AFE is a rare but life-threatening complication of pregnancy caused when amniotic fluid, fetal cells or debris enter the maternal circulation. It has a high mortality rate and serious implications for both mother and infant. AFE should be suspected in pregnant patients experiencing sudden respiratory distress, cardiac collapse, seizures or abnormal bleeding. Prompt diagnosis and aggressive treatment including ventilation, fluid resuscitation, vasopressors and coagulopathy management are required but outcomes remain poor.
Amniotic Fluid Embolism [AFE] Approach to ManagementArun Vasireddy
Amniotic fluid embolism (AFE) is a life threatening obstetric emergency characterized by sudden cardiorespiratory collapse and disseminated intravascular coagulation.
Steiner and Luschbaugh first described AFE in 1941, after they found fetal debris in the pulmonary circulation of women who died during labor. Data from the National Amniotic Fluid Embolus Registry (USA) suggest that the process is more similar to anaphylaxis than to embolism, and the term anaphylactoid syndrome of pregnancy has been suggested because fetal tissue or amniotic fluid components are not universally found in women who present with signs and symptoms attributable to AFE.
The diagnosis of AFE has traditionally been made at autopsy when fetal squamous cells are found in the maternal pulmonary circulation; however, fetal squamous cells are commonly found in the circulation of laboring patients who do not develop the syndrome. The diagnosis is essentially one of exclusion based on clinical presentation. Other causes of hemodynamic instability should not be neglected.
A serious pregnancy complication in which the placenta detaches from the womb (uterus).
Placental abruption occurs when the placenta detaches from the inner wall of the womb before delivery. The condition can deprive the baby of oxygen and nutrients.
Symptoms include vaginal bleeding, stomach pain and back pain in the last 12 weeks of pregnancy.
Depending on the degree of placental separation and how close the baby is to full-term, treatment may include bed rest or a Caesarean (C-section).
Amniotic Fluid Embolism [AFE] Approach to ManagementArun Vasireddy
Amniotic fluid embolism (AFE) is a life threatening obstetric emergency characterized by sudden cardiorespiratory collapse and disseminated intravascular coagulation.
Steiner and Luschbaugh first described AFE in 1941, after they found fetal debris in the pulmonary circulation of women who died during labor. Data from the National Amniotic Fluid Embolus Registry (USA) suggest that the process is more similar to anaphylaxis than to embolism, and the term anaphylactoid syndrome of pregnancy has been suggested because fetal tissue or amniotic fluid components are not universally found in women who present with signs and symptoms attributable to AFE.
The diagnosis of AFE has traditionally been made at autopsy when fetal squamous cells are found in the maternal pulmonary circulation; however, fetal squamous cells are commonly found in the circulation of laboring patients who do not develop the syndrome. The diagnosis is essentially one of exclusion based on clinical presentation. Other causes of hemodynamic instability should not be neglected.
A serious pregnancy complication in which the placenta detaches from the womb (uterus).
Placental abruption occurs when the placenta detaches from the inner wall of the womb before delivery. The condition can deprive the baby of oxygen and nutrients.
Symptoms include vaginal bleeding, stomach pain and back pain in the last 12 weeks of pregnancy.
Depending on the degree of placental separation and how close the baby is to full-term, treatment may include bed rest or a Caesarean (C-section).
Retained placenta can be defined as lack of placental expulsion within 30 minutes of delivery of an infant. it is more common in preterm. Retained Placenta can lead to massive PPH and increase maternal morbidity and mortality.
Uterine Rupture
Deepa Mishra
Assistant Professor (OBG)
Introduction
Uterine rupture is when the muscular wall of the uterus tears during pregnancy or childbirth
Symptoms while classically including increased pain, vaginal bleeding, or a change in contractions are not always present.
Disability or death of the mother or baby may result.
Definition
Uterine rupture is giving way of gravid uterus or dissolution in the continuity of uterine wall anytime after 28 weeks of gestation with or without expulsion of the fetus.
Incidence
Rates of uterine rupture during vaginal birth following one previous C-section, done by the typical technique, are estimated at 0.9%
Rates are greater among those who have had multiple prior C-sections or an atypical type of C-section.
In those who do have uterine scarring, the risk during a vaginal birth is about 1 per 12,000
Risk of death of the baby is about 6%
Etiology
Risk Factors
Previous cesarean section
Myomectomy
Dysfunctional labor
Labor augmentation by oxytocin or prostaglandins
High parity
First pregnancy- very rare
Types of uterine rupture
Complete Rupture
All the layers including peritoneum are torn and the uterine contents escape into the peritoneal cavity.
Usually results in death
Incomplete Rupture
Visceral peritoneum is intact and usually the fetus remains in the uterine cavity
Sign & Symptoms
Uterine dehiscence and abdominal pain and vaginal bleeding
Deterioration of fetal heart rate
Loss of fetal station on manual vaginal exam
Hypovolemic shock due to intrabdominal bleeding
Chest pain between the scapulae, pain during inspiration due to irritation of blood below the perineum
Cessation of uterine contractions
Palpation of fetus outside the uterus
Signs of abdominal pregnancy
Post term pregnancy
Diagnosis
Signs of obstructed labor with dehydration, exhaustion, tachycardia raised temperature tonic contraction , pathological retraction ring
Absent fetal heart sound
On PV hot, dry vagina with a large caput over the presenting part
Prevention
Early diagnosis and management of CPD mal presentation and obstructed labor
Proper selection of cases for vaginal delivery
Carefull monitoring of oxytocin infusion specially in multipara
Avoid intra uterine manipulation no version in single fetus
Instrumental delivery after cervical dilatation
Immediate CS in obstructed labor
Hospital delivery for high risk cases
ECV should be avoided during general anaesthesia
Careful manual removal of placenta
Treatment
Resuscitation with adequate hydration and blood transfusion
Laprotomy
Hysterectomy
Repair
Complication
Rupture uterus with haemorrhage, shock and sepsis
Fetal loss is high in spontaneous and traumatic rupture
Mortality is low in LSCS scar rupture
Placenta previa is a condition in which the placenta lies very low in the uterus and covers all or part of the cervix. The cervix is the opening to the uterus that sits at the top of the vagina. Placenta previa happens in about 1 in 200 pregnancies.
Placenta praevia risk factors include a previous delivery, age older than 35 and a history of previous surgeries, such as a caesarean section (C-section) or uterine fibroid removal.
The main symptom is bright red vaginal bleeding without pain during the second-half of pregnancy. The condition can also cause severe bleeding before or during delivery.
Limited physical activity is recommended. A C-section is often required in severe cases.
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.
amniotic fluid embolism and cardiac arrest in pregnancyprateek gupta
obstetric emergency. amniotic fluid embolism-pathophysiology,clinical presentation, diagnosis, treatment, laboratory investigations and prognosis. cardiac arrest in preganacy and ACLS 2015 guidelines for CPR and new updates
Retained placenta can be defined as lack of placental expulsion within 30 minutes of delivery of an infant. it is more common in preterm. Retained Placenta can lead to massive PPH and increase maternal morbidity and mortality.
Uterine Rupture
Deepa Mishra
Assistant Professor (OBG)
Introduction
Uterine rupture is when the muscular wall of the uterus tears during pregnancy or childbirth
Symptoms while classically including increased pain, vaginal bleeding, or a change in contractions are not always present.
Disability or death of the mother or baby may result.
Definition
Uterine rupture is giving way of gravid uterus or dissolution in the continuity of uterine wall anytime after 28 weeks of gestation with or without expulsion of the fetus.
Incidence
Rates of uterine rupture during vaginal birth following one previous C-section, done by the typical technique, are estimated at 0.9%
Rates are greater among those who have had multiple prior C-sections or an atypical type of C-section.
In those who do have uterine scarring, the risk during a vaginal birth is about 1 per 12,000
Risk of death of the baby is about 6%
Etiology
Risk Factors
Previous cesarean section
Myomectomy
Dysfunctional labor
Labor augmentation by oxytocin or prostaglandins
High parity
First pregnancy- very rare
Types of uterine rupture
Complete Rupture
All the layers including peritoneum are torn and the uterine contents escape into the peritoneal cavity.
Usually results in death
Incomplete Rupture
Visceral peritoneum is intact and usually the fetus remains in the uterine cavity
Sign & Symptoms
Uterine dehiscence and abdominal pain and vaginal bleeding
Deterioration of fetal heart rate
Loss of fetal station on manual vaginal exam
Hypovolemic shock due to intrabdominal bleeding
Chest pain between the scapulae, pain during inspiration due to irritation of blood below the perineum
Cessation of uterine contractions
Palpation of fetus outside the uterus
Signs of abdominal pregnancy
Post term pregnancy
Diagnosis
Signs of obstructed labor with dehydration, exhaustion, tachycardia raised temperature tonic contraction , pathological retraction ring
Absent fetal heart sound
On PV hot, dry vagina with a large caput over the presenting part
Prevention
Early diagnosis and management of CPD mal presentation and obstructed labor
Proper selection of cases for vaginal delivery
Carefull monitoring of oxytocin infusion specially in multipara
Avoid intra uterine manipulation no version in single fetus
Instrumental delivery after cervical dilatation
Immediate CS in obstructed labor
Hospital delivery for high risk cases
ECV should be avoided during general anaesthesia
Careful manual removal of placenta
Treatment
Resuscitation with adequate hydration and blood transfusion
Laprotomy
Hysterectomy
Repair
Complication
Rupture uterus with haemorrhage, shock and sepsis
Fetal loss is high in spontaneous and traumatic rupture
Mortality is low in LSCS scar rupture
Placenta previa is a condition in which the placenta lies very low in the uterus and covers all or part of the cervix. The cervix is the opening to the uterus that sits at the top of the vagina. Placenta previa happens in about 1 in 200 pregnancies.
Placenta praevia risk factors include a previous delivery, age older than 35 and a history of previous surgeries, such as a caesarean section (C-section) or uterine fibroid removal.
The main symptom is bright red vaginal bleeding without pain during the second-half of pregnancy. The condition can also cause severe bleeding before or during delivery.
Limited physical activity is recommended. A C-section is often required in severe cases.
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.
amniotic fluid embolism and cardiac arrest in pregnancyprateek gupta
obstetric emergency. amniotic fluid embolism-pathophysiology,clinical presentation, diagnosis, treatment, laboratory investigations and prognosis. cardiac arrest in preganacy and ACLS 2015 guidelines for CPR and new updates
congenital health problems in children is very serios problem in children ,it is major cause of mortality in children .it can prevented by proper care of mothers during pregnancy .
Breast & it's problems and treatment made by sonal Patelsonal patel
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Antenatal Care Guideline- gestational Age Assessment,Early USG, Nutritional ...sonal patel
Antenatal Care Guideline- gestational Age Assessment,Early USG, Nutritional Supplements,, Food Acquired Infections,medicine, alcohol,smoking, Sexual Intercose avoid, Exercise, Clinical Screening in PPT made by sonal patel
methods of Chromosomal Evaluation in Amniocentesis- Define, Time for test, C...sonal patel
methods of Chromosomal Evaluation in Amniocentesis- Define, Time for test, Complications,and Chorionic Villus sampling ( CVS) , Risk of Procedure, Steps of Procedure in PPT -Define, Time for test made By sonal Patel
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Amenorrhea - Define, Cause, Sign and Symptoms, Type- Pathological and Physiological Amenorrhea and It's Treatment and management, Cushing Syndrome - Define, Causes, Sign And Symptoms in PPT made By Sonal Patel
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Dysfunctional uterine Bleeding is type of Abnormal bleeding from the genital tract- Factore, Types, Diagnosis, Treatment in that one type DUB- Define, sign and Symptoms, Diagnosis, Treatment, Management, hormonal Therapy in PPT made By sonal Patel
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Birth defect system according to System wise in that Respiratory System Birth defect, Cardiovascular System Birth defect,Digestive System Birth defect, Extremity Birth defect made by sonal Patel
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Embryology-all basic definition,Stage wise development of fetus,development of Zygote stage ,development of Embrionic Stage ,development of Fetus Stage all are according week development,Amnione,chorion,Fetal layer, Umbilical Cord developmentmade By sonal Patel
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
- 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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
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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
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.
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
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
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2. AMNIOTIC FLUID EMBOLISM
• AFE is thought to occur when amniotic fluid , fetal cells,
hair, or other debris enter the maternal circulation.
• Ricardo Meyer (1926); reported the presence of fetal cellular
debris in the maternal circulation.
• Steiner and Luschbaugh (1941) described the autopsy
findings of eight cases of AFE.
• Until 1950, only 17 cases had been reported.
• AFE was not listed as a distinct heading in causes of
maternal mortality until 1957 when it was labeled as
obstetric shock.
• Since then more than 400 cases have been documented,
probably as a result of an increased awareness.
3. AMNIOTIC FLUID EMBOLISM
• Overall incidence ranges from 1 in 8,000 to 1 in 80,000
pregnancies.
• 10% of maternal deaths in USA &16% in U.K.
• The first well-documented case with ultimate survival was
published in 1976
(Resnik R, et al. Obstet Gynecol 1976;47:295-8).
• 75 % of survivors are expected to have long-term neurologic
deficits.
• If the fetus is alive at the time of the event, nearly 70 % will
survive the delivery but 50% of the survived neonates will incur
neurologic damage.
4. AMNIOTIC FLUID EMBOLISM
• Time of event:
- During labor.
- During C/S.
- After normal vaginal delivery.
- During second trimester TOP.
• AFE syndrome has been reported to occur as
late as 48 hours following delivery.
5. Risk factors of AFE
• Advanced maternal age
• Multiparity
• Meconium
• Cervical laceration
• Intrauterine foetal death
• Very strong frequent or uterine
tetanic contractions
• Sudden foetal expulsion (short
labour)
• Placenta accreta
• Polyhydramnios
• Uterine rupture
• Maternal history of allergy or
atopy
• Chorioamnionitis
• Macrosomia
• Male fetal sex
• Oxytocin (controversial)
Nevertheless, these and other frequently cited risk factors
are not consistently observed and at the present time
Experts agree that this condition is not preventable.
6. Experimental AFE
The cardiorespiratory effects of acute intravascular injection
of amniotic fluid have been studied in pregnant ewes :
• The initial response was hypotension.
• A 40 % decrease in mean arterial pressure was followed by a 100 %
increase in mean pulmonary artery pressure.
• Little change occurred in the left atrial pressure or the pulmonary artery
wedge pressure.
• A 40 percent fall in cardiac output was associated with the rapid rise in
pulmonary artery pressure.
• These changes resulted in a two- to threefold increase in pulmonary
vascular resistance and a two- to threefold decrease in systemic
vascular resistance.
7. Experimental AFE
• Intravascular injection of amniotic fluid in rhesus
monkeys failed to produce cardiovascular
changes similar to the syndrome observed in
pregnant ewes or humans.
8. Pathophysiology
- Poorly understood.
- Cotton (1996), has proposed a biphasic model.
Phase 1:
Amniotic fluid and fetal cells enter the maternal
circulation biochemical mediators pulmonary artery
vasospasm pulmonary hypertension elevated right
ventricular pressure hypoxia myocardial and pulmonary
capillary damage, left heart failure acute respiratory
distress syndrome
Phase 2:
biochemical mediators DICHemorrhagic phase
characterized by massive hemorrhage and uterine
atony.
9. Pathophysiology
• The similar homodynamic derangements seen with AFE
syndrome , anaphylactic, and septic shock have led
investigators to postulate a substance in amniotic fluid
resulting in the release of primary and secondary
endogenous mediators (i.e. arachidonic acid metabolites)
which might also be responsible for the associated
coagulopathy in AFE.
• The prevention of fatal homodynamic collapse in
experimental AFE with inhibitors of leukotriene synthesis
would support an anaphylactic mechanism for AFE.
10. Pathophysiology
• Measurement of tryptase ( a degranulation
product of mast cells released with histamine
during anaphylactic reactions) levels to further
investigate the anaphylactic nature of AFE.
• The syndrome does not appear to be dependent
on the amount of fluid or particulate matter that
enters the vasculature.
11. Pathophysiology
• To emphasize that the
clinical findings are
secondary to biochemical
mediators rather than
pulmonary embolic
phenomenon; Clark et al
have suggested renaming
this clinical syndrome the
"anaphylactoid syndrome
of pregnancy"
12. Clinical presentation
The classic clinical presentation of the syndrome
has been described by five signs that often occur
in the following sequence:
(1) Respiratory distress
(2) Cyanosis
(3) Cardiovascular collapse cardiogenic shock
(4) Hemorrhage
(5) Coma.
13. Clinical presentation
• A sudden drop in O2 saturation can be the initial
indication of AFE during c/s.
• More than 1/2 of patients die within the first hour.
• Of the survivors 50 % will develop DIC which
may manifest as persistent bleeding from
incision or venipuncture sites.
The coagulopathy typically occurs 0.5 to 4 hours
after phase 1.
14. Clinical presentation
• 10-15% of patients will develop grand mal
seizures.
• CXR may be normal or show effusions, enlarged
heart, or pulmonary edema.
• ECG may show a right strain pattern with ST-T
changes and tachycardia.
15. Diagnosis
• In 1941, Steiner and Luschbaugh described histopathologic
findings in the pulmonary vasculature in 8 multiparous
women dying of sudden shock during labor.
• Findings included mucin, amorphous eosinophilic material ,
and in some cases squamous cells.
• The presence of squamous cells in the pulmonary
vasculature once considered pathognomonic for AFE is
neither sensitive nor specific (only 73% of patients dying from
AFE had this finding).
• The monoclonal antibody TKAH-2 may eventually prove more
useful in the rapid diagnosis of AFE.
16. Laboratory investigations
in suspected AFE
Non specific
• complete blood count
• coagulation parameters
including FDP, fibrinogen
• arterial blood gases
• chest x-ray
• electrocardiogram
• V/Q scan
• echocardiogram
Specific
• cervical histology
• serum tryptase
• serum sialyl Tn antigen
• zinc coproporphyrin
• PMV analysis (if PA
catheter in situ)
17. Differential diagnosis
Obviously depends upon presentation
• Anaphylaxis (Collapse)
• Pulmonary embolus
(Collapse)
• Aspiration (Hypoxaemia)
• Pre-eclampsia or
eclampsia (Fits,
Coagulopathy)
• Haemorrhage (APH ; PPH)
• Septic shock
• Drug toxicity (MgSO4, total
spinal, LA toxicity)
• Aortic dissection
18. Management of AFE
GOALS OF MANAGEMENT:
• Restoration of cardiovascular and pulmonary
equilibrium
- Maintain systolic blood pressure
>90 mm Hg.
- Urine output > 25 ml/hr
- Arterial pO2 > 60 mm Hg.
• Re-establishing uterine tone
• Correct coagulation abnormalities
19. Management of AFE
• As intubation and CPR may be required it is necessary
to have easy access to the patient, experienced help,
and a resuscitation tray with intubation equipment, DC
shock, and emergency medications.
• IMMEDIATE MEASURES :
- Set up IV Infusion, O2 administration.
- Airway control endotracheal intubation
maximal ventilation and oxygenation.
• LABS : CBC,ABG,PT,PTT,fibrinogen,FDP.
20. Management of AFE
• Treat hypotension, increase the circulating volume and
cardiac output with crystalloids.
• After correction of hypotension, restrict fluid therapy to
maintenance levels since ARDS follows in up to 40% to 70%
of cases.
• Steroids may be indicated (recommended but no evidence
as to their value)
• Dopamine infusion if patient remains hypotensive
(myocardial support).
• Other investigators have used vasopressor therapy such as
ephedrine or levarterenol with success (reduced systemic
vascular resistance)
21. Management of AFE
In the ICU
• To assess the effectiveness of treatment and resuscitation, it
is prudent to continuously monitor ECG, pO2, CO2, and urine
output.
• There is support in literature for early placement of arterial,
central venous, and pulmonary artery catheters to provide
critical information and guide specific therapy.
22. Management of AFE
In the ICU
• Central venous pressure monitoring is important to
diagnose right ventricular overload and guide fluid infusion
and vasopressor therapy. Blood can also be sampled from
the right heart for diagnostic purposes.
• Pulmonary artery and capillary wedge pressures and
echocardiography are useful to guide therapy and evaluate
left ventricular function and compliance.
• An arterial line is useful for repeated blood sampling and
blood gases to evaluate the efficacy of resuscitation.
23. Management of AFE
Coagulopathy
• DIC results in the depletion of fibrinogen, platelets,
and coagulation factors, especially factors V, VIII,
and XIII. The fibrinolytic system is activated as well.
• Most patients will have hypofibrinogenemia,
abnormal PT and aPTT and low Platelet counts
• Treat coagulopathy with FFP for a prolonged aPTT,
cryoprecipitate for a fibrinogen level less than 100
mg/dL, and transfuse platelets for platelet counts
less than 20,000/mm3
24. Restoration of uterine tone
• Uterine atony is best treated with massage,
uterine packing, and oxytocin or prostaglandin
analogues.
• Improvement in cardiac output and uterine
perfusion helps restore uterine tone.
• Extreme care should be exercised when using
prostaglandin analogues in hypoxic patients, as
bronchospasm may worsen the situation.
25. Sympathomimetic Vasopressor agent
Dopamine
• Dopamine increases myocardial contractility and systolic
BP with little increase in diastolic BP. Also dilates the renal
vasculature, increasing renal blood flow and GFR.
• DOSE: 2-5 mcg/kg/min IV; titrate to BP and cardiac output.
• Contraindications: ventricular fibrillation, hypovolemia,
pheochromocytoma.
• Precautions: Monitor urine flow, cardiac output, pulmonary
wedge pressure, and BP during infusion; prior to infusion,
correct hypovolemia with either whole blood or plasma, as
indicated; monitoring central venous pressure or left
ventricular filling pressure may be helpful
26. Maternal Mortality in AFE
• Maternal death usually occurs in one of three ways: (1)
sudden cardiac arrest, (2) hemorrhage due to coagulopathy,
or (3) initial survival with death due to acute respiratory
distress syndrome (ARDS) and multiple organ failure
• For women diagnosed as having AFE, mortality rates
ranging from 26% to as high as 86% have been reported.
• The variance in these numbers is explained by dissimilar
case definitions and possibly improvements in intensive
care management of affected patients.
27. Further issues in the
Management
• Transfer:
Transfer to a level 3 hospital may be required once the
patient is stable.
• Deterrence/Prevention:
Amniotic fluid embolism is an unpredictable event.
• Risk of recurrence is unknown. The recommendation for
elective cesarean delivery during future pregnancies in an
attempt to avoid labor is controversial.
• Perimortem cesarean delivery:
After 5 minutes of unsuccessful CPR in arrested mothers,
abdominal delivery is recommended.
28. Medical/Legal Pitfalls
• Failure to respond emergently is a pitfall. AFE is a clinical
diagnosis. Steps must be taken to stabilize the patient as
soon as symptoms manifest.
• Failure to perform perimortem cesarean delivery in a timely
fashion is a pitfall.
• Failure to consider the diagnosis during legal abortion is a
pitfall. A review of the literature indicates that most case
reports of AFE have occurred during late second-trimester
abortions.
29. SUMMARY
• AFE is a sudden and unexpected rare but life
threatining complication of pregnancy.
• It has a complex pathogenesis and serious
implications for both mother and infant
• Associated with high rates of mortality and
morbidity.
• Diagnosis of exclusion.
• Suspect AFE when confronted with any pregnant
patient who has sudden onset of respiratory
distress, cardiac collapse, seizures, unexplained
fetal distress, and abnormal bleeding
• Obstetricians should be alert to the symptoms of
AFE and strive for prompt and aggressive treatment.