is reversible.
Stage2 Decompensate--Maximal compensatory
mechanism are acting but tissue perfusion is
reduced. Vital organ(cerebral , renal, myocardial)
function reduced.
Stage3 Irreversible--Vital organ perfusion badly
impaired. Acute tubular necrosis , severe
acidosis, decreased myocardial perfusion and
contractility the profound decrease in
perfusion leads to cellular death & Organ failure.
5. A high index of suspicion and physical signs of
inadequate perfusion and oxygenation are the
basis of initiating prompt treatment.
Initial management does not rely on knowledge
of the underlying cause.
There are no laboratory tests for shock.
Basic investigations should be sent
e.g.Hb,BT,CT,PCV. Blood for grouping and
cross matching , FB Sugar , routine urine
analysis.
6. Shocked pt requires teamwork--Senior
anaesthetist , obstetrician , physician and
hematologist are to be summoned
immediately.
Obstetrical units should have established
protocols for dealing with shock.
Practice ―FIRE DRILL‖.
MOET,ALSO training courses for individuals
and team.
Active management of shock should start as
soon as it is suspected or expected aiming for
prompt restoration of tissue perfusion and
oxygenation.
7. Resuscitation follows---ABC
A Airway--Patent airway is assured and high
pressure oxygen (15 l/min)using mask/intra tracheal
intubation and anaesthesia machine.
B Breathing--Ventilation checked and supported if
needed .
C Circulation--1 Insert two wide bore cannulas
2 Restore blood volume and
reverse hypotension with
crystalloids/colloids.
3 Initial request for4-6 units of blood
should be sent. O Rh negative
blood may be transfused
8. Monitor the response to therapy - Pulse , BP
, SPO2 /pulse oxymetry, urine output & its pH .
Position of patient - Head down and left lateral
tilt to avoid aortocaval compression which
may further worsen the hypotension.
Vasoactive drugs (inotropes and vasopressors)
are considered if the cause of shock is thought
to be due to myocardial depression or profound
vasodilatation.
These drugs have no part in hypovolumic
shock.
9. Pregnancy produces a hyperdynamic , hypervolaemic
, maternal circulation.
This serves the purpose of saving mother against
haemorrhage to some extent.
Cardiac output increases by 50% , blood volume by
45% reaching a peak at 32-34 wks.
30% loss of fluid may be tolerated without any
tachycardia.
Aortocaval compression aggravates the unstability
seen in haemorrhage.
In antenatal period , uteroplacental hypoperfusion may
occur before maternal signs are evident . Adversely
affects on fetal well-being , can be detected FHR
abnormalities on cardiotocograph.
11. The diagnosis of underlying cause and
definitive treatment is initiated once
resuscitation is under way.
Surgical/ obstetrical--- ectopic
pregnancy, abortion, uterine perforation
,APH, uterine rupture. PPH, inversion of
uterus.
12. A. CELL SALVAGE
Auto transfusion with salvaged red cells avoids the
hazards of homologous transfusion. Blood is removed
from operative site through heparinised suction tubing
and a filter collecting reservoir and processed by
washing and centrifugation to remove contaminating
debris.
The resulting RBC have a haematocrit of 55-80 % and
can be returned to patient quickly.
The risk of amniotic fluid is obviously a concern. Use of
separate suction for amniotic fluid and leukocyte
depletion filter has been found in removing fetal
component from the salvaged blood.
13. Disadvantages of salvaged cell transfusion-
1 Units have capital and maintenance cost.
2 Staff require training and regular
CME/workshops to update itself.
3 Technique is of no use in PPH as faecal and
urine contamination with blood.
14. B.RECOMBINANT ACTIVATED FACTOR VII
rFVIIa promotes clot formation through its
action at many stages in clotting cascade. It
forms a complex with tissue factor a key
initiator in homeostasis, leading to production
of small amount of thrombin and activating
factor V ,VII and platelet aggregation at the site
of injury. Hence aids inconversion of
fibrinogen in to fibrin and formation of clot.
C.PELVIC ARTERIAL EMBOLISATION
15.
16. The failure of heart to provide adequate output
leads to tissue under perfusion.
Back pressure on lungs leads to Pulmonary edema.
Pregnancy puts progressive strain on cardiac
function as pregnancy progresses , the peak being
between 32-34 wks.
Pre existing cardiac disease further increases the
risk.
Cardiac related death are 2nd most common causes
of death in pregnancy and commoner than the
direct leading cause , thromboembolism.
17. Early diagnosis of cardiac lesion.
Surgical correction of operable cardiac lesion
, before pregnancy is planned.
Medical control of decompensated cardiac lesion
by cardiac correction before pregnancy is planned.
Avoiding Pregnancy/MTP at 6-8 wks if cardiac
condition is not under control.
Management of pregnancy in such patients by the
expert team of cardiologist and obstetrician .
Initial Rx of shock is similar , further Rx depends
on cardiac lesionBy the team present in cardiac
ICU
18.
19. Definition - A serious allergic reaction that is
rapid in onset and may result in death.
Aetiology - Pharmacological agents ,insect
stings, foods , latex may trigger
ANAPHYLAXIS
20. Pathophysiology - An exaggerated
immunological response to antigen to which an
individual has been previously sensitized. It is
a type 1 hypersensitivity (IgE mediated)
response causing breakdown and degradation
of mast cells and basophils releasing mediators
(Histamine , Serotonin, Bradikynin ,
Thromboxane , tryptase and leukotrienes) into
plasma . These substances cause increased
mucous membranes secretions , increased
capillary permeability and leakage , marked
vasodilatation and bronchospasm.
22. Symptoms and signs -
4. Gastrointestinal -
nausea , vomiting , abdominal pain .
5. C N S -
Hypotension causes collapse with/without
unconsciousness , dizziness , incontinence
, confusion and throbbing headache .
23. 1. Basic shock management ABC
2. Circulatory management
3. Primary (Special aspect)
- Stop administration of suspected substance
and call for help.
- Subcutaneous 1ml injection of diluted
Adrenaline (1:1000)
- Early intra tracheal intubation-airway edema
will make it problematic later.
- Supine/trendelenberg position with raised
legs increases venous return.
- Start vasopressor drugs and monitor BP.
Rapid infusion for plasma volume expansion ,
with crystalloids
24. 4. Secondary
- Atropine may be given if significant
bradycardia.
- If bronchospasm – nebulise /I V
Amino/Derriphyllin or Beta 2 agonist such as
Salbutamol , Inhaled Ipravent may be
particularly useful for treatment of
bronchospasm in patients on B-blockers.
- Antihistamines - IV Chlorpheniramine.
- Corticosteroids - Effcorlin in I V drip .
Dexamthesone.
Referral to critical care unit.
25. Immediate - Elevated serum Tryptase ,
indicates Mast cell degradation . 3 samples of
blood are taken at 1st,2nd,3rd hr following
suspected reaction.
Late - The aim is to identify causative agent.
Refer to immunologist/allergist for
investigation.
26.
27. Amniotic fluid embolism is a rare , devastating
condition .
It is responsible for (8%) of the direct maternal
deaths .
It’s incidence is 1 in 80,000 - 120,000 .
It is characterized by an abrupt cardiovascular
collapse and coagulopathy during labor or in
the immediate post partum period.
28. Exact mechanism of AFE not clear.
The process is more similar to anaphylactic shock.
Amniotic fluid found in the pulmonary circulation
produces intense pulmonary vasospasm and
pulmonary hypertension.
When ventilation perfusion mismatch occurs
, profound hypoxia ensues.
Hypoxia may account for 50% maternal deaths in 1st hr
of its onset.
Following initial phase there is a phase of
hemodynamic compromise caused by left ventricular
failure . Right heart parameters return to normal . This
mechanism is yet not clear (animal model studies).
29. Delivering woman develops acute dyspnoea
, hypotension ,seizures.
Tachycardia , tachypnoea .
cough - blood tinged frothy sputum .
Cyanosis - circum oral and peripheral .
Fetal bradycardia as a result of hypoxic insult.
Uterine atony - PPH . Dark colored blood which
does not clot DIC .
Pulmonary oedema – typical X- Ray changes
present.
Cardiac arrest.
30. Initial management ABC
Circulatory management
1. Treat hypotension with vasopressors crystalloids
and Colloids I V transfusions .
2. Women who survive the initial phase require ICU
admission and prompt management of DIC and left heart
failure.
3. Coagulopathy is treated with fresh frozen plasma,
cryoprecipitate and platelets as directed by coagulation
studies .
4. Activated recombinant factor VIIa has also being used.
5. Plenty of fresh heparinized blood .
6. Surgery - Perform emergency caesarean surgery in arrested
mother who are un responsive ?
31.
32. There is no loss in intra vascular volume or
cardiac function.
The primary defect is a massive vasodilatation
leading to relative hypovolaemia , reduced
perfusion pressure.
Poor blood flow to tissue tissue anoxia
clinical features of shock .
ABC of initial management.
33.
34. Spinal cord injury may produce hypotension
and shock as a result of sympathetic nervous
system dysfunction . Loss of sympathetic tone
causes wide spread vasodilatation.
Initial management requires ABC , fluid
resuscitation and vasopressor drugs to
counteract vasodilatation .
Atropine may be necessary in high lesions as
bradycardia may occur due to unopposed
vagal activity.
35. 1. Shock may occur during any type of anaesthesia or analgesia
for labour or delivery.
2. Shock caused by general anaesthesia is usually due to adverse
drug reaction (anaphylactic type).
3. High spinal block ---it occurs when over dose of local
anaesthetic drug is administered into epidural or subarachnoid
spaces .
Factors include—
i . Drug dose is reduced in pregnancy.
ii . High spinal block may follow excessive spread of drug
iii . Accidental intrathecal injection of LA intended for
epidural space. Unrecognised dural puncture, migration
of epidural catheter in to intrathecal space.
iv . Hypotension may be aggravated by incorrect positioning ,
absence of lateral tilt -- aortocaval compression.
36. All regional anesthesia techniques produce
sympathetic and motor blockade.
This only becomes problem when it is high and
extensive
1. Hypotension – preceded by nausea or not
feeling well.
2. Bradycardia – unopposed vagal tone due to
blockage of cardio acceleratory fibers(T1-T4)
3. Difficulty in breathing due to paralysis of
intercostal muscles and diaphragm.
4. Upper limb neurological signs (C5-T1) tingling of
fingers and weakness.
37. Basic shock managementABC
Support of cardiovascular system by
Vasopressors , Inotropes.
Intra tracheal intubation and ventilation
support with ventilator.
Sedatives can be used to reduce the awareness
once initial resuscitation is achieved.
38. It is related to high plasma concentration due
to high dose given –I V route , rapid absorption
It may occur during subcutaneous infiltration
or epidural top up.
Intravenous injection of LA while giving
regional blocks pudendal , paracervical
/episiotomy and caudal .
Increased and generous blood supply in
pregnancy aids rapid absorption.
39. CNS - light headedness , tinnitus , dizziness
, circumoral numbness metallic taste , anxiety
, confusion , feeling of impending doom
, generalized tonic-clonic seizures leading to
loss of consciousness and coma , respiratory
depression
CVS – tachycardia , hypotension
, dysrrhythmia and refractory
cardiorespiratory arrest.
Bupivacaine exhibit signs of toxicity in
obstetrical cases.
40. Basic shock management ABC
Special aspects
1. Circulation - Advanced life support with external
cardiac massage and defibrillation . Arrhythmias may
be resistant to conventional therapy.
2.Maintain BP – Vasopressors and inotropic drugs
3.Seizure management – diazepam 5-10 mg I V slowly.
4.Lipid rescue recent work on animals now seems to be
important tool of successful therapy (lipid rescue TM
website).
5. LSCS to salvage baby.
6.Use of sedatives - to reduce the risk of awareness.
41.
42. It remains a significant cause of maternal
death. Mortality Rate due to it , is 3% in
obstetric patients.
43. Nomenclatures -
1 Systemic inflammatory response syndrome (SIRS)
is recognized by presence of one or two of the
following :-
i) temp <36 , or >38 degree centigrade.
ii) HR >90 per minute.
iii) blood gas PaCO2< 4.3KPa (32mmHg).
iv) WBC >12000/mm3 or with immature
neutrophils.
2 Sepsis SIRS with clinical evidence of infection.
44. Nomenclature -
3 Septic shock Sepsis with hypotension despite
adequate fluid resuscitation.
To diagnose it:-
(i)Evidence of infection.
(ii) +ve blood culture
(iii) refractory hypotension , patient requiring
vasopressors /inotropic drugs.
4 Sepsis with multi organ failure(MODS)
Hypotension , hypoxia , oliguria metabolic
acidosis , thrombocytopenia , DIC , depressed
level of consciousness
45. 1. Causative micro organism - E.coli, Streptococcus
type A&B, Klebsiela species, staphylococcus
aureus , these bacteria induce an exaggerated
inflammatory response.
2. Cellwall of these bacteria secrete –lipid A
moiety of lipopolysacharide(Gram-ve)while
Lypoteicholic acid and super antigen Cytotoxins
leading to massive production of cytokinins.
3.Inflammatory cytokinins - activate tissue factor—
Peripheral trigering of coagulation - thrombin
production - cleaving of fibrinogen in to fibrin
46. 4. Cytokinins – disturb body modulators of
coagulation /inflammation -- protien C & S , Anti
thrombin III and tissue factor inhibitor – thus
worsen Coagulopathy by decreasing fibrinolysis.
5. Imbalance between Inflammation , Coagulation &
Fibrinolysis Massive wide spread intravascular
micro thrombi formation.
6. Massive production of cytokinins , Protiens C & S
Interleukins decreased peripheral resistance
vasodilatation hypotension hypovolaemia
decreased Pco2 decreased tissue perfusion
increased cell wall permeability transfer of fluid
intravascular & intracellular to extracellular
compartment tissue edema generalized tissue
anoxia .
52. General--It includes initial management of shock
and circulatory management which requires rapid
blood volume expansion to correct the absolute
and relative hypovolaemia and maintain end
organ perfusion.
Improvement in maternal haemodynamic stability
has direct effect on fetal viability.
LSCS for fetal distress in unstable mother will
drive last nail in her coffin.
If fetal component is source of sepsis , then
delivery becomes the essential part of active
management.
53. Quickly transfer to tertiary medical institution.
Direct arterial and central venous monitoring.
Take samples for culture - blood ,wound ,
higher swab from vagina and uterus , amniotic
fluid , peritoneum , pouch of Douglas .
Intra venous broad spectrum antibiotics against
gram +ve & gram -ve and anaerobes.
Removal of infective tissue P: evacuation of
uterus , colpotomy , laparotomy and if required
caesarean hysterectomy.
Goal related therapy .
54. Early goal – directed therapy - modifying the
initial Rx to achieve mean arterial pressure >65
mmHg , urine out put >0.5 ml/Kg/hr , CVP 8-12
mm Hg and normal mixed venous oxygen
saturation . An effort to reduce end organ damage
and tissue death . It improves outcome in septic
patients.
Insulin therapy - aggressive control of blood sugar
has been demonstrated to improve outcome in
septic patients.
Activated protein C (APC) - Patient with sepsis has
decreased APC levels. Its administration decreases
mortality and reduces organ dysfunction.
55. Corticosteroid therapy ?-- In un selected septic
paient it may worsen outcome because of
secondary infection.
In critically ill patient there may be relative
adrenal insufficiency. In septic shock /the
affected adrenals may not respond to increased
demand of adrenocorticosteroids. Studies on
Cortisone therapy in septic shock , have
different results. Its beneficial effects in
obstetrical sepsis is unknown.
56. 1 .Shock results from acute , generalized , inadequate perfusion of the
tissue.
2.Substandard care is still common in its management patients
death.
3.Sepsis/ haemorrhage are common in obstetrics.
4.Signs of hypovolaemia develop very late because of physiological
changes in pregnancy.
5.Teamwork is required for successful treatment.
6.Obstetrical units Fire drills regularly.
7.Resusctation to maintain tissue perfusion by ABC should be
initiated as soon as shock is diagnosed.
8.Management of underlying cause is secondary task.
9.All therapy Is directed at optimising maternal condition and fetal
wellbeing.