Pemicu 6 KGD Aldi

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Pemicu 6

Blok Kegawatdaruratan
Aldi Firdaus
405140098
LI
1. Menjelaskan ttg ARDS & Gagal Napas
RESPIRATORY FAILURE
RESPIRATORY FAILURE
• Definition
Respiration is gas exchange between the
organism and its environment. Function of
respiratory system is to transfer O2 from
atmosphere to blood and remove CO2 from
blood.

• Clinically
Respiratory failure is defined as PaO2 <60
mmHg while breathing air, or a PaCO2 >50
mmHg.
Respiratory Failure
Respiratory failure may be acute or chronic:
• Acute hypercapnic respiratory failure develops over
minutes to hours. The pH is usually therefore less than 7.3.
• Chronic respiratory failure develops over several days or
longer. There is sufficient time for renal compensation and
an increase in bicarbonate so the pH is usually only slightly
decreased.
• Clinical markers of long-standing hypoxaemia include
polycythaemia and cor pulmonale.
Classification of Respiratory Failure
Respiratory failure is Classifieds into type I or type II relates to
the absence or presence of hypercapnia respectively.
Type 1 respiratory failure is defined as hypoxemia
without hypercapnia, and indeed the PaCO2 may be normal or
low. It is typically caused by a ventilation/perfusion (V/Q)
mismatch; the volume of air flowing in and out of the lungs is not
matched with the flow of blood to the lungs. The basic defect in
Type 1 respiratory failure is failure of oxygenation characterized
by:
PaO2 decreased (< 60 mmHg
(8.0 kPa))

PaCO2 normal or decreased


(<50 mmHg (6.7 kPa))
PA-aO2 increased
Type I: caused by conditions that affect oxygenation
1. Low ambient oxygen (e.g. at 4. Diffusion problem
high altitude). (oxygen cannot enter the
capillaries due to
2. Ventilation-perfusion parenchymal disease,
mismatch (parts of the lung e.g.in pneumonia or ARD
receive oxygen but not S).
enough blood to absorb it,
e.g. pulmonary embolism.
5. Shunt (oxygenated blood
mixes with non-
3. Alveolar hypoventilation oxygenated blood from
(decreased minute volume the venous system,
due to reduced respiratory e.g. right-to-left shunt).
muscle activity, e.g. in
acute neuromuscular
disease); this form can also
cause type 2 respiratory
failure if severe.
Common causes of type I respiratory failure

• Chronic obstructive • Pulmonary hypertension.


pulmonary disease (COPD). • Cyanotic congenital heart
• Pneumonia. disease.
• Pulmonary oedema. • Bronchiectasis.
• Pulmonary fibrosis. • Acute respiratory distress
• Asthma. syndrome.
• Pneumothorax. • Kyphoscoliosis.
• Pulmonary embolism. • Obesity.
Type 2
Hypoxemia (PaO2 <8kPa) with hypercapnia (PaCO2 >6.0kPa).
The basic defect in type 2 respiratory failure is characterized by:

PaO2 decreased (< 60 mmHg


(8.0 kPa))

PaCO2 increased (> 50 mmHg


(6.7 kPa))
PA-aO2 normal
pH decreased
Type 2 respiratory failure is caused by:
• Inadequate alveolar ventilation; both oxygen and carbon
dioxide are affected.
• Defined as the build up of carbon dioxide levels (PaCO2)
that has been generated by the body but cannot be
eliminated.
Type II respiratory failure caused by:

A. Increase airway C. A decrease in the area of


the lung available for gas
resistance (Chronic exchange (such as
obstructive in chronic bronchitis).
pulmonary disease,
asthma, D. Neuromuscular problems
suffocation) (Guillain-Barré
syndrome, myasthenia
gravis, motor neurone
B. Reduced breathing disease).
effort (drug effects,
brain stem lesion, E. Deformed (kyphoscoliosis),
extreme obesity). rigid (ankylosing
spondylitis), or flail chest.
Common causes of type II respiratory failure

• COPD. • Head injuries and neck


• Severe asthma. injuries.
• Drug overdose • Obesity.
poisoning. • Pulmonary oedema.
• Myasthenia gravis. • Adult respiratory
• Polyneuropathy. distress syndrome.
• Poliomyelitis. • Hypothyroidism.
• Muscle disorders
Signs & Symptoms:
Symptoms • Tachycardia and cardiac
• The history may indicate the arrhythmia may result from
underlying cause, e.g. hypoxaemia and acidosis.
paroxysmal nocturnal • Cyanosis.
dyspnoea, and orthopnoea
• Polycythaemia is a
in pulmonary oedema.
complication of long-
• Both confusion and reduced
standing hypoxaemia.
consciousness may occur.
• Cor pulmonale: pulmonary
Signs
hypertension is frequently
• Localised pulmonary present and may induce right
findings are determined by ventricular failure, leading to
the underlying cause. hepatomegaly and peripheral
• Neurological features may oedema.
include restlessness, anxiety,
confusion, seizures, or
Respiratory Failure
Clinical Manifestations
• Sudden or gradual onset
• Severe morning headache
– Rapid, shallow breathing pattern
– Tripod position
• Cyanosis
– Late sign
• Tachycardia and mild hypertension
– Early signs
 A sudden decrease in PaO2 or rapid increase in
PaCO2 indicates a serious condition
Diagnostic considerations
 Respiratory failure is a common and  Those with acute respiratory distress
a life-threatening condition that syndrome (ARDS) require early
demands prompt diagnosis and elective intubation because the
assessment and appropriate duration of respiratory failure is
management. longer.

 Failure to visualize an obvious  Hypercapnic respiratory failure occurs


abnormality on chest radiographs secondary to a variety of causes:
in hypoxemic respiratory failure
suggests the possibility of right-to-
 Increased respiratory muscle load.
left shunting.

 Impaired neuromuscular
 The vast majority of patients in
acute respiratory failure due to function.
cardiogenic pulmonary edema
respond to measures to reduce  Decreased respiratory drive
preload and afterload. caused by central nervous system
(CNS) depression.
Differential Diagnoses

• Acute Respiratory Distress Syndrome • Pneumonia, Viral


• Sleep Apnea • Pneumothorax
• Asthma • Pulmonary Edema
• Atelectasis • Cardiogenic Shock
• Cardiogenic Shock • Pulmonary Edema, Neurogenic
• Cardiomyopathy, Dilated • Pulmonary Embolism
• Cardiomyopathy, Hypertrophic • Pulmonary Fibrosis, Idiopathic
• Cor Pulmonale • Pulmonary Fibrosis, Interstitial
• Diaphragmatic Paralysis • Primary Pulmonary Hypertension
• Emphysema • Secondary Pulmonary Hypertension
• Myocardial Infarction • Respiratory Acidosis
• Pneumonia, Aspiration • Restrictive Lung Disease
• Pneumonia, Bacterial • Shock, Distributive
• Pneumonia, Community-Acquired • Ventilation, Mechanical
• Ventilation, Noninvasive
Investigations:
• Arterial blood gas analysis: • Serum creatine kinase
Confirmation of diagnosis
and troponin I: to help
• CXR: often identifies the
exclude recent
cause of respiratory failure.
• FBC: anemia can contribute
myocardial infarction.
to tissue hypoxia; • Elevated creatine kinase
polycythaemia may indicate may also indicate
chronic hypoxaemic myositis.
respiratory failure.
• Renal function tests and
LFTs: may provide clues to
the aetiology or identify
complications associated
with respiratory failure.
Investigations:
• TFTs (hypothyroidism may
• Right heart catheterization: if
cause chronic hypercapnic
respiratory failure). there is uncertainty about
cardiac function, adequacy of
• Spirometry: useful in the
volume replacement, and
evaluation of chronic
systemic oxygen delivery.
respiratory failure.
• Pulmonary capillary wedge
• Echocardiography: if a
pressure may be helpful in
cardiac cause is suspected
distinguishing cardiogenic
for ARF.
from noncardiogenic oedema.
• Pulmonary function tests in
the evaluation of CRF.
• ECG: to evaluate a
cardiovascular cause.
Management:
• A patient with acute respiratory Hypoxemia
failure generally needs prompt • Ensure adequate oxygen delivery to
hospital admission in an intensive tissues, generally achieved with a
care unit. PaO2 of 60 mm Hg or an arterial
• Many patients with chronic oxygen saturation (SaO2) of greater
respiratory failure can be treated at than 90%.
home, depending on the severity of • Beware the prolonged use of high-
respiratory failure, underlying cause, concentration oxygen in chronic
comorbidities and social sufferers who have become reliant
circumstances. on their hypoxic drive to maintain
• Immediate resuscitation may be an adequate ventilation rate.
required. • Elevating the PaO2 too much may
• Appropriate management of the reduce the respiratory rate so that
underlying cause. the PaCO2 may rise to dangerously
high levels.
Management:
Assisted ventilation: • Non-invasive ventilation
• Mechanical ventilation is used (NIV) has been increasingly
to increase PaO2 and to lower used as an alternative to
intubation.
PaCO2.
• NIV improves survival and
• Mechanical ventilation also reduces complications for
rests the respiratory muscles selected patients with acute
and is an appropriate therapy respiratory failure.
for respiratory muscle fatigue.
• The main indications are
• Weaning patients with chronic exacerbation of COPD,
respiratory failure off of cardiogenic pulmonary
mechanical ventilation may be oedema, pulmonary infiltrates
very difficult. in immunocompromised
patients, and weaning of
previously intubated stable
patients with COPD.
Complications:
• Pulmonary: PE, pulmonary • Polycythaemia.
fibrosis, and complications • Hospital-acquired infection:
secondary to the use of pneumonia, UTI, and catheter-
mechanical ventilation. related sepsis, are frequent
• CVS: Cor pulmonale, • Renal: acute kidney injury
hypotension, reduced cardiac (ARF) and abnormalities of
output, arrhythmias, electrolytes and acid-base
pericarditis, and acute MI. balance are common.
• Gastrointestinal: Gastric • Nutritional: Malnutrition and
distension, haemorrhage, complications related to
ileus, pneumoperitoneum. administration of enteral or
diarrhoea, and duodenal parenteral nutrition.
ulceration caused by stress is • Complications associated with
common in patients with nasogastric tubes, e.g.
acute respiratory failure. abdominal distention and
diarrhea.
Acute Respiratory distress Syndrome
(ARDS)
• Variety of unrelated massive insults injure gas
exchanging surface of Lungs
• First described as clinical syndrome in 1967 by
Ashbaugh & Petty
• Clinical terms synonymous with ARDS
Acute respiratory failure
Capillary leak syndrome
Da Nang Lung
Shock Lung
Traumatic wet Lung
Adult
hyaline membrane disease
Risk Factors in ARDS
Sepsis 3.8%
Cardiopulmonary bypass 1.7%
Transfusion 5.0%
Severe pneumonia 12.0%
Burn 2.3%
Aspiration 35.6%
Fracture 5.3%
Intravascular coagulopathy 12.5%
Two or more of the above 24.6%
PATHOPHYSIOLOGY AND
PATHOGENESIS
• Diffuse damage to gas-exchanging surface
either alveolar or capillary side of
membrane
• Increased vascular permeability causes
pulmonary edema
• Pathology: fluid and RBC in interstitial
space, hyaline membranes
• Loss of surfactant: alveolar collapse
CRITERIA FOR DIAGNOSIS OF ARDS
• Clinical history of catastrophic event
Pulmonary or Non pulmonary (shock, multi system
trauma)
• Exclude
chronic pulmonary diseases left
ventricular failure
Must have respiratory distress
tachypnea >20 breath/minute
Labored breathing
central cyanosis
CXR- diffuse infiltrates
PaO2 <50mmHg FiO2 >O.6
Compliance <50 ml/cm H2O increased shunt
and dead space
MANAGEMENT OF ARDS
• Mechanical ventilation
corrects hypoxemia/respiratory acidosis
• Fluid management
correction of anemia and hypovolemia
• Pharmacological intervention
Dopamine to augment C.O.
Diuretics
Antibiotics
Corticosteroids - no demonstrated benefit
early disease, helpful 1 week later
• Mortality continues to be 50 to 60%
Acute Lung Injury
and
ARDS
Definition
• Acute onset (<7days) respiratory failure/distress
• Diffuse, bilateral infiltrates on CXR
• Absent left atrial hypertension (PAOP ≤18mmHg)
• Or absent clinical evidence of left atrial hypertension
• PaO2/ FiO2 <300mmHg (ALI)
• PaO2/ FiO2 <200mmHg (ARDS)2
Risk Factors
• Alcoholism
• Genetic predisposition
Causes
• Direct Injury1
• Pneumonia
• Aspiration
• Drowning
• Amniotic fluid and fat embolism
• Alveolar haemorrhage
• Smoke, toxic gas inhalation
• Reperfusion (incl rapid drainage pleural effusion)
• Unilateral lung re-implantation
Causes
• Indirect Injury1
• Severe Sepsis
• Massive transfusion
• Shock
• Pancreatitis
• Salicylate/ narcotic overdose
• Anaphylaxis
• Cardiopulmonary bypass
Differential
• LVF
• Fluid overload
• Mitral stenosis
• Lymphangitis carcinomatosis
• Interstitial lung disease1
Physical/ chemical injury
Activation Innate
Inflammatory Cascade

Leakage Protein Rich


Oedema Fluid
Inflammatory Cellular
Infiltrates

Diffusion Abnormalities
V/Q Mismatch

Hypoxia

Respiratory Failure
Physical/ chemical injury
Activation Innate
Inflammatory Cascade

Cellular Infiltrate
Atelectasis
Oedema Fluid

Reduced Thoracic
Compliance +
Vasoconstriction

Hypoxia

Respiratory Failure
Physical/ chemical injury
Activation Innate
Inflammatory Cascade

Small Vessel Thrombosis

Increased Dead Space

Hypoxia

Respiratory Failure
Alveolar
Damage

Hypoxic
Capillary
Damage
Vasoconstriction

Leakage
↑Dead Space Oedema
Fluid

Hypoxia

Inflammatory
↓Thoracic
Cellular
Compliance
Infiltrates

V/Q
Atelectasis
Mismatch
Respiratory Failure

Atelectasis/
Reduced Lung
Compliance

↑ Dead Space Hypoxaemia


Histologically
• Exudative Phase3
• Neutrophilic Infiltrate
• Alveolar Haemorrhage
• Proteinaceous Pulmonary Oedema
• Cytokines (TNF, IL1,8)
» ↑ Inflammation
» ↑ Oxidative Stress and Protease Activity
» ↓ Surfactant Activity
» Atelectasis
Histologically
• Elastase- induced capillary and alveolar
damage3
• ↑ Alveolar flooding
• ↓ Fluid clearance
• Capillary thrombosis
• ↓ Anticoagulant proteins
• ↑ Procoagulant proteins (Tissue Factor)
• ↑ Anti- fibrinolytic Protein (Plasminogen Activator
Inhibitor)
Post Acute Phase
• Fibroproliferative Phase3
– Variable time period
– Fibrosis
– Chronic Inflammation
– Neovascularisation

• Resolution3
– Improvement of hypoxaemia
– Improved dead space and lung compliance
– Resolution radiographic abnormalities
– Can take up to 1 year
– Residual restrictive or obstructive picture
Long Term
• Chronic Respiratory Disease
• Muscle Fatigue
• Muscle Wasting
• Weakness
Treatment
• Ventilation
• Fluid Management
• Steroids
• Other Stuff
Ventilation
• Tidal Volumes
• PEEP
• Positioning
• Weaning Protocols
Tidal Volume
• Recommended 4-6ml/kg4
• High tidal volumes4
• Overdistention of alveoli
• Local inflammatory response resulting in systemic
inflammation
• TNF, IL6, IL10,
Tidal Volume 4

• Low tidal volume ventilation


• Weight
• Predicted not actual
• Plateau Pressure
• ≤30cm H2O
• Resp Rate
• Titrated to pH 7.3-7.45
• PEEP and FiO2
• Adjusted to maintain saturation
• Low tidal volume may result in hypercarbia
• ARMA (Respiratory Management in ALI/ARDS Trial)
• NaHCO3 infusions/ hyperventilation to maintain pH
Tidal Volumes
• Same sedation strategies
• No ↑ duration of ventilation
• High frequency oscillatory ventilation shown
no benefit over low tidal volume ventilation
• 30 day mortality not statistically significant (37% vs
52%, p=0.10)
• Earlier recovery from hypoxia
• Only ventilation strategy shown to
reduce mortality (40% - 31%)4
Fluid Management
• Fluid movement regulated by:
• Starling equation
• Vessel wall
– Ability to filter fluid
– Selective permeability to proteins
Fluid Management
• Study of conservative vs liberal fluid
management5
• 60 day mortality: 25.5 vs 28.4% p=0.30
• 1st 28 days ventilator free: 14.6 vs 12.1 p<0.001
• 1st 28 days ICU free: 13.4 vs 11.2 p<0.001
• Difference in organ failure and need for dialysis not
statistically significant
• No specific mention of CVP/ PAOP levels which to aim
for
• Conservative = 4mmHg Liberal = 10-14mmHg CVP
Steroids
• Theoretical use to ↓inflammatory response
associated with ARDS6
• 2006 study6
• No ↓60 day mortality (28.6% vs 29.2% p= 0.10)
• Use of steroids 14+ days post onset: ↑ mortality
• ↓ need for vasopressors
• ↑ ventilator and shock free days
• ↑ neuromuscular weakness
• Short term improvement in oxygenation
Other stuff
• Extracorporeal membrane oxygenation
• Improvement in oygenation
• No ↑ long term survival
• Vasodilators
• Improved oygenation
• No ↑ long term survival
• Ketoconazole
• Pentoxyfilline
• Nutritional modification
• Antioxidants
• Surfactant
• B2 stimulants1
Emergency Department Summary
• PREVENT!
• Low tidal volume ventilation
• Restrict PEEP
• Restrict Fluids (if possible)
• Initiate Weaning Protocol
• Supine Ventilation
Acute Severe Asthma

Status Asthmaticus
• Exacerbations of asthma  feared by patients
 life-threatening
• Controller therapy : prevent exacerbations
 ICS* and combination inhalers (very
effective)

Harrison’s Principle of Medicine, 18th ed


Clinical Features
• Chest tightness
• Wheezing
• Dyspnea : not or poorly relieved by usual reliever inhaler
• So breathless - unable to complete sentences  may
become cyanotic

Harrison’s Principle of Medicine, 18th ed


Examination
• ↑ ventilation
• Hyperinflation*
• Tachycardia
• Pulsus paradoxus : rare
• Marked fall in spirometric values and PEF (Peak Expiratory
Flow)
• ABG :
– Hypoxia
– PaCO2 low (hyperventilation)
– A normal or rising PaCO2 : impending respiratory failure  requires
immediate monitoring and therapy.
• Chest roentgenogram : not usually informative, but may show
pneumonia or pneumothorax.
Harrison’s Principle of Medicine, 18th ed
Clinical review: Severe asthma, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137395/
Treatment*
• High concentration of oxygen (by face mask)  achieve oxygen saturation of >90%
• High doses of short-acting inhaled β2-agonists (nebulizer or via a metered dose
inhaler with a spacer)
• Not satisfactory response β2-agonists  add : inhaled anti-cholinergic
• Refractory to inhaled therapies  slow infusion of aminophylline
– MONITOR BLOOD LEVELS! Especially in oral theophylline
• IV or nebulizer Magnesium sulfate + inhaled β2-agonists : effective, well tolerated,
but not routinely recommended

• Severely ill patients w/ impending respiratory failure : IV β2-agonists + prophylactic intubation


• Patients with respiratory failure :
– Intubate + institute ventilation
– Conventional bronchodilator
– Not respond  Anesthetic : halothane
– NO Sedatives : may depress ventilation
– Antibiotics : not routinely unless there are signs of pneumonia.

Harrison’s Principle of Medicine, 18th ed


Inhaled β2-agonists
• Safe, effective (obstruction)
• Salbutamol (albuterol: most frequently used
agent : its potency, duration of action (four to
six hours) and β2-selectivity.
– 2.5 mg of salbutamol (0.5 ml) in 2.5 ml NS for each
nebulisation

Clinical review: Severe asthma, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137395/


Anticholinergics and methylxanthines
• Anticholinergics (ipratropium bromide) : controversy
on their ability to offer additional bronchodilation
• Methylxanthines (theophylline) : not generally
recommended, some warrant its use in ED :
– enough data : benefits patients after 24 hours.
– non bronchodilating  action on the diaphragm and anti-
inflammatory effects,

Clinical review: Severe asthma, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137395/


Corticosteroid treatment
• speed the resolution, reduce relapse, reduce
mortality
• Recommended for most patients, especially who
don’t respond to β2-agonists
• Long-term treatment inhaled corticosteroids
– Reduce hospitalization rates in younger patients with
asthma
– Reduce the risk of rehospitalization and all-cause
mortality in elderly asthmatics

Clinical review: Severe asthma, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137395/


Subcutaneous epinephrine and terbutaline
• Considered to :
– who are not responding adequately to continuous
nebulised salbutamol
– who are unable to cooperate (depression of
mental status, apnea, coma)

Clinical review: Severe asthma, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137395/


Clinical review: Severe asthma, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137395/
COPD
Chronic obstructive pulmonary disease
COPD

• Chronic Obstructive Pulmonary Disease

• A progressive disease that affects the lungs,


making it difficult to breathe
COPD: an umbrella term
• Umbrella term used to describe progressive lung
diseases which include:

• Emphysema
• Chronic bronchitis
• Refractory (irreversible) asthma
• Severe bronchiectasis
Other names for COPD
• Chronic Obstructive Lung Disease (COLD)

• Chronic Lower Respiratory Disease (CLRD)


COPD
• Chronic obstructive pulmonary disease (COPD)
is a lung ailment that is characterized by a
persistent blockage of airflow from the lungs.

• It is an under-diagnosed, life-threatening lung


disease that interferes with normal breathing
and is not fully reversible.
Causes
• Most cases of COPD occur as a result of long-term
exposure to lung irritants that damage the lungs and
the airways

•  The most common irritant that causes COPD is


cigarette smoke

• In rare cases, a genetic condition called alpha-1


antitrypsin deficiency may play a role in causing COPD
Who is at risk?
• People who smoke or are exposed to smoke

• People who have a family history of COPD are more likely to


develop the disease if they smoke

• Long-term exposure to other lung irritants also is a risk factor


for COPD

• Almost 90% of COPD deaths occur in low- and middle-income


countries, where effective strategies for prevention and control
are not always implemented or accessible.
Symptoms
• breathlessness
• abnormal sputum (a mix of saliva and mucus
in the airway)
• a chronic cough
• daily activities can become very difficult as
the condition gradually worsens
diagnosis
• A simple diagnostic test called "spirometry“
measures how much air a person can inhale
and exhale, and how fast air can move into
and out of the lungs

• Spirometry can detect


COPD long before its
Symptoms appear. 
Treatment
• COPD has no cure

• Quitting smoking is the most important step


an individual can take to treat COPD

• Other treatments for COPD may include


medicines, vaccines, pulmonary rehabilitation
(rehab), oxygen therapy, and surgery
Managing copd
• COPD symptoms usually slowly worsen over time

• A cold, the flu, or a lung infection may cause


symptoms to intensify

• Prescription antibiotics may treat infections and


other medicines, such as bronchodilators and
inhaled steroids, can help facilitate breathing
Managing COPD
• Avoid lung irritants

• Get ongoing care

• Manage the disease and its symptoms

• Prepare for emergencies


Pleural Effusion

excess quantity of fluid in the pleural


space

Harrison’s Principle of Medicine, 18th ed


Terminology
• Pleuritis (also referred to as pleurisy) = inflammation of the pleura.
Can occur w/ or w/o exudation
• Parapneumonic effusion = A pleural effusion associated with bacterial
pneumonia, bronchiectasis, or lung abscess
• Complicated parapneumonic effusion = parapneumonic effusions that require
tube thoracostomy for their resolution.
• Empyema (or pus in the pleural space) requires the presence of bacteria on
Gram’s staining of the pleural fluid.

• Loculated effusion = Fluid anatomically confined and not freely flowing in the
pleural space
– occur when there are adhesions between the visceral and the parietal pleurae.

Rosen's, 7th ed.


Etiology
Most common
• Western countries : congestive heart failure,
followed by malignancy, bacterial pneumonia,
and pulmonary embolism.
• In other countries : tuberculosis

Rosen's, 7th ed.


Pathogenesis
• Pleural fluid formation (influx) > pleural fluid
absorption (efflux)
• Normal :
– Fluid enters - parietal pleura ( systemic capillaries)
or - interstitial spaces of the lung ( visceral pleura)
or - peritoneal cavity (small holes in the diaphragm)
– Fluid removed - lymphatics (in parietal pleura) &
• Rosen’s : pulmonary capillaries (in visceral pleura)

Harrison’s Principle of Medicine, 18th ed


• Movement of fluid : Starling’s law.
• Direction of pleural fluid flow : difference in hydrostatic
pressure between the systemic and the pulmonary
circulations
• Dynamic equilibrium : influx = efflux, with ±1 L of fluid
traversing the pleural space in 24 hours.
• Amount of fluid that remains in the pleural space is small
(∼0.1–0.2 mL/kg body weight)
• Clinically or radiographically undetectable

Rosen's, 7th ed.


Transudative effusion

• Transudates = ultrafiltrates of plasma, containing very little


protein.
• Develops when : hydrostatic pressure ↑or oncotic pressure ↓
within pleural microvessels.
• Causes :
– CHF (90%) hydrostatic pressure ↑
– Cirrhosis, nephrotic syndrome, malnutrition  hipoalbuminemia 
effusion

Rosen's, 7th ed.


Exudative effusion
• Exudates = high amounts of Etiology :
protein • 1st common form : parapneumonic
• Reflecting an abnormality of the effusion  infection of the adjacent
pleura itself. lung
• 2nd most common form : malignant
Pathogenesis : effusion
• Increased membrane • May also response to inflammatory
permeability or defective abdominal processes : pancreatitis or
lymphatic drainage. subphrenic abscess
• Inflammation in pulmonary or Outcome :
pleura can result in an • Reabsorbed; organize into fibrous
exudative effusion. tissue  pleural adhesions.

Rosen's, 7th ed.


Rosen's, 7th ed.
Clinical Features
• Symptoms : Due to the underlying disease
• Small pleural effusion : asymptomatic
• New PLEf : localized pain or referred to
shoulder
• PF volume >= 500 mL dyspnea on exertion
or at rest (compromised pulmonary function)

Rosen's, 7th ed.


Diagnostic Approach
• Determine whether the effusion is a transudate or an
exudate.
– Transudate : alteration of systemic factors
Causes : LV failure and cirrhosis.
– Exudate : alteration of local factors
Causes : bacterial pneumonia, malignancy, viral infection, and
pulmonary embolism.

• Some pleural effusions may have characteristics of both

Harrison’s Principle of Medicine, 18th ed


Exudative pleural effusions : >= 1 of the criteria
1. Pleural fluid protein : serum protein >0.5
2. Pleural fluid LDH : serum LDH >0.6
3. Pleural fluid LDH > 2/3 normal upper limit for serum

• If >=1 exudative criteria are met AND the patient is clinically thought to have a
condition producing a transudative effusion  measure the protein levels in the
serum – in the pleural fluid
– If this gradient> 31 g/L (3.1 g/dL)  almost all such patients have a
transudative pleural effusion.

• If exudative pleural effusion, obtain the following tests :


description of the fluid, glucose level, differential cell count, microbiologic studies,
and cytology.

Harrison’s Principle of Medicine, 18th ed


• Pleural fluid analyses
– pH <7.3 - parapneumonic effusions, malignancies,
rheumatoid effusions, tuberculosis, and systemic
acidosis.
– pH < 7.0 – empyema (or esophageal rupture).
– pH < 7.0 & glucose <50 mg/dL indications for
tube thoracostomy.

Rosen's, 7th ed.


• Approach to the diagnosis of pleural
effusions.
PF = pleural fluid;
CHF = congestive heart failure;
CT = computed tomography;
LDH = lactate dehydrogenase;
PE = pulmonary embolism;
TB = tuberculosis

Harrison’s Principle of Medicine, 18th ed


• History :
– Viral : prodrome symptoms (low-grade fever, sore throat,
etc)  no?  may be : pulmonary embolism
• Classic physical signs :
– Diminished breath sounds
– Dullness to percussion
– Decreased tactile fremitus
– Occasionally a localized pleural friction rub*
– Massive effusions : signs of mediastinal shift

Rosen's, 7th ed.


• Chest radiography :
– Blunting of the costophrenic angle on the upright chest radiograph
– <250 mL visible in posterior costophrenic gutter on a lateral projection
– 250-500 mL : frontal (AP or PA) projection
– >500 mL :
• hemidiaphragm is obscured*
• upwardly concave meniscus may be seen because pleural fluid has
a tendency to layer higher laterally than centrally
• Pleural fluid can extend up a major fissure and appear as a
homogeneous density in the lower 2/3 of the lung field.
– Massive pleural effusion : totally opacified hemithorax.

Rosen's, 7th ed.


• Ultrasound and CT : localizing effusions and characterizing
underlying lung processes.
Ultrasound
• It can be used to guide thoracentesis and decrease the risk of
complications, particularly in the case of small or loculated
effusions.
• Pleural effusion : hypoechoic fluid located above the
diaphragm w/ loss of the usual mirror-image artifact.

• Pleural effusions < 500 mL, however, can be missed with


bedside radiography.

Rosen's, 7th ed.


Diagnosis
• The presence of free pleural fluid - demonstrated with
– Lateral decubitus radiograph
– Computed Tomography (CT) of the chest, or
– Ultrasound
• If the free fluid separates the lung from the chest wall by >10
mm  therapeutic thoracentesis

Harrison’s Principle of Medicine, 18th ed


Management
Factors indicating the likely need for a procedure more invasive than a thoracentesis (in
increasing order of importance) include:
1. loculated pleural fluid
2. pleural fluid pH < 7.20
3. pleural fluid glucose < 3.3 mmol/L (<60 mg/dL)
4. positive Gram stain or culture of the pleural fluid
5. the presence of gross pus in the pleural space

• If the fluid recurs after the initial therapeutic thoracentesis & presentation of the above
characteristics  repeat thoracentesis
• If the fluid cannot be completely removed with the therapeutic thoracentesis :
– Insert a chest tube and instilling a fibrinolytic (e.g., streptokinase, 250,000 units)
– or performing thoracoscopy with the breakdown of adhesions.
– Decortication : when the above are ineffective.

Harrison’s Principle of Medicine, 18th ed


Effusion Due to Heart Failure
• Most common cause of pleural Diagnostic
effusion : left ventricular failure. • Thoracentesis
Pathogenesis • A pleural fluid N-terminal pro-brain
• Fluid in the lung interstitial spaces natriuretic peptide (NT-proBNP) >1500
exit in part across the visceral pg/mL  effusion secondary to CHF
pleura.
• This overwhelms the capacity of the
lymphatics in the parietal pleura to Best treated with diuretics.
remove fluid. – If the effusion persists  thoracentesis
• Isolated right-sided pleural effusions
are more common than left-sided
effusions in HF.

Harrison’s Principle of Medicine, 18th ed


Hepatic Hydrothorax
• In ~5% of patients with cirrhosis and ascites : pleural
effusion
• direct movement of peritoneal fluid through small
openings in the diaphragm  into the pleural space.
• The effusion is usually right-sided & frequently is
large enough to produce severe dyspnea.

Harrison’s Principle of Medicine, 18th ed


Parapneumonic Effusion
• Associated with bacterial pneumonia, lung abscess, or bronchiectasis
• Probably the most common cause of exudative pleural effusion in the US.
• Empyema = grossly purulent effusion.
• The possibility of a parapneumonic effusion should be considered whenever a
patient with a bacterial pneumonia is initially evaluated.

Presentation :
• Aerobic bacterial pneumonia + pleural effusion  acute febrile illness : chest pain,
sputum production, and leukocytosis.
• Anaerobic infections  subacute illness : weight loss, a brisk leukocytosis, mild
anemia, history of some factor that predisposes them to aspiration.

Harrison’s Principle of Medicine, 18th ed


Effusion Secondary to Malignancy
 2nd most common type of exudative pleural effusion : due to metastatic malignancy
– Lung carcinoma
– Breast carcinoma
– Lymphoma.

DIAGNOSIS
• Most common symptom : Dyspnea  frequently out of proportion to the size of the effusion.
• The pleural fluid is an exudate, and its glucose level ↓ if the tumor burden in the pleural
space is high.
• The diagnosis is usually made  cytology of the pleural fluid.
– If negatif  THORACOSCOPY (if malignancy is strongly suspected)
– At the time of thoracoscopy, a procedure such as pleural abrasion should be performed to effect a
pleurodesis.
– If thoracoscopy is unavailable  NEEDLE BIOPSY of the pleura

Harrison’s Principle of Medicine, 18th ed


Treatment
• Treated symptomatically :
– since the presence of the effusion indicates disseminated disease and
– most malignancies associated with pleural effusion are not curable
with chemotherapy.
• The only symptom : dyspnea
– If the patient's lifestyle is compromised by dyspnea, & if the dyspnea is
relieved with a therapeutic thoracentesis, then one of the following
procedures should be considered:
1. Insertion of a small indwelling catheter; or
2. Tube thoracostomy with the instillation of a sclerosing agent
such as doxycycline, 500 mg.

Harrison’s Principle of Medicine, 18th ed


Mesothelioma
• Primary tumors
• Arise from the mesothelial cells that line the pleural cavities
• Most are related to asbestos exposure.
• Patients : chest pain and shortness of breath.

Examination
• Chest radiograph : Treatment
– pleural effusion • Chest pain : opiates
– generalized pleural thickening, and • Shortness of breath : oxygen
– Shrunken hemithorax and/or opiates.
• Thoracoscopy
• Open pleural biopsy

Harrison’s Principle of Medicine, 18th ed


Effusion Secondary to Pulmonary
Embolization
• DD of undiagnosed pleural effusion  pulmonary embolism.
• Symptom : Dyspnea (most common)
• PF is almost always an exudate.
• Examination : Spiral CT scan or pulmonary arteriography.
• Treatment : treat the pulmonary emboli.
– If the effusion increases in size after anticoagulation  the patient
probably has recurrent emboli or another complication (such as a
hemothorax or a pleural infection)

Harrison’s Principle of Medicine, 18th ed


Tuberculous Pleuritis
• Most common cause of an exudative pleural effusion
– Relatively uncommon in the United States.
• Usually associated with primary TB and a hypersensitivity
reaction to tuberculous protein in the pleural space.

Symptoms :
o Fever
o Weight loss
o Dyspnea
o Pleuritic chest pain.

Harrison’s Principle of Medicine, 18th ed


EXAMINATION
• PF is an exudate, predominantly small lymphocytes.
• High levels of TB markers in PF :
– Adenosine deaminase > 40 IU/L
– Interferon > 140 pg/mL, or
– Positive polymerase chain reaction (PCR) for tuberculous DNA).
• Culture of the PF
• Needle biopsy of the pleura
• Thoracoscopy

TREATMENT : Treat the pulmonary TB


Effusion Secondary to Viral Infection
• Undiagnosed exudative pleural effusions.
• No diagnosis is established for ~20% of exudative effusions
• Resolve spontaneously with no long-term residua.
• Should not be too aggressive in trying to establish a diagnosis for the
undiagnosed effusion, particularly if the patient is improving clinically.
AIDS
• Pleural effusions are uncommon in such patients.

Harrison’s Principle of Medicine, 18th ed


Chylothorax
• Thoracic duct is disrupted and chyle accumulates in the pleural space.
• Causes :
– Trauma : most common
– Tumors in the mediastinum
• Symptoms : dyspnea

EXAMINATION
• Chest radiograph : large pleural effusion
• Thoracentesis : milky fluid
• Biochemical analysis : triglyceride >1.2 mmol/L (110 mg/dL)
• No obvious trauma : lymphangiogram and a mediastinal CT scan to assess
the mediastinum for lymph nodes.

Harrison’s Principle of Medicine, 18th ed


TREATMENT
• Treatment of choice : insertion of a chest tube +
administration of octreotide.
– Fail  pleuroperitoneal shunt (Unless the patient has chylous ascites)
• Should not undergo prolonged tube thoracostomy with chest
tube drainage  will lead to malnutrition and immunologic
incompetence.
Hemothorax
• Thoracentesis reveals bloody pleural fluid  obtain hematocrit on
the pleural fluid.
• Hct in PF > ½ Hct in the peripheral blood

• Causes :
– Trauma : most common
– Rupture of a blood vessel
– Tumor
• Treatment :
– Tube thoracostomy  allows continuous quantification of bleeding.
– If the bleeding emanates from a laceration of the pleura  apposition of the
two pleural surfaces
– If the pleural hemorrhage > 200 mL/h  thoracoscopy or thoracotomy.

Harrison’s Principle of Medicine, 18th ed


Miscellaneous Causes of Pleural Effusion
• There are many other causes of pleural effusion
• Key features :
– PF amylase level ↑  esophageal rupture or pancreatic disease
– Febrile, PMN cells in the PF, and has no pulmonary parenchymal abnormalities  an
intraabdominal abscess
– Benign ovarian tumors can produce ascites and a pleural effusion (Meigs' syndrome), as
can the ovarian hyperstimulation syndrome.
– Several drugs can cause pleural effusion; the associated fluid is usually eosinophilic.
– Pleural effusions commonly occur  coronary artery bypass surgery (CABG)
– Effusions occurring within the 1st weeks are typically left-sided and bloody, with large
numbers of eosinophils, and respond to one or two therapeutic thoracenteses.
– Effusions occurring after the first few weeks are typically left-sided and clear yellow,
with predominantly small lymphocytes, and tend to recur.
– Other medical manipulations that induce pleural effusions include abdominal surgery;
radiation therapy; liver, lung, or heart transplantation; or the intravascular insertion of
central lines.

Harrison’s Principle of Medicine, 18th ed


Harrison’s Principle of Medicine, 18th ed
Harrison’s Principle of Medicine, 18th ed
Pleural disease in ED :
• Asymptomatic pleural effusion  tension
pneumothorax
Nontraumatic pleural problems:
• spontaneous pneumothorax and
• pleural inflammation with effusion.
Pneumothorax
Pneumothorax
Pneumothorax : presence of free air in the
intrapleural space.
• Simple : no communication with the
atmosphere or any shift of the
mediastinum or hemidiaphragm.
• Communicating (combat injuries,
secondary to shotgun wounds)  paradox
• Tension
Pneumothorax
Graded according to the degree of collapse :
• small pneumothorax <=15% of the pleural
cavity
• moderate 15 - 60%, and
• large >60%
Pneumothorax
• A spontaneous pneumothorax : absence of any external
precipitating factor, either traumatic or iatrogenic.
– Primary spontaneous pneumothorax = without clinically apparent lung
disease.
– Secondary spontaneous pneumothorax = underlying pulmonary disease
process.
• A traumatic pneumothorax : results from penetrating or
nonpenetrating chest injuries.
• A tension pneumothorax : the pressure in the pleural space is
positive throughout the respiratory cycle.
Traumatic Pneumothorax
Traumatic pneumothoraces can result from both penetrating and
nonpenetrating chest trauma.
– most often caused by a fractured rib that is driven inward, lacerating
the pleura.
– without a fracture when the impact is delivered at full
inspiration with the glottis closed  tremendous increase
in intra-alveolar pressure and the subsequent rupture of
the alveoli.
Treatment Traumatic Pneumothorax
• Traumatic pneumothoraces should be treated with tube thoracostomy
(unless they are very small).
– Hemopneumothorax is present, one chest tube  in the superior part of the
hemithorax to evacuate the air ; and another  in the inferior part of the hemithorax to
remove the blood.
• Iatrogenic pneumothorax (type of traumatic pneumothorax)
– Due to transthoracic needle aspiration, thoracentesis, and the insertion of central
intravenous catheters, trocar?.
– supplemental oxygen or aspiration  unsuccessful  tube thoracostomy.
Pathophysiologic
• Intrapleural pressure is negative (less than atmospheric), −10 mm Hg to −12 mm Hg
(inspiration), −4 mm Hg during expiration.
• Intrabronchial and intraalveolar pressures are negative during inspiration (−1 to −3
mm Hg) and positive during expiration (+1 to +3 mm Hg).
• The alveolar walls and visceral pleura  barrier 
– separates the intrapleural and intraalveolar spaces and
– maintains the pressure gradient.
– defect occurs  air enters the pleural space (loss of negative pressure  lung collapses) until
either the pressures equalize or the communication seals.
• A large pneumothorax  restrictive ventilation impairment, with reduced vital
capacity, functional residual capacity, and total lung capacity.
• Shunting of blood through nonventilated lung tissue  acute hypoxemia, although
over time this effect is mitigated by compensatory vasoconstriction in the collapsed
lung.
Primary Spontaneous Pneumothorax
• 90% due to rupture of apical pleural blebs, small cystic spaces
that lie within or immediately under the visceral pleura.
• disruption of the alveolar-pleural barrier occurs when a
subpleural bulla (or bleb), typically located at the lung apex,
ruptures into the pleural space.
• degradation of elastic fibers within the lung and an imbalance
in the protease-antiprotease and oxidantantioxidant systems
 bullae.
• almost exclusively in smokers  suggests ps have subclinical
lung disease.
• one-half  recurrence.
Clinical Features
• Suddenly while at rest.
• Ipsilateral chest pain and dyspnea
– the pain is typically “pleuritic” in nature (i.e., often described as sharp and made worse with deep
inspiration), but it often evolves over time into a dull, steady ache.
– extreme dyspnea is uncommon (absence of underlying lung disease or tension pneumothorax)
• Cough
• asymptomatic or have only nonspecific complaints
• delay presentation (1 week or >)
• Without treatment  resolve spontaneously within 24 to 72hrs (pneumothorax is still present)
• Physical findings (degree of symptoms) :
– A mild sinus tachycardia (common)
– decreased or absent breath sounds with hyperresonance to percussion (large pneumothorax)
– unilateral enlargement of the hemithorax
– decreased excursion with respirations
– Absent tactile fremitus
– inferior displacement of the liver or spleen.
– etc
Treatment
• Small primary spontaneous pneumothorax (i.e., <20% of the
hemithorax)  6 hours of observation (in ED-based
observation unit )  repeat chest radiograph (before
discharge)  discharged  follow-up evaluation in 24 hours
 air travel and underwater diving must be avoided until the
pneumothorax has completely resolved.
• Larger primary spontaneous pneumothoraces (i.e., ≥20% of
the hemithorax)  aspiration with an intravenous catheter 
6 hours chest radiograph  no reaccumulation of the
pneumothorax  the catheter is removed  discharge
Treatment
The initial recommended treatment : simple aspiration (less invasive,
equally effective as chest tube drainage)
if lung does not expand or has a recurrent pneumothorax
attached to a water-seal device or to a one-way Heimlich valve and managed like a small-
caliber chest tube (tube thoracostomy).
thoracoscopy with stapling of blebs and pleural abrasion (almost 100% successful in
preventing recurrences).

Tube thoracostomy small-caliber (7–14F) :


• first-line intervention in uncomplicated cases or
• after a less invasive approach (i.e., observation or simple aspiration) fails
Secondary Spontaneous Pneumothorax
• Underlying lung disease  (Most) due to chronic obstructive
pulmonary disease
• Lack of pulmonary reserve in these ps  more life-
threatening than it is in normal individuals.
Clinical Features
• Poor pulmonary reserve  dyspnea (nearly
universal) even when the pneumothorax is small.
• tend not to resolve on their own.
• Physical findings (overlap considerably with the
underlying lung disease) :
– hyperexpansion and distant breath sounds
• COPD presents with an exacerbation of dyspnea?
 pneumothorax should be considered
Pathophysiology
• P. jiroveci pneumonia, cytotoxic  repeated
episodes of inflammation  bullous and cystic
changes.
• COPD  chronic exposure to cigarette smoke
 development of large, thin-walled bullae 
risk for rupture
Treatment of spontaneous pneumothorax

2 goals :
1. To evacuate air from the pleural space, and
2. To prevent recurrence
Treatment
• Less invasive approaches (i.e., observation or simple aspiration)  lower
success rates.
 standard size (20–28F) thoracostomy tube.
 larger tube size (≥28F)  detectable pleural fluid or an anticipated need
for mechanical ventilation.
 suction (with a pressure of 20 cm H2O) lung fails to reexpand after
drainage through a water-seal device or Heimlich valve for 24 to 48 hours.
• Ps is not a good operative candidate or refuses surgery  pleurodesis
(attempted by mechanical pleural abrasion or by the intrapleural injection
of a sclerosing agent such as doxycycline).
Tension Pneumothorax
• This condition usually occurs during mechanical ventilation or resuscitative
efforts.
• The positive pleural pressure is life-threatening :
– Ventilation is severely compromised and
– The positive pressure is transmitted to the mediastinum  decreased venous return to
the heart and reduced cardiac output.
Diagnosis :
• Difficulty in ventilation during resuscitation or high peak inspiratory
pressures during mechanical ventilation  strongly suggests the
diagnosis.
• enlarged hemithorax with no breath sounds
• hyperresonance to percussion
• shift of the mediastinum to the contralateral side.
• the alveolar-pleural defect  a one-way valve  air pass into
the pleural space during inspiration  trapping it there during
expiration  progressive accumulation of intrapleural air and
increasingly positive intrapleural pressure  compression of
the contralateral lung with asphyxia  worsening hypoxia
• Intrapleural pressure exceeding 15 to 20 mm Hg  decreased
diastolic filling & cardiac output hypoxia, acidosis, and
shock
Clinical Features
• Asphyxia and decreased cardiac output
• Tachycardia (often >120 beats/min) & hypoxia (common)
• Hypotension is a late and ominous finding
• Distention of the jugular veins (common, difficult to detect)
• Displacement of the trachea to the contralateral side
(uncommon finding, usually occurring only in the
immediately preterminal phase )
• etc
Treatment
• Medical emergency! (inadequate cardiac output or marked
hypoxemia).
• Suggest?  decompressed  intravenous catheter or by
immediate tube thoracostomy
– (temporizing procedure) : large-bore needle should be inserted into the
pleural space through the second anterior intercostal space  large
amounts of gas escape from the needle after insertion (diagnosis is
confirmed).
– (definitive management) : thoracostomy tube (needle should be left in
place until tube is inserted).
• Obesity?
Diagnosis of Pneumothorax
• Chest radiograph
– standard
– CT scan  gold standard
– Bedside ultrasound  rapid and accurate
• Tension  treatment should not be delayed (chest radiograph confirmed?
X)
• Pneumothorax susp  standard radiograph  not seen  expiratory film
(occasionally helpful in identifying a small apical pneumothorax, routine
used does not improve diagnostic yield)
• critically ill patients for whom only a supine chest radiograph  “deep
sulcus” (i.e., a deep lateral costophrenic angle)  suggest pneumothorax.
Treatment of Pneumothorax
Simple observation or aspiration with a catheter to video-
assisted thoracoscopic surgery or thoracotomy :
• severity of signs
• presence of underlying pulmonary disease
• other comorbidities, history of previous pneumothoraces
• patient reliability, degree and persistence of the air leak,
and
• available follow-up monitoring
 therapeutic options
Treatment of Pneumothorax
Observation  simple aspiration  small/standard/large caliber tube 
water seal/+ Heimlich valve  suction  surgical intervention : resection
of bullae and pleurodesis (+video-assisted thoracoscopic surgery or
thoracotomy).

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