respiratory emergencies in emergency medicine

1. Respiratory Emergencies

2. Asthma
• Asthma is a chronic respiratory disease characterized by periods of
variable and recurring symptoms, airflow obstruction, and bronchial
hyperresponsiveness that manifests clinically as attacks of impaired
breathing
• Asthma is an inflammatory disease; repetitive episodes of acute
superimposed on chronic airway inflammation are responsible for
alterations in airway function and result in irreversible structural
airway changes
• Asthma is thus a complex interaction of the immune system, the
environment, and genetic predispositions, which combine to alter
airway structure and function

8. European Respiratory Society/American Thoracic Society Definitions
of Severe and Uncontrolled Asthma
• Severe asthma for patients 6 years old and older is defined as:
Asthma which requires treatment with guidelines suggested
medications for Global Initiative for Asthma steps 4 to 5 asthma (high-
dose ICS and LABA or leukotriene modifier/ theophylline) for the
previous year or systemic corticosteroids for ≥50% of the previous
year to preventing it from becoming “uncontrolled” or which remains
“uncontrolled” despite this therapy

10. Uncontrolled asthma is defined as one of the following:
• Poor symptom control (ACQ consistently >1.5, ACT <20 (or “not well controlled” by
NAEPP/Global Initiative for Asthma guidelines)
• Frequent severe exacerbations: Two or more bursts of systemic corticosteroids (>3
days each) in previous year
• Serious exacerbations: At least one hospitalization, ICU stay, or mechanical
ventilation in the previous year
• Airflow limitation: After appropriate bronchodilator, withhold FEV1<80% predicted
(in the face of reduced FEV1 as less than the lower limit of normal)/FVC defined
• Controlled asthma that worsens on tapering of these high doses of ICS or systemic
corticosteroids (or additional biologics)

12. Treatment

20. COPD
• Global Initiative for Chronic Obstructive Lung Disease (GOLD)
collaborators have updated their defnition of COPD as “a preventable and
treatable disease characterized by persistent airflow limitation that is
usually progressive and associated with an enhanced chronic inflamatory
response in the airways and the lungs to noxious particles or gas.”
• The definition specifically avoids mention of chronic bronchitis and
emphysema, two entities that have been traditionally included in the
definition of COPD
• the GOLD collaborators focus on airflow limitation as the principle feature
of the disease. Airflow limitation is a direct result of a combination of
parenchymal destruction and small airways disease. Both processes are a
consequence of chronic inflammatory changes and present clinically in
varying degrees amongst patients with COPD

22. • Progressive inflammation in COPD leads to airway limitation and obstruction.
However, not all patients who smoke or have exposure to noxious stimuli
develop COPD, raising the possibility that other contributory factors such as
genetics and environmental factors
• In COPD, evidence of airway inflammation is found from the trachea down to
the smallest peripheral airways. In the larger, more proximal airways, an
increase in both the number and size of mucous-secreting goblet cells can
result in the formation of mucous plugs, which further contributes to airflow
obstruction.
• Damage to the endothelium impairs the mucociliary response that clears
bacteria and mucous. Airway resistance and flow limitation are mainly due to
damage to the distal, smaller airways where the diameter is 2 mm or less.
• In cigarette smokers, the parenchymal damage will typically present in a
centriacinar pattern, especially in the early stages of the disease. Emphysema
is no longer routinely used in the definition of COPD, because it is a pathologic
and anatomically defined condition.

23. • Chronic bronchitis on the other hand is a clinical condition defined by the
presence of chronic productive cough for 3 months in each of 2 successive
years, where other causes of chronic cough have been excluded. Most patients
with COPD will have mixed features of both conditions.
• There is compelling evidence that protease/anti-protease imbalance plays a role
in the modification of the inflammatory cascade and resultant parenchymal
destruction seen in COPD. Protease-mediated destruction of connective tissues,
including elastin results in lung parenchymal damage and resultant emphysema.
• Anti-proteases protect against connective tissue destruction and are an integral
component in the pathogenesis of patients with congenital α1-antitrypsin
deficiency.
• Congenital α1-antitrypsin deficiency accounts for a small percentage of COPD
patients and is recognized by the lack of the anti-protease enzyme that inhibits
the protease enzyme, neutrophil elastase. The deficiency of this anti-protease
results in uninhibited protease action, parenchymal destruction, and severe
panacinar emphysema.

33. Proposed Indications for Mechanical Ventilation
• Respiratory arrest Worsening level of consciousness despite maximal
therapy
• Cardiovascular instability (shock, heart failure)
• NIPPV failure or exclusion criteria
• Severe dyspnea with use of accessory muscles and paradoxical abdominal
motion
• Severe tachypnea
• Life-threatening hypoxia
• Severe acidosis and hypercapnia
• Other complications (metabolic abnormalities, sepsis, pneumonia,
pulmonary embolism [PE], barotraumas, massive pleural effusion)

34. Pneumonia
• Pneumonia involves symptoms and signs of lower respiratory tract
infection (breathlessness, productive cough, and fever) usually
associated with CXR abnormalities. Pneumocystis pneumonia may
occur with minimal or no CXR changes. Consider pneumonia in
patients with septicaemia or acute confusional states.
• Pneumonia commonly results from microaspiration of upper
respiratory pathogens into the sterile lower respiratory tract. If the
challenge of invading organisms overwhelms host defenses, microbial
proliferation leads to inflammation, an immune response, and clinical
pneumonia.

36. • In patients admitted in the ICU the most common aetiologies were S. pneumoniae
(62%), atypical pathogens (14%) and polymicrobial aetiologies (11%). The most
frequent polymicrobial pattern was S. pneumoniae and viral infection, particularly
influenza virus .
• The microbial pattern of the severe CAP has changed over the years, with the decrease
of atypical pathogens, especially Legionella and the increase of viral pneumonia
• A large number of micro-organisms other than S. pneumoniae must be considered,
especially Pseudomonas aeruginosa, and CA—MRSA. The risk factors for Pseudomonas
pneumonia include
o ◆ Recent hospitalization.
◆ Frequent (>4 courses per year) or recent administration of antibiotics (last 3 months).
◆ Severe disease (FEV1 < 30%) and oral steroid use (>10 mg of prednisolone daily in the last 2
weeks).
• Accordingly, the risk factors for community-acquired methicillin-resistant
Staphylococcus aureus (CA-MRSA), an emerging problem, are participating in contact
sport, living in crowded or unsanitary conditions, intravenous drug abuse
• CA-MRSA is the most common pathogen isolated in community-acquired skin and soft
tissue infections. It causes severe, rapidly progressing pneumonia with sepsis, often in
children or healthy young adults with influenza

37. American Thoracic Society/Infectious Disease Society of America
Definitions of Hospital Acquired, Ventilator-Associated, and Health
Care–Associated Pneumonia
• Hospital-acquired pneumonia (HAP)—occurs ≥48 hr after admission and
does not appear to be incubating at the time of admission
• Ventilator-associated pneumonia (VAP)—occurs >48–72 hr after
endotracheal intubation
• Health care–associated pneumonia (HCAP)—occurs in a non hospitalized
patient with extensive health care contact defined by one or more of the
following exposures
• IV therapy, wound care, or IV chemotherapy within the prior 30 days Residence in a
nursing home or other long-term care facility
• Hospitalization in an acute care hospital for 2 or more days within the past 90 days
• Received hemodialysis within the prior 30 day.

38. Organ colonization time-evolution during ICU stay.
*At 48 hours 80% of ETT are colonized, but heavy colonization occurs at
60–96 hours.

44. Criteria for ICU admission.
One of the major or three
or more of the minor
criteria would indicate ICU
admission

49. Pneumothorax
• Pneumothorax is defined as the presence of air in the intrapleural space
and can range from a benign to a life-threatening process.
• A spontaneous pneumothorax occurs in the absence of any external
precipitating factor, traumatic or iatrogenic.
• Primary spontaneous pneumothorax occurs in individuals without clinically
apparent lung disease.
• Secondary spontaneous pneumothorax arises in the context of an
underlying pulmonary disease process.
• Tension pneumothorax is a life-threatening complication resulting from
pressure in the pleural cavity causing hemodynamic compromise.

52. Causes of Secondary Spontaneous Pneumothorax
AIRWAY DISEASE
• Chronic obstructive pulmonary disease
• Asthma
• Cystic fibrosis
INFECTIONS
• Necrotizing bacterial pneumonia,
• lung abscess
• Pneumocystis jiroveci
• pneumonia
• Tuberculosis
INTERSTITIAL LUNG DISEASE
• Sarcoidosis
• Idiopathic pulmonary fibrosis
• Lymphangiomyomatosis
• Tuberous sclerosis
• Pneumoconioses
NEOPLASMS
• Primary lung cancers
• Pulmonary or pleural metastases

57. The classic radiographic appearance is that of a thin, visceral pleural line lying parallel to the chest wall,
separated by a radiolucent band devoid of lung markings. The average width of this band can be used to
estimate the size of the pneumothorax, such as with the Rhea method

58. British Thoracic Society
guidelines define size
based on measurement
of the intrapleural
distance at the level of
the hilum: small, less than
1 cm; moderate, 1 to 2
cm; and large, more than
2 cm.
The American College
of Chest Physicians
measures from the apex
to the cupola(chest wall
apex)—small is less than
3 cm, and large is more
than 3 cm.

61. Deep venous thrombosis

62. • The triad of venous injury, slow blood flow, and hypercoagulability are the
cardinal inciting mechanisms for VTE, and most clinical decision rules for VTE
incorporate these factors.

65. Diagnosis
• Diagnosis of DVT and PE starts with an estimation of the pretest
probability (PTP).
• the LEFt score:
• 1 point in case of left (L) leg suspicion,
• 1 point for edema (E), and
• 1 point if the suspicion occurred during the first trimester (Ft) of pregnancy,
• with a score of 0 or 1 tantamount to a low PTP
• The PTP dictates the pathway for diagnostic testing

67. A three-point
ultrasound includes
the common femoral,
femoral, and
popliteal veins. A
whole-leg ultrasound
includes a three-
point ultrasound and
the peroneal and
tibial calf veins.

70. • Upper extremity DVT can cause PE, and all patients with DVT above the elbow
require definitive treatment.: About half of all upper extremity DVTs are
associated with an indwelling catheter, and peripherally inserted central
catheters (PICCs) carry the highest risk.
• Acute PE from an axillary vein Isolated upper occurs in about 9% of patients
with arm DVT, although the PE tends to be less severe from upper extremity
DVT
• only venous ultrasound has been adequately validated as a method to
diagnose and exclude upper extremity DVT

71. PULMONARY EMBOLISM
• A PE results when a clot that formed hours, days, or sometimes weeks
earlier in the deep veins dislodges, travels through the venous system, and
traverses the right ventricle into the pulmonary vasculature.
• The mortality of diagnosed and treated pulmonary embolism is 7%. Many
more people die from undiagnosed PE. Venous thromboembolism
develops in patients already suffering from sepsis, cancer, or COPD or in
patients recovering from stroke, MI, surgery, and joint replacement.
• Pulmonary embolic disease can result in a variety of symptoms often
misdiagnosed as asthma, anxiety, pneumonia and ACS

74. • The right ventricle normally pumps through a pulmonary vascular tree with a
low resistance to fluid flow, and young persons without cardiopulmonary
disease (eg, congestive heart failure, chronic obstructive lung disease,
advanced sarcoidosis, pulmonary fibrosis, scleroderma, primary pulmonary
hypertension) can tolerate at least 30% obstruction from a clot, with minimal
symptoms or signs.
• Pulmonary infarction, in contrast, can produce severe pleuritic pain Although
a segmental pulmonary artery constitutes only about 1/16 of the entire
pulmonary vascular circuit, a clot lodged deeply in a segmental artery can
obstruct blood flow to a sufficient degree to cause tissue necrosis.

78. Pulmonary Embolism Rule-Out Criteria (PERC
Rule)
Low pretest probability for PE by the treating emergency clinician’s
unstructured estimate, plus all the following must be true:
• Age < 50 yr
• Pulse rate < 100 beats/min
• Oxygen saturation < 94%
• No hemoptysis
• No unilateral leg swelling
• No recent major surgery or trauma
• No prior pulmonary embolism or deep venous thrombosis
• No hormone use

80. • Chest radiography seldom provides specific information, but is useful to
suggest alternative diagnoses, such as pneumonia, congestive heart failure, or
pneumothorax.
• If symptoms have been present for 3 days or more, a pulmonary infarction may
be visible on chest x-ray as an apex central, pleural-based, wedge-shaped area
of infiltrate, producing the so-called Hampton’s hump finding. Unilateral lung
oligemia (Westermark’s sign) is a rare radiographic manifestation of a large PE.
• When PE causes electrocardiographic changes, this is usually a result of acute
or subacute pulmonary hypertension. The most common effects of pulmonary
hypertension on the ECG are rapid heart rate, symmetric T-wave inversion in
the anterior leads (V1–V4), the McGinn White S1Q3T3 pattern, and incomplete
or complete right bundle branch block
• In the ED, inability to identify a cause of chest symptoms or specific signs may
be an important cue to evaluate the patient for PE

82. PLEURAL INFLAMMATION AND
EFFUSION
• Pleural effusion implies the presence of an abnormal collection of fluid in
the pleural space.
• A pleural effusion associated with bacterial pneumonia or lung abscess is
termed a parapneumonic effusion. The term pleural empyema (or
pyothorax) implies the presence of actual pus in the pleural space. Fluid
that is anatomically confined and not freely flowing within the pleural
space is termed a loculated effusion.
• Loculated effusions occur when there are adhesions between the visceral
and parietal pleurae