Volume I:
First Thirty Minutes
- Section 1
  Acute Care Algorithm/ Treatment Plans/ Acronyms
- Section 2
  Universal Approach
  - CALS Universal Approach To Emergency Advanced Life Support
- Section 3
  Steps 1-6
- Section 4
  Preliminary Impression/Focused Clinical Pathways
Volume II:
Resuscitation Procedures
Volume III:
Definitive Care

Pathway 6: Adult Respiratory

The team continues the resuscitation along the pathway suggested by the initial clinical impression. Each pathway includes a complete, thorough, and rapid physical examination with additional history taking. The team leader is wary of conditions that may not be apparent. To obtain additional clinical data or to correct a missed or newly developed condition, the team leader repeats the initial survey if the patient is not responding satisfactorily.

During the initial survey, the airway was assessed and appropriate measures were taken to assure an open airway and adequate ventilation. If this has not been done, return to the initial survey and do it now. If it was not necessary to secure the airway at that time but the airway becomes compromised, return to the initial survey and secure the airway, utilizing the approaches outlined.

In this pathway, choose the section(s) most closely corresponding to the problem at hand. For example, fever, cough, and dyspnea are most likely suggestive of pneumonia or pulmonary embolism and may be used as a starting point. In patients with known or suspected co-existing diseases (such as CHF and COPD), go to all pertinent pathways and sections. If after a thorough history and physical exam the nature of the patient’s respiratory condition is uncertain (perhaps due to lack of history or associated symptoms), go to the Dyspnea section.

Because of the close anatomic and physiologic relationships between the respiratory and cardiovascular systems, consider the following:

Cardiac pain tends to be substernal and constant; pulmonary pain tends to be peripheral and associated with respiration.
All that wheezes is not asthma: Patients with CHF may wheeze.
Myocardial ischemia may present as painless dyspnea.
Pulmonary embolism involves both systems and may be insidious in its multiple presentations.

Text Number	Diagnosis/Condition	Related Materials
1	Dyspnea	Vol I—Pathway 2 Cardiovascular Emergencies
2	Upper Airway: General	VolII—Air Skills 12 Tracheal Foreign Body Removal
3	Upper Airway: Angioedema	Vol III— AIR3 Heliox Treatment Airway 8 Anaphylaxis
4	Upper Airway: Epiglottitis	Vol III—PED3 Epiglottitis
5	Upper Airway: Foreign Body(ies)	Vol II—Air Skills 12 Tracheal Foreign Body Removal; Vol III—AIR3 Heliox Treatment
6	Acute Respiratory Distress Syndrome: Non-cardiogenic Pulmonary Edema	Vol II—Breath Skills 1 Chest Tube Insertion, Circ Skills; Vol III—AIR4 Ventilator Management
7	Asthma/Anaphylaxis	Vol III—AIR8 Anaphylaxis; AIR1 Rapid Sequence Intubation, AIR3 Heliox Treatment, AIR4 Ventilator Management, AIR7 Status Asthmaticus
8	Chronic Obstructive Pulmonary Disease (COPD)	Vol III—END/M6 Acid-Base, AIR7 Status Asthmaticus, AIR5 Noninvasive Ventilatory Support
9	Pneumonia and Aspiration	Vol III—IN1 Adult Pneumonia
10	Pulmonary Embolism	Vol II—Circ Skills 3 Central Venous Pressure Measurement; Vol II—Air Skills; Vol III—AIR4 Ventilator Management
11	Pneumothorax and Pneumomediastinum	Vol I—Step 3 Initial Survey; Vol II—Breath Skills 1 Chest Tube Insertion
12	Massive Hemoptysis	Vol II—Air Skills 3 Orotracheal Intubation; Vol II—Breath Skills 3 Endobronchial Tube

Dyspnea
Dyspnea is a subjective symptom, a perceived inability to breathe normally, causing anxiety and/or fear, which then amplify the sensation. A viscous cycle ensues, which may mislead caregivers to focus on the anxiety and discount the underlying disease. Both need to be addressed. The goal is to detect and treat life-threatening or serious causes of dyspnea. Think in terms of organ systems to organize the clinical process:

Upper Airway

• allergic reaction
• foreign body
• mass
• stenosis
• tracheomalacia

Pulmonary
• air embolism
• adult respiratory distress syndrome
• aspiration
• asthma
• COPD
• interstitial lung disease
• mass
• pleural effusion
• pneumonia
• pneumothorax
• pulmonary embolism
• pulmonary hypertension

Cardiac
• arrhythmia
• CHF
• pericardial effusion
• myocardial ischemia
• valvular heart disease

Neuromuscular Disorders
• Guillain-Barre syndrome
• myasthenia gravis
• myopathy
• neuropathy

Hematologic/Metabolic
• abnormal hemoglobin: CO, methemoglobin
• acidosis
• anemia
• electrolyte disorders: calcium, phosphate, potassium
• fever/sepsis
• thyrotoxicosis

Psychogenic
• hyperventilation
• panic disorder

Miscellaneous
• de-conditioning
• diaphragm encroachment: massive ascites; pregnancy
• drug withdrawal

If the survey has not explained the underlying cause of dyspnea, consider the assessment of the patient in the approximate order presented. Some assessments are performed simultaneously:

Evaluate pulse oximetry findings: saturations less than 90% to 92% indicate the need for oxygen, further evaluation, and probable admission. Note that oximetry does not evaluate ventilation/CO₂ status, and a normal value does not rule out a pulmonary embolism or abnormal hemoglobin.
Perform Peak Expiratory Flow Rate (PEFRs) to help diagnose/exclude reactive airway disease: normal values direct the search toward other causes; improvement of abnormal values with bronchodilator therapy is presumptive evidence of the disease.
Obtain a chest x-ray. If abnormal, try to obtain prior x-rays for comparison to evaluate whether the findings are new or unchanged. Classic findings (ie, pneumothorax, CHF) suggest the cause of dyspnea. Indefinite findings (atelectasis, effusion, infiltrate, non-classic patterns for CHF/ARDS) need further evaluation. If the x-ray is normal, continue the assessment. Be aware that clinical presentations may be apparent before being visible in the x-ray findings. Obtain delayed x-rays as needed.
Reconsider the risks for the cardiac diseases in the preceding list, and test appropriately: ECG, cardiac enzymes, echocardiography, stress testing. (Vol I—Pathway 2 Cardiovascular Emergencies)
Reconsider the risks for pulmonary embolism and test appropriately: bedside echocardiography, V/Q scanning, helical CT. (See Pulmonary Embolism, # 10 below.)
Obtain a bedside hematocrit for patients at risk of anemia.
Obtain ABG for patients with suspected acidosis and/or ventilatory insufficiency.
Evaluate continued unexplained hypoxia and/or distress. Consider evolving ARDS by thinking of its precipitating conditions. For example, is your patient at risk for aspiration?
Consider psychogenic disorders only in a young healthy person with a normal exam, normal oximetry values, and a prior history of similar attacks. It is a diagnosis of exclusion.
Note that deconditioning dyspnea—exertional dyspnea in obese, sedentary patients—is also a diagnosis of exclusion.

DOs and DON’Ts of DYSPNEA

DO:

Assume that anxiety will complicate the evaluation. Deal with anxiety proactively and appropriately. Repeated honest reassurance and explicit explanations help to alleviate anxiety.
Take explicit histories as directed in the preceding list. Some patients don’t volunteer information, don’t understand their disease or previous similar experiences, or do minimize symptoms. Example: Distinguish between the work-up for pulmonary embolism/deep vein thrombosis and the actual diagnosis. Distinguish between blood clots and what may be mistaken for them, such as hematomas or varicose veins.
A thorough exam: thrush in the mouth in someone complaining of dyspnea on exertion highly suggests pneumocystis carinii pneumonia (and underlying HIV/AIDS).
Monitor closely those patients on oxygen: while treating hypoxia, oxygen can take away the respiratory drive of COPD patients, leading to CO₂ narcosis.
Obtain the PA and lateral chest x-ray, unless the patient is unstable and requires a portable x-ray.
Obtain ABGs in patients with altered mental status, suspected CO₂retention, and suspected acidosis.
Recognize the constraints of the ABG. The A-a gradient is accurate only on room air, and an abnormal gradient only suggests diseases. A normal gradient does not rule out pulmonary embolism.
Suspect pulmonary embolism in cases with modest or equivocal findings. Unlike other serious causes of dyspnea, which present with severe symptoms, pulmonary embolism may present subtly.

DON’T:

Assume anxiety is the cause of dyspnea.
Treat anxiety with sedatives unless you are prepared to undergo full evaluation and full respiratory support, including intubation and mechanical ventilation.
Obtain ABGs to rule out hypoxia if pulse oximetry is normal on room air.
Assume infallibility of testing. Helical CTs can miss small peripheral emboli.
Assume that pulmonary infiltrates are pneumonia. It may be impossible for radiologists to distinguish between pneumonic and embolic infiltrates.
Assume that this episode has the same cause as the last. New conditions emerge.
Assume that the absence of pain rules out myocardial ischemia or pulmonary embolism.
Assume that dyspnea in pregnancy is physiologic. Pregnancy is a risk factor for pulmonary embolism and eclampsia, both of which cause dyspnea.

Upper Airway: General

Additional anatomical predictors of airways difficult to intubate include:

limited mouth opening
narrow mouth
long teeth
large tongue
small intra-oral cavity
poor view of posterior structures
narrow submental angle
submental and submadibular swelling
deviated trachea
neck swelling and scars

Ask the patient to describe, point to, localize the problem. Ask directed questions about symptoms in relation to breathing, coughing, and swallowing. Important clues of significant upper airway problems include stridor (audible inspiratory noise), drooling, sitting bolt upright, muffled voice or hoarseness (involvement at the level of the cords), and paradoxical movement of the torso with inspiration (the abdomen moves outward while the sternum moves inward).

Carefully inspect all structures involving the airway as many disease processes take place in the head and neck regions. Do not be satisfied with only a look in the throat. Take the extra steps involved to visualize the airway to the level of the cords either directly (laryngoscopy or fiber-optic nasopharyngoscopy) or indirectly (mirror laryngoscopy). Use topical anesthesia if necessary to gain the cooperation of the patient to obtain visualization. (Vol II—Air Skills 12 Tracheal Foreign Body Removal)

Upper Airway: Angioedema
Rapid sequence intubation may be contraindicated in patients with angioedema. Paralyzing the patient may take away the muscle tone and positioning that is keeping the airway minimally open. Awake intubation (nebulized 4% lidocaine, IV sedation, and laryngoscopy or fiberoptic intubation) is an alternative. Be prepared for immediate cricothyroidotomy.

Angioedema (localized soft tissue swelling involving deeper layers) may be due to several different causes, which are responsive to different treatment regimens. Remember, angioedema from different causes may look the same. It may be impossible to distinguish these causes by history, especially if you are seeing the first episode. (Vol III—AIR8 Anaphylaxis) Various kinds of angioedema and their treatments follow:

Acquired angioedema. Manage the patient’s airway. There will be variable to no response to epinephrine, antihistamines, and corticosteroids. Give C₁ INH (C₁ esterase inhibitor concentrate) to patients with a deficiency. Use fresh frozen plasma if C₁INH is not available.^a
Allergic angioedema. Manage the patient’s airway. Administer epinephrine, antihistamines, corticosteroids.
Angiotensin-converting enzyme (ACE) inhibitor angioedema. Manage the patient’s airway. There will be poor or little response to epinephrine, antihistamines, and corticosteroids.
Hereditary angioedema. Manage the patient’s airway. Administer intravenous C₁INH (or fresh frozen plasma if C₁INH is not available). This condition will not respond to epinephrine, antihistamines, corticosteroids.

An approach to patients with angioedema includes the following:

Airway management: the same for all entities. (Vol I—Step 3 Initial Survey)

Utilize O₂ as indicated. Heliox (80% helium, 20% oxygen) may help. (Vol III—AIR3 Heliox Treatment)

Unless you know that the patient has acquired or hereditary angioedema, administer the following medications:

Epinephrine IM, SQ, or IV. Choice of route depends on severity.

IM/SQ: 0.01 mL/kg (up to 0.3 mL) of 1:1000 solution. Repeat every 5 min prn.
IV: 1 mg in 250 cc D₅W carefully titrated to response under direct supervision while monitoring BP and cardiac rhythm.

H1 and H2 Antihistamines (give both):

Corticosteroids:

Methylprednisolone 125 mg IV

If the patient has no response to epinephrine (antihistamines and steroids take longer to act), consider glucagon 1 to 2 mg IV every 5 min titrated to effect; may need a drip at 1 to 5 mg/h.

For cases of hereditary angioedema (and those cases of acquired angioedema that have the C₁ INH), administer either:

C₁-inhibitor concentrate:^b 500 to 1000 U IV or
Fresh frozen plasma 2 U IV

Remove the allergen source from the patient:
- Remove the stinger from an insect bite with a blade to avoid possible injection of more allergen.
- If a substance has been ingested, give activated charcoal 1 g/kg PO or via NG tube. (After administration of charcoal, do not give medications orally.)

Monitor patient carefully for response to therapy, adverse outcomes, and disease progression.

Upper Airway: Epiglottitis (Vol III—PED3 Epiglottitis)

Adult epiglottitis (acute inflammation and swelling of the epiglottis and surrounding tissue) can have a very rapid onset with progression to airway obstruction. Do not underestimate this potential. Epiglottitis is usually caused by bacteria (Hemophilus influenza, group A Streptococcus, or Staphylococcus), but the epiglottis can become inflamed by other agents. How seriously ill a patient appears depends on the degree of illness at the time care is sought. In the past, seeing a thumbprint sign of a swollen epiglottis on a soft tissue lateral cervical x-ray was considered diagnostic; however, direct visualization of the actual area of involvement is now used for diagnosis. A normal appearing epiglottis and surrounding tissue structures rule out this condition.

Start the patient on ceftriaxone 1 to 2 g IV. Take blood cultures, and if the patient is intubated, take cultures of the epiglottal area. Racemic epinephrine, beta-agonists, sedation, and steroids are either not helpful or can make the condition potentially worse. Consult an ENT surgeon. If you have decided not to intubate at this time, observe the patient in intensive care unit conditions under close supervision, and be prepared to do an emergency cricothyrotomy or formal tracheostomy at any time.

Upper Airway: Foreign Body (ies)
For the patient with partial obstruction or passage of the foreign body further down the pulmonary tree, continue to support the patient, closely observe for any deterioration, and arrange to have the foreign body emergently removed by bronchoscopy by a specialist. (Rigid bronchoscopy is done in the operating room under general anesthesia; flexible bronchoscopy may be done in the procedure room under topical anesthesia with or without sedation, depending on the situation.)

Use Heliox as a temporizing measure to assist oxygenation as needed. (Vol III—AIR3 Heliox Treatment)
Obtain a PA and lateral chest x-ray and examine for the foreign body and complications, such as atelectasis, mediastinal shift, air trapping, pneumothorax, or compensatory contralateral emphysema. Aspirated foreign bodies commonly lodge in the right main stem bronchus or lower lobe.
Prepare the patient for the procedure. Pre-bronchoscopy steroids (methyprednisolone 125 mg IV) and a broad-spectrum antibiotic (cefazolin 1 g IV) may serve to reduce the complications of swelling and infection.

For complete tracheal obstruction, see Vol II—Air Skills 12 Tracheal Foreign Body Removal.

Acute Respiratory Distress Syndrome (ARDS)
ARDS is a hypoxemic respiratory failure syndrome consisting of non-cardiogenic pulmonary edema that is associated with numerous precipitating conditions including:

infection—sepsis, pneumonia
shock—especially septic and traumatic
aspiration—near drowning, GI aspiration
toxic inhalation(s)
trauma—pulmonary contusion, multiple long bone fractures, pelvic fractures
multiple transfusions
disseminated intravascular coagulation
drug overdose—aspirin, heroin, barbiturates, others

Onset from time of initial insult may vary from hours to days, so most patients will become symptomatic from ARDS while being evaluated for the primary cause after admission. The stage in which ARDS presents will guide evaluation and therapy. A patient who has dyspnea in the early stages of ARDS may be difficult to diagnose, as chest x-ray changes may be initially absent. (Findings may not indicate the changes occurring in the pulmonary tissue.) Maintain a high index of suspicion for early onset ARDS, and do not send the patient home with a history consistent with developing ARDS. These patients can deteriorate rapidly, and they have high morbidity and mortality.

Dyspnea is the main presenting symptom, and pulse oximetry guides further ABG testing for hypoxia. The chest x-ray is helpful for the diagnosis. Classic findings are bilateral diffuse alveolar/interstitial infiltrates. For patients in obvious pulmonary edema, echocardiography is helpful in differentiating ARDS from cardiogenic pulmonary edema, which is treated differently. If echocardiography is not available, other factors (besides the history of precipitating conditions) that can help differentiate this process from cardiac pulmonary edema include:

an often normal ECG (other than tachycardia)
no S3 gallop on cardiac exam
no hepatojugular reflux
no peripheral edema
no cardiomegaly on chest x-ray (although chest x-ray is not a sensitive test for cardiomegaly)

Recent attention has been given to the blood test called brain natriuretic peptide (BNP) in differentiating CHF from other conditions.

Unlike cardiogenic pulmonary edema, there are no medications per se for this disease in its early stages. Treatment is directed at cardiopulmonary support and the underlying condition(s). Intubate and mechanically ventilate those patients with clinical signs of respiratory failure and/or hypoxemia refractory to oxygen therapy. PEEP is often utilized. (Vol II—Breath Skills 1 Chest Tube Insertion, Vol II Circ Skills; Vol III—AIR4 Ventilator Management) Also utilize those portals that relate to the underlying conditions. Avoid excessive fluid administration. Even with appropriate fluid management, cardiac support may require vasopressors such as dopamine or dobutamine. Admit these high mortality patients to the intensive care unit with critical care consultation.

Asthma/Anaphylaxis^1,2
Hemodynamically stable patients with anaphylaxis involving the lower airways generally exhibit bronchospasm with accompanying wheezing. Furthermore, some patients with asthma are allergic, and these two conditions interplay. Asthma and anaphylaxis are considered here because of their similarities.
(Remember, all that wheezes is not asthma or allergies; wheezing may also occur with CHF, foreign body, pulmonary embolism, pneumonia, and other rarer causes.)

Anaphylaxis
This section addresses the respiratory manifestations of anaphylaxis. For a patient with anaphylaxis who is hemodynamically unstable, see Vol III—AIR8 Anaphylaxis.

If a patient has no history of asthma, a good history for allergen exposure and/or anaphylactoid response, and a clear upper airway but has dyspnea/wheezing, proceed as follows:

Begin oxygen therapy if oxygen saturation is < 92%.
Give 0.3 mL of epinephrine 1:1000 either IM (probably better absorption) or SQ. This dose may be repeated every 5 to 10 minutes for a total of 3 doses.
Treat bronchospasm with inhaled albuterol 2.5 to 5.0 mg and/or use nebulized ipratropium bromide (Atrovent) 0.5 mg if patient is on beta blockers. Repeat albuterol and/or ipratropium every 20 minutes prn for a total of three doses.
If the patient is not improving, consider continuous nebs (see Vol III—AIR7 Status Asthmaticus).
After initial treatment, give H1 and H2 antihistamines (diphenhydramine 50 mg PO or IV and cimetidine 300 mg PO or IV).
Decrease the antigen load:

If an oral ingestion precipitated the attack, give activated charcoal 1 g PO or NG. (After administration of activated charcoal, give further medications via another route.)
Stinger removal: if the anaphylactic reaction is the result of a bee sting, inspect the site to see if the stinger is still there. Lift the stinger out of the skin with a blade to avoid injecting more venom. Cold packs may decrease absorption. If patient is hypotensive, consider applying a venous tourniquet proximal to the sting until the hypotension has been relieved.

Give corticosteroids such as prednisone 60 mg PO or methylprednisolone 125 mg IV.
Monitor the patient for worsening/no improvement. (Vol III—AIR8 Anaphylaxis)

Asthma

For the patient who has asthma or probably has either asthma and/or anaphylatic bronchospasm (and no other reason to wheeze, such as CHF, COPD, pulmonary embolism, foreign body exposure, pneumonia) proceed as follows:

For the potentially unstable patient who is not yet intubated, prepare for intubation while performing the following:

Oxygen or Heliox therapy to keep saturation > 90% to 92% (Vol III—AIR3 Heliox Treatment)
Continuous nebulized beta agonist therapy with albuterol, 10 to15 mg/hour. (Vol III—AIR7 Status Asthmaticus)
Nebulized ipratropium bromide, 0.5 mg; may repeat every 20 minutes as needed for a total of three doses.
Methylprednisolone 125 mg IV

While not routine, the following interventions may be used in an attempt to avoid the need for intubation:

Terbutaline 0.25 mg SQ or 0.3 cc epinephrine 1:1000 IM/SQ
Magnesium 2 g IV over 5 to 10 minutes (if no renal failure)
Consider BiPAP (Bi-level Positive Pressure Ventilation -- see Vol III —AIR5 Noninvasive VentilatorySupport.)
Proceed with rapid sequence intubation (RSI)/airway management if the patient is not improving (Vol III—AIR1 Rapid Sequence Intubation, AIR7 Status Asthmaticus, AIR4 Ventilator Management)

When ventilating a patient with asthma, allow extra time for exhalation. Patients with severe asthma have a problem with hyperinflation (“auto-PEEP”). Ventilate the patient slowly, at a rate of 8 to 10 times/minute

For the stable patient:

Oxygen to keep saturation > 90% to 92%.
Inhaled albuterol, 2.5 to 5.0 mg; repeat every 20 minutes prn for a total of three doses.
Inhaled ipratropium bromide, 0.5 mg; repeat every 20 minutes prn for a total of three doses.
If the patient is not improving, consider continuous nebs (see Vol III—AIR7 Status Asthmaticus)
Consider pulmonary function tests (PEFR or FEV1) to help guide further management.
Asymptomatic/resolved symptoms and PEFR/FEV1> 70% predicted: Evaluate for outpatient management. (Vol III—AIR7 Status Asthmaticus)
Continued symptoms and PEFR/FEV1>70% predicted: Continue inhalation therapy while reassessing for alternative conditions (See Dyspnea, #1 this pathway.)
Continued moderate symptoms and PEFR/FEV1 from 40% to 70% predicted: Continue inhalation therapy. Consider terbutaline 0.25 mg SQ or 0.3 cc epinephrine 1:1000 IM/SQ. Add methyprednisolone 125 mg IV and continue assessment. (Vol III—AIR7 Statis Asthmaticus)
Continued severe exacerbation and PEFR/FEV1 from 40% to 70% predicted: Continue inhalation therapy. Consider terbutaline 0.25 mg SQ or 0.3 cc epinephrine 1:1000 IM/SQ. Add methyprednisolone 125 mg IV. Consider magnesium 2 g IV over 20 minutes followed by a 2 g/hour drip. Consider Heliox inhalation and terbutaline IV. Closely assess response and see Vol III—AIR7 Status Asthmaticus for other considerations.

Chronic Obstructive Pulmonary Disease (COPD)
COPD patients often have other diseases, which precipitate and/or interact with acute exacerbations. Further, other causes of dyspnea can co-exist in the COPD patient: asthma/wheezy bronchitis, pulmonary embolism, myocardial infarction, CHF, pneumonia, lobar atelectasis, pneumothorax, and volume overload. A thorough history and associated symptoms help to focus management; previous records help to establish baseline status. Utilize other pathways and portals as necessary. As in many emergency situations, evaluation and treatment may have to proceed in tandem. Monitoring oxygenation and ventilation status is an important aspect of management of COPD exacerbations. Patients with saturation values less than 92% on pulse oximetry need treatment; however, some COPD patients are chronically hypoxic. COPD patients who retain CO₂ may be dependent on their hypoxic drive as a means to ventilate. Necessary oxygen treatment can take this hypoxic drive away, leaving the patient to become lethargic/obtunded from further CO₂ retention. Pulse oximetry does not determine the ventilation/CO₂status. Closely observe COPD patients on oxygen. Use ABGs to evaluate pH and ventilatory status in patients who are in severe distress, have altered mental status, and may have acidosis. (Vol III—END/M6 Acid-Base) Whereas COPD patients may have a baseline compensatory respiratory acidosis (elevated pCO₂ with a normal pH), acute respiratory acidosis reflects decompensation from their baseline, and metabolic acidosis can signal impending cardio-respiratory failure. Recent guidelines suggest that acute spirometry does not have a role in the emergency treatment of COPD (unlike its role in a primary care setting).

Routine testing besides ABGs that is helpful in the acute setting of COPD includes the chest x-ray and the ECG. Multifocal atrial tachycardia (MAT) is commonly associated with COPD and is often confused with atrial fibrillation. However, this dysrhythmia is often caused by hypoxia and is not treated with anti-arrhythmics but by reversing the hypoxia. Otherwise, laboratory testing is directed to specific needs, such as a theophylline level ifpatients have tremors, have arrhythmias while on aminophylline, or are vomiting.

Initial treatment of acute exacerbations of COPD in patients not intubated includes:

Oxygen to keep saturations > 90%; closely observe for obtundation.
Inhaled albuterol: 2.5 to 5 mg via nebulilzer or MDI with spacer; may repeat every 20 min or sooner prn. (For continuous nebulization, see Vol III— AIR7 Status Asthmaticus.)
Inhaled ipratropium: 0.5 mg via nebulilzer or MDI with spacer; may repeat every 20 min prn.
Corticosteroids: prednisone 40 to 60 mg PO or methylprednisolone 125 mg IV.
Early use of non-invasive ventilation support (NIV) in moderate-to-severe dyspnea and tachypnea may prevent the need for intubation and mechanical ventilation. (Vol III—AIR5 Noninvasive Ventilatory Support)

Pneumonia and Aspiration
Pneumonia

Triage the patient with cough and fever appropriately for the safety and well being of the staff (and the community at large). Place a mask on the patient. Minimize exposure to others.
Take the patient in respiratory distress or extremis directly to the treatment room, utilizing appropriate precautions against exposure until history can stratify the communicable risk further. Obtain the history.
Obtain a rapid chest x-ray.
For a cough longer than 2 weeks associated with a history of night sweats, weight loss, fever, or a cough associated with HIV/AIDS, IV drug use, recent incarceration, homelessness, immigration from a developing country, or history of tuberculosis /tuberculosis exposure, take appropriate precautions: Place patient in an isolation room with respiratory precautions until the chest x-ray is read for tuberculosis or, when HIV/AIDS is suspected, until sputum culture results are read. (The chest x-ray can be normal in HIV/AIDS patients with active tuberculosis.)

Many diseases can mimic pneumonia, as many conditions present with a combination of respiratory symptoms, fever, and infiltrate on chest x-ray. Common conditions include CHF, pulmonary embolism, COPD exacerbation, and aspiration. Ascertain risk factors for pulmonary embolism and investigate accordingly. Furthermore, symptoms of pneumonia, including elevation of the temperature, may be absent in geriatric or debilitated patients. Patients with suspected pneumonia and normal oral temperatures should have a rectal temperature taken. The history and physical should be conducted with HIV/AIDS in mind, as these patients are at risk for tuberculosis and pneumocystis carinii pneumonia, which require a different approach to treatment. Oral thrush in this setting is highly suggestive of HIV-related pneumocystis carinii pneumonia.

In the face of pneumonia, two main management decisions face the team:

which patients to admit and where, and
which antibiotic(s) to use initially (empirically).

Admission Considerations

History is paramount in the management of pneumonia. Criteria for patients at high risk and needing admission include:

geriatric patients
debilitated patients/poor nutritional status
patients with alcoholism
IV drug abusers (Also, investigate for endocarditis.)
patients with underlying diseases such as diabetes, CHF, renal failure, liver disease, CVA, anemia, neuromuscular disease
immunosuppressed/compromised patients: steroid use, immunosuppression agents, chemotherapy agents, HIV/AIDS, sickle-cell disease, asplenia/splenectomy, connective tissue disorders, neoplastic disease, organ/bone marrow transplants
resistant microorganisms (recent hospitalization, nursing home residence, recent antibiotic use)
social situation: caregiver, transportation, communication, financial considerations
altered mental status
hypoxia
tachypnea (> 30 breaths per minute)
hypotension
vomiting/unable to keep food down
chest x-ray with multi-lobar disease, effusions, and/or cavitations
extrapulmonary infection
metabolic acidosis

Direct your testing to specific situations, and don’t delay antibiotic treatment in acutely ill patients with pneumonia because of testing.

Chest x-ray is essential for diagnosis and management. Chest x-ray uncovers not only the pneumonia but also high-risk findings such as multi-lobar disease, effusions, and cavitations. Therefore, do not treat without one. The chest x-ray has its limitations. Clinical findings may be apparent before, and even a radiologist may be unable to distinguish between the infiltrates of pneumonia and pulmonary embolism. (Note that a V/Q scan is also unlikely to make this distinction.)
ABGs are useful in evaluating hypoxic patients with underlying pulmonary disease, patients with altered mental status, patients suspected of having metabolic acidosis, and patients with pneumocystis carinii pneumonia. (The need for steroids rise when PaO₂ is < 70 mm Hg.)
The white blood cell count may not be useful in the setting of cancer chemotherapy.
Patients who are seriously ill need at least a hematocrit, glucose, sodium, and pH.
Blood cultures are recommended on hospitalized patients (although they have limited yield). Sputum testing in emergency conditions is more controversial; it may be reasonable in those less ill patients being hospitalized.

Use your judgment in discharging low-risk patients with pneumonia to outpatient management. Factor in their psychosocial situation. Home IV therapy may be appropriate in certain situations.

Admit acutely ill patients to the appropriate level of care using your clinical judgment. Patients with HIV/AIDS who are admitted need to be placed in isolation until tuberculosis has been ruled out.

Treatment Considerations

Use oxygen to keep saturations > 92%.
Treat bronchospasm with inhaled albuterol: 2.5 mg via nebulization or MDI with spacer.
Watch closely for worsening respiratory status.
Monitor hydration status carefully. Treat dehydration with IV fluids. If a patient is in shock, give a bolus of NS and guide fluid resuscitation with CVP measurements and urinary output. Avoid over-hydration and possible pulmonary edema.
If a pleural effusion is present, consider performing a thoracentesis. Empyemas (pus in the pleural space) need placement of a chest tube and ongoing drainage. Note: this is not an emergency procedure, should not interfere with ongoing evaluation and treatment, and can be done hours after antibiotics have been started.
Promptly administer empiric antibiotic therapy. No combination of criteria available in the initial investigation period can reliably establish the cause of pneumonia with perhaps the exception of the findings of anaerobic lung abscess on chest x-ray (cavity with an air-fluid level) or a classic tuberculosis chest x-ray (scarring, apical cavitation, hilar adenopathy). One consequence is that the terms typical and atypical as applied to pneumonia are being abandoned except when they refer to antibiotic susceptibility. Empiric therapy covers microorganisms for both. Account for where the patient resides, disposition, and the antibiotic resistance patterns within your locale. (Note that the distinction between community-acquired and nosocomial pneumonia may be open to debate, depending on how long the patient has been away from a hospital or nursing home setting.)
Outpatient setting antibiotic selection (non-immunocompromised): choose between a macrolide, a fluoroquinolone, or doxycycline. Optimal duration of coverage remains unclear.
Inpatient setting antibiotic selection: see antibiotic management in Vol III—IN1 Adult Pneumonia.

Aspiration
Aspiration is foreign material entering the respiratory system. What happens after that depends on the nature of the aspirate, how much has been aspirated, and how the body reacts to this insult. Micro-aspiration is a common event, usually handled well by bodily mechanisms. Those micro-aspiration events that are not handled well, along with macro-aspiration events, give rise to pneumonic reactions generally referred to as pneumonia or pneumonitis. This usually occurs in patients with impaired airway protection. The two main categories are infectious and chemical pneumonitis. If distinguishable, they are treated differently:

Infectious pneumonitis in a community setting is usually caused by aerobic and anaerobic oropharyngeal flora. In a hospital or nursing home setting, gram-negative and resistant Staphylococcus organisms also need to be considered. Complications include lung abscess and/or empyema. Treatment is covered under pneumonia above and in Vol III—IN1 Adult Pneumonia.

Chemical pneumonitis is caused by aspirating gastric contents. This may or may not include particulate matter. Large volumes and/or high acidity worsen the reaction and consequences, which can include mechanical obstruction, bronchospasm, ARDS (see #6 ARDS in this pathway), respiratory failure, and nosocomial bacterial pneumonia. Mortality may be high.

Treatment consists of:

removal of obstructions by tracheobronchial suction/bronchoscopy (Vol II—Air Skills 16 Transtracheal Needle Ventilation)
bronchodilator agents for bronchospasm
respiratory support with oxygen; CPAP and intubation are utilized if needed. Mechanically ventilated patients may benefit from PEEP.
no antibiotic therapy unless infection develops

Patients at risk for gastric aspiration should be protected.

Intubate the airway if it can’t be maintained and protected by the patient.
Elevate the head of the bed to a 30- to 45-degree angle, if possible.
Decrease gastric acidity with antacids/H2 blockers.
Feed through an NG tube or gastric tube, if necessary. Check residual gastric volume regularly.

Pulmonary Embolism
Pulmonary embolism is common and highly variable in its presentation. While diagnosing pulmonary embolism may be straightforward, diagnosis may also be difficult as pulmonary embolism may mimic other diseases. Pulmonary embolism may be fatal in healthy people who don’t appear critically ill. Pulmonary embolism may be a co-morbid illness. The patient may appear well or be in full cardiac arrest. Blood clots may be difficult to detect both at their source (often the deep veins of the legs) and in their final destination, clogging the pulmonary vascular system and interfering with gas exchange. Maintain a high index of suspicion for pulmonary embolism and take unexplained and/or isolated dyspnea seriously.

Risk factors are important in the diagnostic process. Risk factors include recent immobilization, lower extremity immobilization/cast, a recent trip in a sitting position longer than 4 hours, history of deep vein thrombosis or pulmonary embolism, family history of thromboembolic disease, recent surgery or trauma, indwelling venous catheters, history of cancer, advanced age, heart failure, and obesity. These factors along with the acute history and examination form the basis for the diagnosis.

Symptoms associated with pulmonary embolism include dyspnea, anxiety, cough (may be bloody), syncope, new wheezing, chest pain (usually pleuritic in nature), and others.

Physical findings associated with pulmonary embolism include: fever (although a rectal temp higher than 102°F is unlikely in pulmonary embolism), tachycardia, Kussmaul’s sign (neck vein distension with inspiration, signifying an increase in right-sided CVP), an accentuated second heart sound, pulmonary rales, wheezing, unilateral leg swelling, calf tenderness, palpable venous cords (especially in the popliteal fossa), or a leg in a cast. Pulmonary embolism is a cause of obstructive shock. Check for an elevated CVP (>12 cm H₂O) in the ominous context of hypotension. (Vol II—Circ Skills 3 Central Venous Pressure Measurement)

Even with all these factors absent, the patient may still have a significant pulmonary embolism, which can quickly progress to death. Patients may even be therapeutically anticoagulated and still have pulmonary embolism. With such a wide variation in its presentation, the differential diagnosis list is extensive. Clinical variables alone cannot guide a treatment decision. Because of this and the fact that pulmonary embolism is a common cause of unexpected death in most age groups, diagnostic testing for patients at risk for pulmonary embolism continues until it is ruled in or out or another diagnosis is clear.

Diagnostic Testing Considerations

Form the best clinical impression from the history and physical examination and consider the patient to be in one of two categories: low or high probability of having pulmonary embolism. Diagnostic tools such as the Wells criteria1 (reproduced at the end of this section on pulmonary embolism) are useful for assessing the pre-test probability of pulmonary embolus. While this may be useful in interpretation of results, many patients fall into the moderate risk category in which a definitive diagnosis is almost entirely dependent on laboratory and imaging results.
No blood test changes the clinical likelihood category of the patient. Quantitative D-dimer testing has a reported sensitivity of > 90% in detection of venous thrombosis and pulmonary embolus.²Used in conjunction with imaging studies (CT, V/Q scan, and/or venous ultrasound and Doppler), a quantitative D–dimer level may be helpful in interpreting equivocal results. While some advocate performing this test prior to deciding on imaging studies,³ it may be more practical to perform the test concurrently with imaging studies.
While ABGs may be helpful, the pO₂, oxygen saturation levels, and the alveolar-arterial gradient have no predictive value for pulmonary embolism in the typical population of patients suspected to have pulmonary embolism. These values can all be normal in pulmonary embolism.
Chest x-ray is mandatory but non-diagnostic for pulmonary embolism. (Even radiologists cannot distinguish a pulmonary embolism infiltrate from pneumonia.) Chest x-ray helps to rule in or out other causes and interpret other findings. Common pulmonary embolism findings are infiltrate and effusion. If an infiltrate is seen, a subsequent V/Q scan will be non-diagnostic, so go directly to another diagnostic test such as an enhanced helical CT scan or angiography.
Helical (spiral) CT with contrast or CT angiography has become the most widely used modality for the diagnosis of pulmonary embolus. Contraindications are limited to contrast allergy, inability to tolerate a contrast load due to renal insufficiency or metformin treatment, or concerns about radiation exposure in early pregnancy. As there are a number of chest CT scanning protocols, make certain that the CT technician and radiologist know that the scan is being performed for diagnosis of pulmonary embolism.
The ventilation-perfusion scan (V/Q scan) is an important diagnostic modality. (Note that the scan cannot distinguish pulmonary embolism from pneumonia.) To use this test, you must categorize the patient’s risk into either high or low probability of having pulmonary embolism before getting the test. Test results should be reported to you as either diagnostic or non-diagnostic.

Diagnostic scans come in one of two forms, both of which may be used to guide clinical management if they are consistent with your pretest clinical risk assessment.

Normal scan means there are no perfusion defects noted. If the pretest probability was low, chances are good that the patient does not have pulmonary embolism. (Note that a small number of patients can have pulmonary embolism, even with a normal test). If the pretest probability was high, you need to investigate further for pulmonary embolism.
High probability scan: One of numerous defect patterns that highly suggest pulmonary embolism. If the pretest probability was low, get another confirmatory test (D-dimer and/or venous ultrasound), especially if the patient is not an ideal candidate for fibrinolytics. If the pretest probability was high, begin treatment for pulmonary embolism.

Non-diagnostic scan: One of numerous defect patterns that are equivocal. (This category includes the former categories of low and intermediate probability of PE.) An important concept is that a non-diagnostic scan is not a diagnostic endpoint. A definitive test must be performed for either pulmonary embolism or an alternative diagnosis.
Duplex ultrasound, which means concurrent imaging and Doppler flow recording, of the lower extremities is useful when positive: Demonstrating the presence of deep vein thrombosis virtually proves the diagnosis of pulmonary embolism. A negative study does not rule out pulmonary embolism or markedly reduce its probability.
Pulmonary angiography remains the most definitive test for pulmonary embolism diagnosis; however the advent of CT scanning for pulmonary embolus has to a large extent rendered angiography unnecessary. A positive study provides certainty; a negative study properly done provides greater than 90% certainty that pulmonary embolism doesn’t exist. (A negative study can’t visualize the really small emboli.)
Echocardiography—transthoracic or transesophageal—can identify right heart strain (RV hypokinesis and/or dilatation, tricuspid regurgitation), pulmonary hypertension, or large clots in the primary branches of the pulmonary tree. Bedside ultrasound may show evidence of right ventricular enlargement due to a major occlusion of a pulmonary artery. As a rule, the right ventricle should normally appear smaller than the left on apical 4-chamber view.⁴
ECG testing is rarely helpful. The classic right heart strain pattern shows up infrequently and is only suggestive, not diagnostic, of pulmonary embolism. Massive pulmonary embolism may be associated with symmetric T wave inversion in V1-4.

Management Considerations

Administer oxygen therapy to all patients suspected of having pulmonary embolism, as increased alveolar oxygen may promote pulmonary vasculature vasodilatation.
Intubate and mechanically ventilate if there are signs of respiratory failure. (Vol II—Air Skills; Vol III—AIR 4 Ventilator Management). Support circulation using CVP measurements as a guide. (Vol II—Circ Skills 3 Central Venous Pressure Measurement)
1. Without invasive monitoring or a cautious fluid trial and measurement, you can’t know whether the preload of additional fluid will help or harm a heart struggling to pump against high outflow pressures caused by an obstruction. If the patient’s condition worsens, stop immediately. Note that improvement with fluids does not mean that the patient is stabilizing; the primary problem hasn’t changed.
2. Bedside echocardiography is useful in the hemodynamically unstable patient whose heart might be failing from obstructive shock generated by pulmonary embolism.
3. Patients in cardiac arrest because of pulmonary embolism will not respond to CPR and treatment suggested by the ACLS protocols. Obstruction to oxygenated blood flow to the heart (and brain) is the cause. Emergency cardiopulmonary bypass can provide a bridge to operative embolectomy. Short of that, bilateral thoracotomy with pulmonary artery massage may be of some benefit.
Medication mainstays in the treatment of pulmonary embolism are fibrinolytics and anticoagulants. Be familiar with the precautions, risks, and contraindications of these agents before using them.
1. Fibrinolytics (clot dissolvers) should be considered in all pulmonary embolism patients without contraindications to therapy (and deep vein thrombosis patients without proven evidence of pulmonary embolism and no contraindications to fibrinolytics). Clear-cut indications include:
  - hemodynamically unstable patients with proven pulmonary embolism (Give immediately.)
  - pulmonary embolism patients with right heart strain and exhausted cardiopulmonary reserves
  - empiric treatment in unstable/deteriorating patients with highly suspected pulmonary embolism (and unlikely aortic dissection) who won’t survive long enough to get a confirmatory study
  - proven massive pulmonary embolism
  - pulmonary embolism patients at risk for multiple episodes into the future

Quicker-acting agents such as alteplase or reteplase are preferred. (Others that have been used include urokinase and streptokinase.)

Alteplase: 100 mg IV over 2 hours. (An accelerated, 90-minute schedule using the same amount but based on body weight has also been used.)
Reteplase: 10 units IV bolus and repeat in 30 minutes. In cardiac arrest situations, the 20 units have been given at once.

Order coagulation studies to be done 4 hours after therapy.

Anticoagulation with either of the following drugs is started upon suspicion of deep vein thrombosis or pulmonary embolism in order to inhibit clot extension. (They do not dissolve the clot.)

full-dose (low molecular weight heparin) enoxaparin (Lovenox): 1 mg/kg SQ every 12 hours. No need for coagulation studies. Preferred choice.
full dose IV heparin (different from cardiac dose heparin) can be used but can be difficult to titrate. (Note that heparin is used differently in certain clinical states involving fibrinolytics.) It may be given either concurrently with fibrinolytic therapy for pulmonary embolism, or it can be held and restarted after fibrinolytic has been given.

Consultation should not delay diagnosis or therapy. The team leader ultimately makes the decision to start fibrinolytic and/or anticoagulation therapy. Interventional radiologists may be helpful for directed fibrinolysis. Emergency surgical thromboembolectomy is indicated in those cases where fibrinolysis fails, is not tolerated, or is contraindicated.

Pulmonary Embolism Caveats

Deep vein thrombosis when diagnosed is believed to signify pulmonary embolism. Deep vein thrombosis below the knee is just as important as above the knee.
Pulmonary embolism is common during pregnancy and post partum for several months. Diagnose and treat a patient with pulmonary embolism who is pregnant the same as you would a non-pregnant patient.
Pulmonary embolism is more common as age increases. Do not dismiss respiratory symptoms in the geriatric patients.

Wells Clinical Prediction Rule for Pulmonary Embolism (PE)

Clinical Feature	Points
Clinical symptoms of DVT	3
Other diagnosis less likely than PE	3
Heart rate > 100 bpm	1.5
Immobilization/surgery within past 4 weeks	1.5
Previous DVT or PE	1.5
Hemoptysis	1
Malignancy	1
Total points
PE=pulmonary embolism; DVT=deep vein thrombosis.
Risk score interpretation (probability of PE): >6 points: high risk (PE incidence 78.4%) 2 to 6 points: moderate risk (PE incidence 27.8%) <2 points: low risk (PE incidence 3.4%)

Pneumothorax and Pneumomediastinum

Tension pneumothorax is addressed in Vol I—Step 3 Initial Survey.

Traumatic pneumothorax treatment is straightforward: Insert a chest tube. Vol II—Breath Skills 1 Chest Tube Insertion)

Nontraumatic (or spontaneous) pneumothorax occurs when a bleb on the surface of the lung ruptures and air escapes into the negative pressure pleural space. The gas pressure equilibrates across the tear, which may or may not seal. Vital capacity and PaO₂tend to decrease. This situation tends to be more serious or life threatening when the underlying lung is not normal (such as in COPD), when the pneumothorax is large, and/or when the patient is geriatric. Usually the patient is at rest when this happens. Symptoms may vary, and the patient may not come in for days. Therefore, this clinical condition may vary considerably on presentation. Symptoms may include ipsilateral chest pain and dyspnea.

The chest x-ray is usually diagnostic. Expiratory films may help to see a small pneumothorax. It may be difficult to estimate the size of the pneumothorax. Base therapy on the overall clinical status of the patient.

Management includes interventions to re-expand the lung. Patients who have waited a number of days before seeking treatment may be at increased risk for pulmonary edema when the lung is re-expanded. (How suction is used may play a role in re-expansion pulmonary edema.)

Give oxygen: increased O₂ saturation speeds the re-absorption of the free pleural air.
Ensure hemodynamic stability before proceeding with expansion attempts.
Consider sedation and analgesia needs before placing a chest tube. (Vol III—SED1 Procedural Sedation)
Re-expansion treatment varies depending on factors such as the baseline status of the underlying lung prior to the pneumothorax, whether the patient is symptomatic, and the size of the pneumothorax.
- If lungs are normal, there are no symptoms, and the pneumothorax is < 15%, consider observation without invasive intervention.
- If lungs are normal, the pneumothorax is <15%, but the patient is symptomatic, consider needle thoracostomy and aspiration.
- If the lungs are normal, the pneumothorax is >15%, and the patient is symptomatic, proceed with tube thoracostomy. (Vol II—Breath Skills 1 Chest Tube Insertion)
- If lungs are abnormal, proceed with tube thoracostomy. (Vol II—Breath Skills 1 Chest Tube Insertion)

Connect the chest tube to an underwater-seal drainage apparatus or a Heimlich valve (rather than a suction device) in order to avoid re-expansion pulmonary edema.

Obtain a repeat chest x-ray to confirm placement and lung re-expansion.

Arrange for pleurodesis by a consultant in cases with underlying abnormal lungs.

Consider prophylactic antibiotics.

Nontraumatic pneumomediastinum usually occurs when intrathoracic pressures become elevated due to conditions such as coughing, asthma, vomiting, Valsalva maneuvers, smoking crack cocaine, childbirth, angioedema, and seizures. Perivascular alveoli rupture and air dissects into connective issues, travels to the mediastinum, and then tracks superiorly. Once the air reaches the neck spaces, it can spread diffusely through the body’s subcutaneous tissues (crepitus may be felt subcutaneously). Patients may or may not have symptoms such as dyspnea or chest pain that radiates to the back and neck and is worsened by cough or deep breathing. It is usually benign and self-limited in the absence of serious comorbid disease; however, most patients are admitted for observation of signs of serious complications. These follow:

pneumothorax (the free air can rupture through the mediastinal parietal pleura)
mediastinitis
malignant pneumomediastinum (pressure high enough to cause cardiopulmonary failure)

In contrast, pneumomediastinum due to esophageal rupture has high mortality. This may occur under similar conditions, such as vomiting, forceful swallowing, straining, and weight lifting. Also ask about any recent medical procedures involving the upper GI system, suggesting iatrogenic perforation with delayed symptoms. Presentations vary from mild to acutely ill and septic. Symptoms include dyspnea, chest pain, abdominal pain, and vomiting blood. Physical findings include fever, tachycardia, tachypea, decreased breath sounds, crunching heart sounds, and palpable subcutaneous emphysema. Chest x-ray findings are suggestive but usually non-diagnostic and can include pneumomediastinum, pleural effusion, pneumothorax, mediastinal widening, air-fluid levels, and mediastinal emphysema. Early diagnosis and treatment is crucial. Emergency treatment consists of:

Airway and ventilation management
Hemodynamic stabilization considerations
Early consultation during the diagnostic work-up to ascertain esophageal perforation, which may include staging gastrografin swallows, endoscopy, non-contrast CT, and/or barium esophagography.
Once the diagnosis is established, antibiotics and an emergency cardiothoracic surgical referral for esophageal repair are indicated.

Massive Hemoptysis (Vol II—Breath Skills 3 Endobronchial Tube)

Quantifying the amount of blood that a patient coughs up can be somewhat arbitrary. For the patient with active/massive/gross bleeding from the respiratory system, or respiratory bleeding with respiratory insufficiency, or respiratory bleeding and unstable hemodynamics:

Position patient in Trendelenburg with bleeding side down (best breath sounds up).
Orotracheally intubate with large ET tube (8.00 mm). (Vol II—Air Skills 3 Orotracheal Intubation) If left-sided bleeding is suspected, do not place ET tube in the right main stem bronchus because of risk of occluding the right upper lobe bronchus. In right-sided bleeding, it may be beneficial if possible to place the ET tube into the left main stem bronchus for selective ventilation.
Alternatively, intubate with a left endobronchial tube in order to ventilate and suction the lungs separately.
Suction blood from the tracheobroncheal tree to improve oxygenation.
Resuscitate with normal saline 1 to 2 L IV; order and use blood as necessary.
Call for stat pulmonary/thoracic surgery consult.
- Bronchoscopy is performed to maintain ventilation and direct endobronchial blockade. (Rigid bronchoscopy may be better for massive bleeding.)
- When bleeding has been isolated, choices for definitive therapy include embolization, surgical resection, or both.
- Prepare the patient with these end goals in mind.

Chest x-ray after intubation.

For a patient who is stable in whom you suspect pulmonary embolism as a cause of bleeding, see #10 this portal. For the other stable patients, obtain a chest x-ray and continue to evaluate for the possible cause/site of bleeding.

Many underlying disorders can cause blood from the respiratory tract:

cancer
coagulopathy
drugs (anticoagulants, others)
iatrogenic causes
idiopathic causes
infection (bronchitis, tuberculosis, pneumonia, fungal, others)
heart problems (mitral stenosis, others)
lung disease (bronchiectasis, COPD, others)
trauma
vascular disorders (pulmonary embolism, pulmonary AV malformation, pulmonary infarction, others)

Further work-up may include CT scan or pulmonary angiography.

References

National Institutes of Health. National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report III: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: U.S. Department of Health and Human Services; 2007.
Institute for Clinical Systems Improvement. Health Care Guideline: Diagnosis and Treatment of Asthma. 9th ed. June 2010. http://www.icsi.org/asthma__outpatient/asthma__diagnosis_management_of__guideline_.html. Accessed October 6, 2010.
Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients’ probability of pulmonary embolism: increasing the model’s utility with the SimpliRED D-dimer. Thromb Haemost. 2000;83:416-420.
Stein PD, Hull RD, Patel KC et al. D-Dimer for the exclusion of acute venous thrombosis and pulmonary embolism: a systematic review. Ann Intern Med. 2004;140:589-602.
American College of Emergency Physicians Clinical Policies Committee; Clinical Policies Committee Subcommittee on Suspected Pulmonary Embolism. Clinical policy: critical issues in the evaluation and management of adult patients presenting with suspected pulmonary embolism. Ann Emerg Med. 2003;41:257-270.
Ma OJ, Mateer JR. Emergency Ultrasound. New York, NY: McGraw-Hill, 2002.

Pathway 6: Adult Respiratory

DOs and DON’Ts of DYSPNEA

DO:

DON’T:

References

Edition 13-October 2011