Respiratory distress syndrome: Pathology Review
Summary
TLDRThe script discusses two cases of respiratory distress: Mike, a 55-year-old with pneumonia leading to ARDS, characterized by rapid lung inflammation, hypoxia, and a PF ratio below 300, not caused by heart failure. Donna, a premature infant, develops NRDS due to surfactant deficiency, presenting with respiratory distress and a characteristic chest x-ray pattern. The script explains the pathophysiology, diagnosis criteria, and treatment approaches for both conditions, emphasizing the importance of supportive care and surfactant therapy.
Takeaways
- 💉 Mike, a 55-year-old man, presented with shortness of breath, fever, and cough, which led to a pneumonia diagnosis after a chest x-ray showed a right lower lobe infiltrate.
- 🚑 Despite IV antibiotics, Mike's condition worsened, and he developed septic shock with hypoxemia, requiring intubation, IV fluids, and vasopressors.
- 📉 A repeat x-ray revealed bilateral alveolar opacities, a PF ratio of 109, and heart failure was ruled out by echography, leading to a diagnosis of acute respiratory distress syndrome (ARDS).
- 👶 Donna, an infant born at 36 weeks via C-section, developed respiratory distress hours after birth, presenting with tachypnea, chest retractions, and nasal flaring.
- 🩻 Donna’s chest x-ray showed a diffuse reticulogranular ground glass appearance with air bronchograms, confirming neonatal respiratory distress syndrome due to surfactant deficiency.
- 🫁 Type 2 pneumocytes are responsible for producing surfactant, which prevents alveolar collapse. Damage to these cells contributes to both ARDS and neonatal respiratory distress syndrome.
- 🔥 ARDS is characterized by alveolar damage caused by conditions like sepsis, leading to fluid accumulation in the alveoli, pulmonary edema, and impaired gas exchange.
- 🩸 Diagnosis of ARDS involves acute onset (within 1 week), bilateral lung opacities on imaging, a PF ratio below 300, and ruling out cardiac causes.
- 🛠️ Treatment of ARDS focuses on supportive care, such as mechanical ventilation with positive end-expiratory pressure (PEEP) and low tidal volumes to prevent further lung damage.
- 👶 Neonatal respiratory distress syndrome is often linked to premature birth, maternal diabetes, or C-section delivery. It is treated with continuous positive airway pressure (CPAP) or surfactant therapy.
Q & A
What led to Mike's diagnosis of pneumonia?
-Mike's diagnosis of pneumonia was based on his presentation of shortness of breath, high fever, and cough, along with a chest x-ray showing a right lower lobe infiltrate.
What complications did Mike experience after being treated for pneumonia?
-Despite treatment, Mike developed hypoxia and hypotension, eventually progressing to septic shock. A repeat x-ray showed bilateral alveolar opacities, indicating acute respiratory distress syndrome (ARDS).
What are the four criteria used to diagnose acute respiratory distress syndrome (ARDS)?
-The four criteria for diagnosing ARDS are: (1) acute onset within one week, (2) bilateral opacities on chest imaging, (3) a PF ratio below 300 mmHg, and (4) respiratory failure not due to cardiac causes like heart failure.
What role do type 2 pneumocytes play in lung function and injury response?
-Type 2 pneumocytes produce surfactant, which reduces surface tension in the alveoli, preventing their collapse. They also proliferate in response to lung injury and can differentiate into type 1 and type 2 cells.
What is the mechanism behind the development of pulmonary edema in ARDS?
-In ARDS, the alveolar-capillary membrane becomes more permeable due to inflammation, allowing fluid to leak into the alveoli, leading to pulmonary edema. This impairs gas exchange and worsens respiratory function.
What findings on Mike's arterial blood gas analysis supported his ARDS diagnosis?
-Mike's arterial blood gas analysis revealed a PF ratio of 109 mmHg, which is significantly below the threshold for ARDS, indicating severely impaired gas exchange.
What are the risk factors for neonatal respiratory distress syndrome (NRDS) in Donna's case?
-Donna's risk factors for neonatal respiratory distress syndrome include her premature delivery at 36 weeks gestational age and being delivered by C-section, which can reduce the stress-induced glucocorticoid surge needed for surfactant production.
What are the characteristic findings of neonatal respiratory distress syndrome on chest x-ray?
-The characteristic chest x-ray findings for neonatal respiratory distress syndrome include diffuse reticulogranular ground glass appearance with air bronchograms.
What are the key differences between ARDS and neonatal respiratory distress syndrome (NRDS)?
-ARDS is caused by widespread lung inflammation in response to various triggers, such as sepsis or trauma, while NRDS is caused by a deficiency of surfactant in newborns, often due to prematurity. ARDS affects older individuals, while NRDS primarily affects preterm infants.
What treatment options are available for neonatal respiratory distress syndrome (NRDS)?
-Initial treatment for NRDS includes nasal continuous positive airway pressure (CPAP) to keep the alveoli open. If this fails, endotracheal intubation and intratracheal surfactant therapy are used. Antenatal corticosteroids are also given to mothers at risk of preterm delivery to reduce the severity of NRDS.
Outlines
🩺 Emergency Cases: Adult and Infant Respiratory Distress
The paragraph presents two cases admitted to the emergency department. Mike, a 55-year-old man, shows symptoms of pneumonia and progresses to septic shock with severe respiratory failure, characterized by bilateral alveolar opacities and a low PF ratio, fulfilling criteria for acute respiratory distress syndrome (ARDS). Donna, an infant delivered by cesarean section, shows signs of neonatal respiratory distress with symptoms such as tachypnea, chest wall retractions, and nasal flaring. Her chest x-ray indicates a reticulogranular ground glass appearance typical of neonatal respiratory distress syndrome.
🫁 Physiology and Pathophysiology of ARDS
This section explains normal lung physiology focusing on type 1 and type 2 pneumocytes, with an emphasis on the role of surfactant in reducing alveolar surface tension. It describes ARDS as a condition caused by widespread lung inflammation due to factors like sepsis and trauma, leading to alveolar damage. The inflammatory response involves cytokines and neutrophils that exacerbate lung damage, resulting in increased capillary permeability, pulmonary edema, surfactant loss, and alveolar collapse. The formation of a hyaline membrane further impairs lung function, leading to severe respiratory symptoms and systemic effects like shock.
📊 Diagnosis and Management of ARDS and Neonatal RDS
This paragraph outlines the diagnostic criteria for ARDS, which include acute onset, bilateral lung opacities, a PF ratio below 300, and exclusion of cardiac causes. The role of echocardiography and pulmonary capillary wedge pressure in differentiating ARDS from heart failure is highlighted. The management primarily involves treating the underlying cause and supportive care with mechanical ventilation, emphasizing positive end-expiratory pressure (PEEP) and low tidal volumes to prevent further lung injury. It also discusses neonatal respiratory distress syndrome (RDS), its risk factors like prematurity and maternal diabetes, symptoms, and diagnostic imaging findings, including the ground glass appearance and air bronchogram. Treatment includes antenatal corticosteroids, nasal CPAP, and surfactant therapy, with potential complications of oxygen therapy in neonates.
Mindmap
Keywords
💡Pneumonia
💡Acute Respiratory Distress Syndrome (ARDS)
💡Septic Shock
💡Surfactant
💡Hypoxemia
💡Neonatal Respiratory Distress Syndrome (NRDS)
💡PF Ratio
💡Ground Glass Appearance
💡Pulmonary Edema
💡Positive End-Expiratory Pressure (PEEP)
Highlights
Mike, a 55-year-old man, is admitted to the emergency department with shortness of breath, high fever, and cough.
Chest x-ray reveals a right lower lobe infiltrate, suggestive of pneumonia.
Mike is started on IV antibiotics for pneumonia.
Mike becomes hypoxic and hypotensive, leading to a diagnosis of septic shock.
Repeat x-ray shows newly developed bilateral alveolar opacities, ruling out heart failure as the cause.
Arterial blood gas analysis reveals a PF ratio of 109, indicating severe respiratory distress.
Donna, an infant, is delivered by cesarean section at 36 weeks gestational age with an Apgar score of 9.
Donna develops tachypnea, chest wall retractions, and tachycardia a few hours after delivery.
Chest x-ray for Donna shows diffuse reticulogranular ground glass appearance, typical for neonatal respiratory distress.
Type 1 and Type 2 pneumocytes are crucial for gas exchange and lung injury response.
ARDS is characterized by widespread inflammation leading to respiratory failure, often triggered by conditions like sepsis.
The main site of injury in ARDS is the alveolar capillary membrane, leading to pulmonary edema.
ARDS diagnosis requires acute symptoms, bilateral opacities on x-ray, a PF ratio below 300, and ruling out heart failure.
Treatment for ARDS involves supportive care with supplemental oxygen and mechanical ventilation.
Neonates with respiratory distress syndrome present with signs of progressive respiratory failure.
Risk factors for neonatal respiratory distress syndrome include prematurity, maternal diabetes, and C-section delivery.
Diagnosis of neonatal respiratory distress syndrome is confirmed with chest radiography showing specific patterns.
Treatment for neonatal respiratory distress syndrome starts with nasal continuous positive airway pressure.
Mike's case meets all criteria for an ARDS diagnosis based on clinical presentation and test results.
Donna's case is consistent with neonatal respiratory distress syndrome, confirmed by chest x-ray findings.
Transcripts
two people are admitted to the emergency
department Mike a 55 year old man
presents with shortness of breath high
fever and cough a chest x-ray was
ordered and it showed a right lower lobe
infiltrate which is suggestive of
pneumonia
he was then started on IV antibiotics
but the following day Mike became
hypoxic and hypotensive because his
hypotension didn't improve despite
intubation IV fluids and vasopressors he
is diagnosed with septic shock
next a repeat x-ray detected newly
developed bilateral alveolar opacities
heart echography ruled out heart failure
and arterial blood gas analysis revealed
a PF ratio of 109 milligrams of Mercury
then there was Donna an infant delivered
by cesarean section at 36 weeks
gestational age with an apgar score of 9
at Birth a few hours after delivery she
develops tachypnea chest wall
retractions with nasal flaring and
tachycardia aside from increased work of
breathing her physical examination
findings are normal a chest x-ray was
ordered and it showed diffuse
reticulogranular ground glass appearance
with air bronchograms
now both people are in respiratory
distress
but first a bit of physiology normally
when you breathe in the air reaches the
alveoli which are made up of two types
of pneumocytes first type 1 pneumocytes
are thin and have a large surface area
that can facilitate gas exchange
more important for the exams are the
type 2 pneumocytes which are smaller
thicker and have the ability to
proliferate in response to lung injury
they are in charge of making a fluid
called surfactant which contains various
phospholipids this lets it act like
droplets of oil that coat the inside of
the alveoli decreasing surface tension
so if it's missing the alveoli will
collapse these cells also act like stem
cells meaning they can give rise to type
1 cells and type 2 pneumocytes
okay so acute respiratory distress
syndrome or ards is characterized by
rapid onset of widespread inflammation
in the lungs which can lead to
respiratory failure Arts is not a
primary disease as it is usually
triggered by conditions like sepsis
aspiration trauma and pancreatitis
now art starts when these conditions
cause alveolar damage and a high yield
fact is that the injury triggers the
pneumocytes to secrete inflammatory
cytokines like tnf Alpha and
interleukin-1 this subsequently leads to
neutrophil Recruitment and they will
release toxic mediators like reactive
oxygen species and proteases which will
damage the lungs even more
you'll need to know that the main site
of injury is the alveolar capillary
membrane which becomes more permeable
causing fluid to move into the alveoli
resulting in pulmonary edema this fluid
can impair gas exchange leading to
hypoxemia furthermore the edema can also
wash away the surfactant coating of the
alveoli to the point where it can't
reduce surface tension anymore and as a
result the alveoli collapse and finally
dead cells and protein-rich fluids start
to pile up in the alveolar space and
over time it forms this waxy hyaline
membrane which look like a layer of
glassy material
individuals with Arts present with
serious symptoms and signs that require
urgent investigation the inflammation
process and impaired gas exchange lead
to Fever shortness of breath tachypnea
chest pain hypotension hypoxia and
cyanosis more often than not ards will
lead to shock due to hypotension the
excess fluid in the lungs can cause a
crackling sound called rails during
auscultation which is the sound of
collapsed alveoli popping open with
inspiration
keep in mind that additional symptoms
might provide clues to the underlying
cause
for example epigastric abdominal pain
radiating to the back along with the
history of gallstones indicate acute
pancreatitis
diagnosis of ards is typically made when
the individual presents all of the next
four criteria which you should
definitely remember for your exams first
the symptoms have to be acute meaning an
onset of one week or less second and
particularly high yield a chest x-ray or
CT scan shows opacities or white out in
both lungs which is due to pulmonary
edema
the third is What's called the PF ratio
it's the partial pressure of oxygen in
the arterial blood divided by the
percent of oxygen in the inspired air
also called the fraction of inspired
oxygen in ards gas exchange is defective
so the PF ratio is below 300 millimeters
of mercury and the lower this ratio gets
the more severe the condition
fourth the respiratory distress must not
be due to cardiac causes like heart
failure often this is assessed by using
an echocardiogram to look for evidence
of heart failure like an ejection
fraction below 55 percent in systolic
heart failure and abnormal relaxation of
The myocardium and diastolic heart
failure
another clue is the pulmonary capillary
wedge pressure which is measured by
inserting a catheter into a small
pulmonary arterial branch in heart
failure this is elevated because more
blood remains in the left side of the
heart and it prevents pulmonary venous
return the blood backs up into the
pulmonary vessels and the increase in
pressure pushes fluid into the
interstitium of the lungs resulting in
edema in ards the pressure is normal
since the edema is caused by leaky
capillaries instead of increased
pressure
treatment of ards ultimately comes down
to treating the condition that triggered
it however the most important initial
step is supportive care like
supplemental oxygen or mechanical
ventilation a high yield fact to
remember is that it's vital to maintain
positive end expiratory pressure which
is where the pressure in the lungs is
kept slightly above atmospheric pressure
even after exhalation because this
prevents the alveoli from collapsing
it's also good to have low tidal volumes
to prevent over inflation of the damaged
alveoli another important thing to watch
out for is positive pressure ventilation
which can cause compression of pulmonary
vessels which leads to pulmonary
hypertension decreased pulmonary venous
return this will reduce cardiac output
and hypotension might worsen now even
with supportive care the macrophages
clean up old cell debris that attract
and activate fibroblasts which are cells
that secrete collagen and form scar
tissue in the alveolar walls if the
there's enough Scar Tissue it can still
lead to a decrease in lung compliance or
the ability of lungs to expand and come
back to their original size remember
that this means the individual will have
residual symptoms all of their lives
next neonatal respiratory distress
syndrome is a disease of the newborn
caused by a deficiency of surfactant
this results in alveoli that can't stay
open and the newborn has to work hard to
breathe resulting in the development of
progressive and diffuse atelectasis now
there are some risk factors associated
with the disease that are commonly
tested first there's prematurity usually
because the lungs are not mature enough
to produce surfactant next maternal
diabetes can cause increased insulin
levels in the infant which interferes
with surfactant production C-section
delivery is another cause normal birth
is a very stressful process for the
infant and this increases glucocorticoid
levels which causes the pneumocytes to
release more surfactant during a
C-section there's no boost of
glucocorticoids which can cause a
deficiency of surfactant
for symptoms at Birth the newborn might
be asymptomatic because they receive
oxygen via the umbilical cord before
birth a few hours later
initial clinical signs like dyspnea
tachypnea tachycardia and hypoxemia will
develop eventually respiratory failure
will manifest and the baby will present
with chest wall retractions expiratory
grunting nasal flaring or nasal widening
while breathing eventually they might
become cyanotic another fact you need to
remember is that since the O2 pressure
in the blood will be lower than normal
the ductus arteriosus might not close a
small patent ductus arteriosus or PDA
might not cause additional symptoms but
a large one might lead to heart failure
now you'll be able to diagnose neonatal
respiratory distress syndrome by chest
radiography or CT where typical findings
include low lung volume and the classic
diffuse reticulogranular ground glass
appearance this shows up as a contrast
between the black aerated alveoli and
the white or gray ones where there's
alveolar atelectasis another feature is
air bronchogram where the air filled
bronchi appears dark in contrast to the
surrounding white or gray atelectatic
tissue arterial blood gases usually show
hypoxemia and hypercapnia now we can
also assess lung maturity before the
baby is born with amniocentesis where a
sample of amniotic fluid is drawn to
measure the lecithin single myelin ratio
in amniotic fluid both of which are
surfactant components a ratio under 1.5
is predictive of neonatal respiratory
distress syndrome other tests include
the foam stability index and surfactant
albumin ratio which are similar to The
lecithin sphingomyelin ratio test
regarding treatment something essential
to remember is that antenatal
corticosteroid therapy should be
administered to all pregnant individuals
at 23 to 34 weeks gestation who are at
an increased risk of preterm delivery
this is done to prevent or decrease the
severity of the syndrome in newborns
without respiratory failure nasal
continuous positive airway pressure is
the preferred initial intervention
however keep in mind that some
complications of supplemental oxygen can
include retinopathy of prematurity
intraventricular hemorrhage and
bronchopulmonary dysplasia if this fails
endotracheal intubation and
intratracheal surfactant therapy is
needed
all right as a quick recap acute
respiratory distress syndrome happens
when inflammation causes diffuse
alveolar injury and pulmonary edema the
four criteria of ards are it develops
within a week affects both lungs causes
the PF ratio to dip below 300
millimeters of mercury and is not due to
heart failure or other cardiac causes
treatment includes supplemental oxygen
and mechanical ventilation
neonatal respiratory distress syndrome
is caused by a deficiency of surfactant
often this is due to prematurity
maternal diabetes or delivery through
C-section diagnosis is based on a
clinical picture of the infant with the
onset of progressive respiratory failure
and chest radiography showing low lung
volume diffuse reticulogranular ground
glass appearance and Air bronchogram
treatment begins with nasal continuous
positive airway pressure if this fails
endotracheal intubation and
intratracheal surfactant therapy are
needed
now back to our cases
so Mike presents with a cute onset of
shortness of breath high fever and cough
which together with the chest x-ray
showing a right lower lobe infiltrate
led to a diagnosis of pneumonia he was
then started on intravenous antibiotics
but his respiratory symptoms only got
worse the next day Mike developed
hypoxemia and septic shock despite
appropriate treatment the x-rays
detected newly developed bilateral
alveolar opacities heart echography
ruled out heart failure and arterial
blood gas analysis revealed a severely
decreased PF ratio these four factors
mean Mike met all the criteria needed
for an Arts diagnosis
Donna was delivered prematurely by
C-section but she initially had a good
apgar score however soon after delivery
she developed signs of respiratory
distress tachypnea and subcostal
retractions with nasal flaring and
tachycardia given her history and risk
factors a diagnosis of neonatal
respiratory distress syndrome should be
high on the differential list this was
actually confirmed by a chest x-ray
showing the classic reticulogranular
ground glass appearance with air
bronchograms
helping current and future clinicians
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