An embolus is a solid, liquid, or gaseous mass that breaks off and travels through the bloodstream, lodging in and blocking smaller blood vessels. Pulmonary embolisms originate from deep leg vein thrombi in 95% of cases and can cause infarction or blockage of lung tissue. Systemic embolisms originate from heart mural thrombi in 80% of cases and commonly impact the brain or lower extremities. Fat embolisms occur after bone fractures and burns, causing pulmonary insufficiency, neurological issues, and thrombocytopenia. Air embolisms enter the circulation through chest or obstetric injuries and can block major blood vessels. Amniotic fluid embolisms are a rare
Ischemia is defined as a condition of inadequate blood supply to an area of tissue.
Infarction- Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage
Public Health Significance- Long-term exposure to other lung irritants also is a risk factor for COPD leading to IHD. Examples of other lung irritants include secondhand smoke, air pollution, and chemical fumes and dust from the environment or workplace.
Ischemia is defined as a condition of inadequate blood supply to an area of tissue.
Infarction- Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage
Public Health Significance- Long-term exposure to other lung irritants also is a risk factor for COPD leading to IHD. Examples of other lung irritants include secondhand smoke, air pollution, and chemical fumes and dust from the environment or workplace.
Coagulation: In medicine, the clotting of blood. The process by which the blood clots to form solid masses, or clots.
More than 30 types of cells and substances in blood affect clotting. The process is initiated by blood platelets. Platelets produce a substance that combines with calcium ions in the blood to form thromboplastin, which in turn converts the protein prothrombin into thrombin in a complex series of reactions. Thrombin, a proteolytic enzyme, converts fibrinogen, a protein substance, into fibrin, an insoluble protein that forms an intricate network of minute threadlike structures called fibrils and causes the blood plasma to gel. The blood cells and plasma are enmeshed in the network of fibrils to form the clot.
This PowerPoint, designed by East Stroudsburg University student Kristen O'Connor, is a PowerPoint designed for middle school science students on cell organelles.
General Pathology Notes
Embolism Definition And Types
Paradoxical embolus
Retrograde embolus
Arterial (systemic) thromboembolism
Venous thromboembolism
Pulmonary Thromboembolism
Contrasting features of pulmonary thrombosis and pulmonary thromboembolism
Consequences Of Pulmonary Embolism
Natural history of pulmonary embolism
Systemic Embolism
Non-traumatic causes
Pulmonary fat embolism
Consequences Of Fat Embolism
Systemic fat embolism
Gas Embolism
Air Embolism
Venous Air Embolism
Arterial Air Embolism
Effects The effects of decompression sickness
Clinical effects of decompression sickness
Amniotic Fluid Embolism
Morphologic Features
- 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
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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
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.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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.
2. Def: An embolus is a detached
intravascular solid, liquid, or
gaseous mass that is carried by the
blood to a site distant from its point
of origin.
3. Almost all emboli represent some
part of a dislodged thrombus
Unless specified embolism means
Thromboembolism
4. Rare forms of emboli
droplets of fat
bubbles of air or nitrogen
Cholesterol emboli from AS debri
tumor fragments
bits of bone marrow, or even
foreign bodies such as bullets
5. Effect of embolus
Occlusion
Emboli lodge in vessels too small to permit
further passage, resulting in partial or
complete vascular occlusion
7. Clinical outcome
Depends on: the site of origin &
the site of lodgment
The clinical outcomes are best
understood from the standpoint of
whether emboli lodge in the pulmonary
or systemic circulations.
9. PULMONARY
THROMBOEMBOLISM
•Incidence of 20 to 25 per 100,000 hospitalized patients
•In more than 95% of instances, venous emboli originate from deep
leg vein thrombi
•Depending on the size of the embolus, it may occlude the main
pulmonary artery, impact across the bifurcation (saddle embolus), or
pass out into the smaller, branching arterioles
•in general, the patient who has had one pulmonary embolus is at
high risk of having more.
•Rarely, an embolus may pass through an interatrial or
interventricular defect to gain access to the systemic circulation
(paradoxical embolism)
10. • Most pulmonary emboli (60% to 80%) are clinically silent because they are
small. With time, they undergo organization and are incorporated into the
vascular wall in some cases, organization of the thromboembolus leaves
behind a delicate, bridging fibrous web.
• Sudden death, right heart failure (cor pulmonale). or cardiovascular
collapse occurs when 60% or more of the pulmonary circulation is
obstructed with emboli.
• Embolic obstruction of medium-sized arteries may result in pulmonary
hemorrhage but usually does not cause pulmonary infarction because of the
dual blood flow into the area from the bronchial circulation. A similar
embolus in the setting of left-sided cardiac failure (i.e., with sluggish
bronchial artery flow), however, may result in a large infarct.
• Embolic obstruction of small end-arteriolar pulmonary branches usually
does result in associated infarction.
• Multiple emboli over time may cause pulmonary hypertension with right
heart failure.
PULMONARY
THROMBOEMBOLISM
11. Consequences of Pul.embolism
• The morphologic consequences depend on the
size of the embolic mass and the general state
of the circulation
• Large emboli - Sudden death often ensues -
acute cor pulmonale (ECG-elecromechanical
dissociation)
• Smaller emboli
– with good CVS – hemorrhages
resorption & reconstitution of
the preexisting architecture
– with CVS compromise - 10% infarction
12. Here is large pulmonary
thromboembolus seen in cross
section of this lung. The
typical source for such
thromboemboli is from large
veins in the legs and pelvis.
13.
14. Figure 4-17 Large
embolus derived from a
lower extremity deep
venous thrombosis and
now impacted in a
pulmonary artery branch
18. Non thrombotic forms of pul.emboli
• uncommon but potentially lethal
• air (may be iatrogenic)
• bone marrow (after trauma and bone
marrow necrosis in sickle cell patients)
• fat (trauma and surgery)
• amniotic fluid (during parturition) and
• foreign bodies (in I/V drug abusers)
19. SYSTEMIC THROMBOEMBOLISM
• refers to emboli travelling within the
arterial circulation
• Common source: Mural thrombi in heart
(80%)
• Less common source: Aorta (AS,
Aneurysm)
21. SYSTEMIC THROMBOEMBOLISM
The major sites for arteriolar embolization
• Lower extremities (75%) and
• Brain (10%)
• the intestines, kidneys, spleen, and upper
extremities involved to a lesser extent
22. SYSTEMIC THROMBOEMBOLISM
The consequences of systemic emboli
depend on:
the extent of collateral vascular supply in the
affected tissue
the tissue's vulnerability to ischemia and
the caliber of the vessel occluded
in general, arterial emboli cause infarction of
tissues downstream of the obstructed
vessel
23. Tissues supplied by end-arteries
without significant collateral
supplies will be the most
susceptible.
Obstruction of blood supply
leads to ischemia which when
prolonged leads to necrosis and
atrophy.
Where there is reperfusion after
ischemic necrosis the tissues will
show a hemorrhagic necrosis.
Where there is infection by
Clostridia (gram positive bacilli),
gangrene sets in.
24. FAT EMBOLISM
• Presence of microscopic fat globules in
the circulation
• Causes: # of long bones
Soft tissue trauma
Burns
25. FAT EMBOLISM
Fat embolism syndrome is characterized by
pulmonary insufficiency,
neurologic symptoms,
anemia, and
Thrombocytopenia
Symptoms:
typically begin 1 to 3 days after injury,
sudden onset of tachypnea, dyspnea, and
tachycardia
26. FAT EMBOLISM
Fat embolism syndrome: Pathogenesis
mechanical obstruction and
biochemical injury
Fat globule platelet complexes
Fat globule RBC complexes
Release of FFA > toxic injury to endothelium >
inflammation > further damage to the vessels
27. FAT EMBOLISM
Demonstration of fat embolism in
specimens:
By means of frozen sections
Routine processing dissolves fat
28. Figure 4-18 Bone marrow embolus in the pulmonary circulation. The
cleared vacuoles represent marrow fat that is now impacted in a distal
vessel along with the cellular hematopoietic precursors.
29. AIR EMBOLISM
• Gas bubbles within the circulation can
obstruct vascular flow
• Entry of gas into circulation occurs during
Obstetric procedures
Chest wall injury
30. AIR EMBOLISM
Dose: should be > 100ml to produce
any clinical effect
Bubbles act like physical obstructions and
may coalesce to form frothy masses
sufficiently large to occlude major vessels
31. AIR EMBOLISM
Decompression sickness:
Scuba and deep sea divers,
underwater construction workers, and
individuals in unpressurized aircraft
Gas: Nitrogen
Clinically: bends, chokes, ischemia, infarction
Treatment: slow decompression
Caisson disease: chronic form of decompression
sickness
32. AMNIOTIC FLUID EMBOLISM
Uncommon complication of laborUncommon complication of labor
Has a mortality rate of 20% to 40%
Clinically: sudden severe dyspnea, cyanosis, and
hypotensive shock, followed by seizures and coma
Pathogenesis: DIC
The underlying cause: infusion of amniotic fluid or fetal
tissue into the maternal circulation via a tear in the
placental membranes or rupture of uterine veins
The classic findings: the presence in the pulmonary
microcirculation of squamous cells shed from fetal skin,
lanugo hair, fat from vernix caseosa, and mucin derived
from the fetal respiratory or gastrointestinal tract
Depending on the site of origin, emboli may lodge anywhere in the vascular tree; the clinical outcomes are best understood from the standpoint of whether emboli lodge in the pulmonary or systemic circulations.
PULMONARY THROMBOEMBOLISM:
Incidence of 20 to 25 per 100,000 hospitalized patients
Although the rate of fatal pulmonary emboli (as assessed at autopsy) has declined from 6% to 2% over the last quarter century
pulmonary embolism still causes about 200,000 deaths per year in the United States.
In more than 95% of instances, venous emboli originate from deep leg vein thrombi
They are carried through progressively larger channels and usually pass through the right side of the heart into the pulmonary vasculature. Depending on the size of the embolus, it may occlude the main pulmonary artery, impact across the bifurcation (saddle embolus), or pass out into the smaller, branching arterioles ( Fig. 4-17 ). Frequently, there are multiple emboli, perhaps sequentially or as a shower of smaller emboli from a single large mass; in general, the patient who has had one pulmonary embolus is at high risk of having more. Rarely, an embolus may pass through an interatrial or interventricular defect to gain access to the systemic circulation (paradoxical embolism). A more complete discussion of pulmonary emboli is presented in Chapter 15 ; an overview is offered here.[43][44]
The morphologic consequences of embolic occlusion of the pulmonary arteries depend on the size of the embolic mass and the general state of the circulation. Large emboli may impact in the main pulmonary artery or its major branches or lodge at the bifurcation as a saddle embolus ( Fig. 15-27 ). Sudden death often ensues, owing largely to the blockage of blood flow through the lungs. Death may also be caused by acute failure of the right side of the heart (acute cor pulmonale). Smaller emboli can travel out into the more peripheral vessels, where they may cause infarction. In patients with adequate cardiovascular function, the bronchial arterial supply can often sustain the lung parenchyma despite obstruction to the pulmonary arterial system. Under these circumstances, hemorrhages may occur, but there is no infarction of the underlying lung parenchyma. Only about 10% of emboli actually cause infarction. Although the underlying pulmonary architecture may be obscured by the suffusion of blood, hemorrhages are distinguished by the preservation of the pulmonary alveolar architecture; in such cases, resorption of the blood permits reconstitution of the preexisting architecture
====================
A large pulmonary embolus is one of the few causes of virtually instantaneous death. During cardiopulmonary resuscitation in such instances, the patient frequently is said to have electromechanical dissociation, in which the electrocardiogram has a rhythm but no pulses are palpated because of the massive blockage of blood in the systemic venous circulation.
Here is another large pulmonary thromboembolus seen in cross section of this lung. The typical source for such thromboemboli is from large veins in the legs and pelvis.
This pulmonary thromboembolus is occluding the main pulmonary artery. Persons who are immobilized for weeks are at greatest risk. The patient can experience sudden onset of shortness of breath. Death may occur within minutes.
Figure 4-17 Large embolus derived from a lower extremity deep venous thrombosis and now impacted in a pulmonary artery branch
A pulmonary thromboembolus travels from a large vein in the leg up the inferior vena cava to the main pulmonary arteries as they branch. Such thrombi embolize most often from large veins in the legs and pelvis where thrombi form with stasis.
This is the microscopic appearance of a pulmonary embolus (PE) in a major pulmonary artery branch
Figure 4-14 Mural thrombi. A, Thrombus in the left and right ventricular apices, overlying a white fibrous scar. B, Laminated thrombus in a dilated abdominal aortic aneurysm.
The major sites for arteriolar embolization are the lower extremities (75%) and the brain (10%), with the intestines, kidneys, spleen, and upper extremities involved to a lesser extent.
The major sites for arteriolar embolization are the lower extremities (75%) and the brain (10%), with the intestines, kidneys, spleen, and upper extremities involved to a lesser extent.
Figure 4-18 Bone marrow embolus in the pulmonary circulation. The cleared vacuoles represent marrow fat that is now impacted in a distal vessel along with the cellular hematopoietic precursors
AMNIOTIC FLUID EMBOLISM :
Amniotic fluid embolism is a grave but fortunately uncommon complication of labor and the immediate postpartum period (1 in 50,000 deliveries). It has a mortality rate of 20% to 40%, and as other obstetric complications (e.g., eclampsia, pulmonary embolism) have been better managed, amniotic fluid embolism has become an important cause of maternal mortality. The onset is characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma. If the patient survives the initial crisis, pulmonary edema typically develops, along with (in half the patients) DIC, owing to release of thrombogenic substances from amniotic fluid.[51][52]
The underlying cause is the infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins. The classic findings are therefore the presence in the pulmonary microcirculation of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tract. There is also marked pulmonary edema and changes of diffuse alveolar damage ( Chapter 15 ) as well as systemic fibrin thrombi indicative of DIC.