current diagnosis & treatment emergency medicine, 7e chapter 13

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CURRENT Diagnosis & Treatment Emergency Medicine, 7e >

Chapter 13. Respiratory DistressC. Keith Stone, MD

Immediate Management of Life-Threatening ProblemsSee Figure 13–1.

FIGURE 13–1.

Management of severe respiratory distress.

Assess Severity and Give Immediate Necessary Care

Patients in severe respiratory distress should receive simultaneous evaluation and therapy (see Figure 13–1). Providing and maintainingan adequate airway is the first consideration. Quickly assess the severity of distress by noting the patient's general appearance. Patientsstruggling to breathe demonstrate a greater use of chest and accessory muscles than the normal quiet use of the diaphragm. Anypatient with severe respiratory distress should receive immediate oxygen supplementation during assessment and treatment. Rapidlyperform a focused examination of the oropharynx, neck, lungs, heart, chest, and extremities. A plain film chest X-ray (CXR) with PA andlateral views, if possible, provides valuable information and should be obtained as soon as possible.

Assess Adequacy of Oxygenation

Pulse Oximetry

Bedside pulse oximeters measure the percent saturation of oxygen in capillary blood. Pulse oximetry is particularly useful during

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procedural sedation and during attempts at endotracheal intubation because of the real-time availability of the information. However, thisinformation is incomplete because pulse oximeters do not measure the PCO2 or detect the presence of hypoventilation leading torespiratory acidosis.

Arterial Blood Gases

Arterial blood gases provide, in essence, the same information about arterial oxygen saturation as does pulse oximetry, but arenecessary to provide valuable information about the effectiveness of ventilation. The blood gas provides measurement of pH, PO2, andPCO2. Arterial blood gases should be obtained in patients who are in severe respiratory distress, especially if pulse oximetry identifiesthat they require high concentrations of oxygen.

Cardiac Arrest

Clinical Findings

In unresponsive patients, check for airway patency and properly position the head and jaw to open the airway (Chapter 9). Evaluaterespiratory effort and assist ventilations if inadequate. Ventricular fibrillation results in rapid loss of consciousness usually within 5–10seconds. Such patients usually become apneic but may have perfunctory respiratory effort while unconscious. Such agonal breathing willbe shallow and ineffective. It is important to recognize the situation as a primary cardiac event. The treatment is immediate defibrillation.

Basic and advanced life support is covered in Chapter 9.

Severe Upper Airway Obstruction

See also Chapter 10.

Clinical Findings

Unless the patient has progressed to apnea unwitnessed, high-grade upper airway obstruction is usually obvious from pronouncedstridorous respirations. Retractions of the supraclavicular and suprasternal areas of the chest indicate that there is significant obstruction.Patients with complete airway obstruction will not be able to breathe or speak. Patients may have a visible swelling or mass in the neck.The tongue may be swollen, as may other structures in the mouth. Laryngoscopy may reveal a foreign body, tumor, or other obstructionin the larynx or trachea.

Treatment

(See also Chapter 9). Upper airway obstruction is most often due to soft tissue swelling secondary to infection or angioedema. Therapyshould be directed to reduce the edema either by cooling or by vasoconstriction and treating the underlying infection or allergy.Epinephrine, either topically, by inhalation, or parentally, is the most effective medication for angioedema but caution should be exercisedbecause of the associated cardiovascular effects. Direct laryngoscopy coupled with the use of forceps is the best method of removingobstructing foreign bodies. Obstructing liquids and particulate matter can be removed with a rigid suction device with a blunt tip(Yankauer). Foreign bodies such as meat may be removed by the Heimlich maneuver. A physician skilled in difficult airway managementshould care for these patients and may use adjuncts such as fiberoptic intubating bronchoscopy for diagnosis or securing the airway. Ifless invasive methods fail, immediate cricothyrotomy or tracheostomy is required (Chapter 7).

Disposition

Patients with easy, uncomplicated removal of an obstructing foreign body may be sent home following a period of observation withinstructions to eat more slowly, chew more thoroughly, and swallow more carefully. Patients who have lost consciousness but otherwiseappear well should be examined and observed in the emergency department and hospitalized only if symptoms develop or persist. Somepatients will have aspirated some material into the lungs, and hospitalization is appropriate if significant aspiration is suspected.

Altered Mental Status with Shallow Breathing

Clinical Findings

Altered mental status in a patient with obvious respiratory distress may be due to carbon dioxide retention or profound tissue hypoxia.However, the patient may have unlabored shallow respirations. Absence of a gag reflex (unprotected airway) or severe hypercapnia orhypoxemia on arterial blood gas studies (ie, respiratory failure) together with clinical assessment of underlying causes of altered mentalstatus support the necessity for endotracheal intubation in the emergency department.

Treatment

Ventilatory support should be given until endotracheal intubation can be accomplished. Provide high-flow (10–15 L/min) supplemental

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oxygen by nonrebreather mask or bag-valve-mask ventilation, as indicated.

As soon as oxygenation and carbon dioxide exchange have been partially corrected by assisted ventilation, the patient should beintubated. An endotracheal tube provides a definitive airway by preventing aspiration and facilitating effective respiratory support. If thereis doubt about the need for intubation, err on the side of intubation. Evaluation and treatment of other causes of altered mental statusshould follow airway management (Chapters 17, 18, 19, and 20 and 37).

Disposition

Hospitalize these patients for further diagnosis and treatment.

Tension Pneumothorax

Clinical Findings

Tension pneumothorax may develop as a result of trauma or may occur during positive pressure ventilation. Spontaneous pneumothorax(SP) rarely produces a tension pneumothorax. Specific physical signs of tension pneumothorax include shift of the trachea to thecontralateral side, and distended neck veins. Often these signs are difficult to appreciate, especially during a tense and sometimeschaotic trauma resuscitation. Clinical suspicion is the key to the diagnosis.

Treatment

Provide supplemental oxygen 100% by mask. Tube thoracostomy (Chapter 7) is the definitive treatment. Needle decompression shouldbe rarely, if ever, be required. Tube thoracostomy can be justified by clinical examination without a CXR and is usually preferable toneedle decompression. If a delay in performing tube thoracostomy is unavoidable and the patient is in severe distress, a large-bore (14–16-guage) needle may be placed through the second intercostal space in the midclavicular line. A rush of air verifies successfuldecompression of the hemithorax. Follow needle decompression with tube thoracostomy when the situation permits.

Disposition

Hospitalize these patients for further treatment.

Massive Aspiration

Clinical Findings

If the patient with severe respiratory distress has vomitus with particulate matter in the oropharynx, significant aspiration is likely.Aspiration may be observed sometimes during airway procedures. Vomitus, tube feedings, or particulate food particles may be observedin the oropharynx or suctioned from the airway. Following such an episode, the patient with aspiration will typically become hypoxic withtachypnea and respiratory distress. Fever and tachycardia frequently occur. Hypotension may develop. An infiltrate, sometimesextensive, usually appears on CXR especially in the dependent areas of the lungs. Aspiration pneumonia is a common cause ofrespiratory morbidity and mortality in elderly and debilitated patients.

Treatment

The airway should be suctioned to clear the aspirated material. Administer oxygen to correct hypoxia. Chemical pneumonitis resultingfrom aspiration does not require antibiotics but there is usually such difficulty in distinguishing aspiration pneumonitis from bacterialpneumonia that most clinicians begin treatment with broad-spectrum antibiotics. Corticosteroids have no proven value in the treatment ofaspiration pneumonia and, in fact, may be deleterious.

Disposition

Hospitalize these patients for definitive treatment.

Severe Pulmonary Edema

See also Chapters 33 & 35.

Clinical Findings

Patients with acute pulmonary edema present with severe dyspnea and labored breathing. This may be the presenting manifestation ofcardiac disease, may represent decompensation of previously managed congestive heart failure (CHF), or be noncardiac in origin. Mostpatients have rales at the base of both lungs but in some cases, all one can appreciate is wheezing, prolonged expiration, anddiminished breath sounds. Most of these patients are elderly or have known cardiac disease such as cardiomyopathy, coronary artery, orvalvular heart disease. Jugular venous distension and lower extremity edema are unreliable predictors of the presence and severity ofpulmonary congestion. The CXR will usually demonstrate interstitial (Figure 13–2) and sometimes alveolar edema. The work of breathing




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is greatly increased when the lungs are congested and edematous. Varying degrees of hypoxia are usually present. Brain natriureticpeptide (BNP) testing is helpful, especially in differentiating CHF from COPD. A level of greater than 100 pg/dL is consistent with acutedecompensated heart failure. The level of BNP correlates with the severity of CHF.

FIGURE 13–2.

The radiographic appearance of severe pulmonary edema.

Treatment

Patients should be treated with 100% oxygen by a nonrebreather mask. Furosemide should be given with the initial dose of 40 mg.Doses of 80–160 mg should be used if the patient already takes diuretics or has renal insufficiency. Severe hypertension is usuallypresent and is responsible for much of the reduced cardiac output and high left atrial pressure. Reducing it rapidly is a priority.Nitroglycerin by intravenous infusion is the best choice of a vasodilator in this setting starting at 5–10 μg/min. A higher dose may be usedif the blood pressure is very high. Sublingual nitroglycerin should be used prior to establishing the infusion.

Angiotensin-converting enzyme inhibitors are important in the long-term management of heart failure but their role in the acutelydecompensated patient is yet unclear. β blockers are useful in the long-term management of CHF but are best avoided in the acutelydecompensated patient. Bilevel positive airway pressure (BiPAP) with an expiratory level of 5 cm H2O and an inspiratory level of 15 cmH2O is most commonly used to provide noninvasive ventilatory support and my obviate the need for endotracheal intubation.

Disposition

Many of these patients are severely ill on presentation but improve dramatically with treatment. Most will still need to be hospitalized. Thepresence of chest pain, hypotension, or arrhythmia increases the risk of complications. Some patients with mild exacerbations of CHFthat are referable to an easily reversible cause, such as medication noncompliance, may be discharged if they respond well to treatment.

Severe Asthma, Chronic Obstructive Pulmonary Disease


Clinical Findings

Patients with asthma or chronic obstructive pulmonary disease may present with severe dyspnea and respiratory distress. However,dyspnea in this group of patients is less likely to be postural and cough is more common and troublesome. Patients with asthma orchronic obstructive pulmonary disease usually have wheezing on auscultation of the chest. Also common are tachypnea, tachycardia,cyanosis, chest hyperexpansion, and globally diminished breath sounds. Severe episodes are characterized by inability to speak in fullsentences, oxygen saturations < 92%, use of accessory muscles, pulsus paradoxus, confusion, and a quiet chest on auscultation. CXRshows only hyperexpanded lung fields unless another pathologic process such as bacterial pneumonia is present. These patientsfrequently have viral or (rarely) bacterial tracheobronchitis, or exposure to an allergen has exacerbated their chronic underlying disease.Peak expiratory flow rate is the most practical objective test of airway obstruction and the response to treatment available.

Treatment





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Oxygen

Give oxygen, 1–3 L/min, to raise arterial saturation to at least 95% or PO2 to between 60 and 80 mm Hg without causing respiratorydepression and a marked increase in arterial PCO2. Pulse oximetry is preferred, but arterial blood gas analysis may be indicated to helpdirect therapy. Noninvasive ventilation may be attempted to avoid tracheal intubation and mechanical ventilation. However, intubationmay be necessary if a patient is in acute respiratory failure.

β-Adrenergic Sympathomimetic Bronchodilators

In adults, β-adrenergic sympathomimetic bronchodilators should be given in aerosol form if possible; otherwise, they may be givenparenterally. A typical regimen is albuterol, 0.2–0.3 mL in 3 mL normal saline, delivered by nebulizer every 20–30 minutes. β-agonistsmay be nebulized in combination with ipratropium bromide (0.5 mg, up to three doses). For patients who are able to use them properly,metered-dose inhalers are as efficacious as nebulized therapy.

In general, parenteral therapy offers little benefit over nebulization, except in the most extreme cases. If used, parenteral therapyincludes epinephrine, 0.2–0.3 mL (1:1000 dilution) every 20–30 minutes subcutaneously, or terbutaline, 0.25 mg subcutaneously every2–4 hours. Parenteral therapy may have value in younger patients with severe exacerbation. However, parenteral administration ofsympathomimetics can produce marked tachycardia and may induce myocardial ischemia, especially in elderly patients or those withpreexisting coronary artery disease. Therefore, they should be used cautiously in this group and be withheld if chest pain or extremetachycardia develops.

Corticosteroids

Corticosteroids should be given early to patients who do not respond adequately to nebulized or parenteral β-adrenergic agents. Therecommended regimen is methylprednisolone, 125 mg intravenously initially, or prednisone, 60 mg orally. If the patient is to bedischarged from the emergency department, a short course of oral steroids may be considered.

Magnesium Sulfate

Magnesium sulfate has a bronchodialiting effect that may be of benefit in asthma. Its use should be reserved for life-threateningbronchospasm, which is refractory to all other interventions. Adult dosing of magnesium sulfate is 1–2 g intravenously over 15–30minutes; pediatric dosage is 40 mg/kg intravenously. Effects are short-lived after the infusion is discontinued. Blood pressure should bemonitored and the infusion stopped if hypotension occurs. Intravenous calcium should be immediately available to counteract cardiacdysrhythmias related to magnesium. Deep tendon reflexes will be lost once serum magnesium concentration reaches 7–10 mEq/L(normal concentration is 1.5–2.0 mEq/L); the infusion should be stopped if reflexes are lost. At higher concentrations, respiratorydepression and cardiac arrest may occur. However, the dose used for asthma is relatively low (approximately one-fourth the dose usedin preeclampsia).

Disposition

Hospitalize patients with significant bronchospasm that does not respond promptly to treatment, or those with moderate bronchospasmthat fails to improve after several hours of treatment.

Further management of patients with these disorders is discussed in Chapter 33.

Barnard A: Management of an acute asthma attack. Aust Fam Physician 2005;34:531–534 [PubMed: 15999162] .

Hammer J: Acquired upper airway obstruction. Paediatr Respir Rev 2004;5:25–33 [PubMed: 15222951] .

Holley AD, Boots RJ: Review article: management of acute severe and near-fatal asthma. Emerg Med Australas 2009;21:258–268 [PubMed: 19682010] .

Jessup M, Abraham WT, Casey DE et al: 2009 focused update: ACC/AHA guidelines for the diagnosis and management of heart failurein adults. Circulation 2009;119:1977–2016 [PubMed: 19324967] .

Keel M, Meier C: Chest injuries-what is new? Curr Opin Crit Care 2007;13:674–679 [PubMed: 17975389] .

Maher TM, Wells AU: Acute breathlessness. Br J Hosp Med 2007;68:M40–M43 [PubMed: 17419463] .

Masip J: Non-invasive ventilation. Heart Fail Rev 2007;12:119–124 [PubMed: 17492379] .

Paintal HS, Kuschner WG: Aspiration syndromes: 10 clinical pearls every physician should know. Int J Clin Pract 2007;61:846–852 [PubMed: 17493092] .

Leigh-Smith S, Harris T. Tension pneumothorax—time for a re-think? Emerg Med J 2005;22:8–16 [PubMed: 15611534] .

Further Diagnostic Evaluation

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Diagnostic Information

After supplemental oxygen has been started and life-threatening problems have been corrected, proceed as follows:

1. Obtain brief history directed toward cardiopulmonary disease and comorbidities, including potential triggers or causes, previoussimilar episodes, previous need for mechanical ventilation, and duration of this attack of dyspnea.

2. Obtain complete list of prescribed and unprescribed medications (current and recent past), including most recent dosage history andhistory of steroid use.

3. Conduct physical examination of the heart, lungs, abdomen, extremities, and other areas as indicated.

4. Obtain complete blood count, urinalysis, serum creatinine or blood urea nitrogen, serum electrolytes, and glucose, depending on thepatient's history and examination findings.

5. Monitor pulse oximetry and peak expiratory flow rate and conduct dyspnea scale assessment. Arterial blood gas may be performedon the basis of pulse oximetry or concomitant clinical findings.

6. Order CXR and electrocardiogram, if indicated.

7. Order additional indicated tests such as d-dimer or other imaging studies (ie, chest computed tomography [CT] scan, ventilation–perfusion scan).

Interpretation of Diagnostic Data

Information gathered from the history, physical exam, and ancillary testing, usually will allow the emergency physician to identify thecause of dyspnea (further discussed below and in Table 13–1).

Table 13–1. Esseyntials of Diagnosis of Diseases Causing Dyspnea and Respiratory Distress.a

Disorder SpecificCondition

OnsetHistory

SymptomsOther ThanDyspnea

Sans Chest X-ray Comment

Chest walldefect Flail chest Trauma Pain with

respirationParadoxicalmotion of chestwall

Rib fracturesCoexistentpneumothoraxcommon

Muscularweakness

Gradualonset

Weaknessof othermuscles

Weakness ofnonrespiratorymuscles

NormalDiminishedinspiratoryforce

Pulmonary Pneumothorax.Suddenonset;occasionallytrauma

Cough andchest paincommon

Tympany anddecreasedbreath sounds;decreasedblood pressureand trachealshift if tension

Lung collapse;mediastinal shiftif tension

Hydrothorax Gradualonset

Dullness anddecreasedbreath sounds

Pleural effusion(decubitusviews)

Atelectasis Variableonset Variable Signs of

atelectasis

Loss offunctionallungparenchyma

Pulmonaryedema

Usuallyabruptonset(hours todays)

Coughcommon;dyspnea onexertion,paroxysmalnocturnaldyspnea,orthopnea

Bibasilar rales(occasionalwheezing);jugular venousdistention withor withoutperipheraledema

Bilateral,alveolarinfiltrates, oftensymmetric

Most commoncause iscardiogenic,in which casethe patient willhaveassociatedsigns of

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heartfailure

Pneumonia

Usuallyabruptonset(hours todays)

Cough,pleurisycommon

Rales with orwithout dullnessover affectedareas; fever

Patchy alveolarinfiltrates,usuallyasymmetric

Leukocytesand oftenbacteriasputum

Diffuseinterstitialdisease

Previousdyspneacommon

Cough Often dry ralesInterstitialdisease (ornegative)

Patient oftena ware ofdiagnosis

AspirationAbruptonset;history ofvomiting

CoughVomitus inoropharynx, oron endotrachealsuction

Normal orinfiltrate

Usuallyassociatedwith coma orobtundation,underlyingdisease

Airwaydisease

Upper airwayobstruction

Oftensuddenonset

Hoarsenessor aphonia

Inspiratorystridor Normal

Soft tissue X-rays of neckmay behelpful

AsthmaUsuallypreviousattacks

Wheezing

Wheezing;hyperinflationand decreasedbreath soundsin statusasthmaticus

HyperinflationPatientusually awareof diagnosis

Chronicobstructivelung diseaseand cysticfibrosis

Previousdyspneacommon;onsetvariable

Cough,wheezing

Wheezing;hyperinflationand decreasedbreath sounds

Hyperinflation;occasionalpneumonitis

Clubbing withcystic fibrosis;patient usuallyaware ofdiagnosis

Pulmonaryvasculardisease

Acutepulmonaryembolism

Abruptonset

Cough,pleurisy,hemoptysis

Tachycardia;occasionallysigns of acutecor pulmonale

Usually normal;occasionallyinfiltrates,atelectasis,elevatedhemidiaphragm.“Hampton'shump”

Ventilation-perfusion lungscan, CTangiogram,pulmonaryarteriogramfor diagnoses,D-dimer

Repeatedsmallpulmonaryemboli

Gradualonset

Rarely,pleurisy orchest pain

Occasionallysigns of corpulmonale

Rarely helpful

May requireformalpulmonaryfunction testsfor diagnosis

Miscellaneous Pleurisy Oftenabrupt

Pleuriticpain

Rub (about80%) Normal

Rule outpulmonaryembolism

Metabolicacidosis

Gradualonset

Often notdyspneic Hyperventilation Normal

Low arterialblood pH andbicarbonate

NeurogenicUsually notdyspenic

Sign of cardiacor neurologicdisease

NormalStroke, heartfailure areusual causes

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Psychogenic

Previousattackscommon;abruptonset withstress

Circumoraland acraltingling

Tetany Normal

Reliefobtained withrebreathingsystem (e.g.,paper bag).Low PCO2

aThe most helpful tests or findings are shaded.

Disposition

(See also Miscellaneous Conditions.) If the clinical workup suggests a significant acute abnormality, but an exact diagnosis cannot bemade that would permit specific therapy to be started, hospitalize the patient even if the clinical status would not otherwise warranthospitalization. Sometimes more than one abnormality is present in the same patient (eg, acute exacerbation of chronic bronchitis andpneumonia).

Emergency Treatment of Specific Disorders

Chest Wall Defects

Flail Chest

Clinical Findings

Flail chest is an uncommon condition from blunt force trauma that is usually apparent on physical examination as a painful paradoxicalmotion of the rib cage or sternum (inward with inhalation and outward with exhalation). Crepitation or subcutaneous emphysema may benoted on examination together with decreased breath sounds on the affected side. A full trauma evaluation should be undertaken toidentify any associated injuries.

Treatment

Provide supplemental oxygen. Use a bag-mask to support ventilation of patients with obvious hypoventilation. Continuously monitor pulseoximetry. Intubation for respiratory support need not be performed immediately if the patient demonstrates adequate ventilation andoxygenation. However, endotracheal intubation and positive-pressure ventilation are likely to be required for hypoxia or hypoventilationdue to pain should trigger intervention. Provide analgesia (morphine, 1–4 mg intravenously, or fentanyl, 25–50 μg intravenously), andwatch carefully for signs of respiratory depression.

Disposition

All patients with flail chest injuries require hospitalization and consideration for ICU admission for aggressive pulmonary toilet and paincontrol.

Neuromuscular Diseases

Clinical Findings

Patients with dyspnea or respiratory distress associated with progressive neuromuscular disease usually have hypoventilation(decreased pulse oximetry readings or arterial blood gases showing hypoxemia and hypercapnia) and objective weakness of othermuscle groups, though the latter is not always present. Among many possible causes are Guillain–Barré syndrome, myasthenia gravis,hypokalemic periodic paralysis, botulism, and tick paralysis.

Treatment and Disposition

Evaluate respiratory status using pulse oximetry, arterial blood gas analysis, and pulmonary function tests (eg, vital capacity and maximalinspiratory force). Intubation may be postponed if initial blood gas levels are satisfactory. Specific therapy should focus on theneuromuscular disease (Chapter 37). Immediate hospitalization is usually indicated.

Pulmonary Collapse

Moderate degrees of pulmonary collapse that do not cause severe respiratory distress or obvious physical findings can be apparent onCXR. Treatment depends on the specific cause as discussed below.




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Pneumothorax

Clinical Findings

Clinically, pneumothorax is classified as spontaneous or traumatic. SP is divided into primary SP (no underlying lung disease) orsecondary SP (clinically apparent underlying lung disease). The patient often has chest pain and respiratory distress, with decreasedbreath sounds and tympany elicited by chest percussion of the affected side. The degree of dyspnea or respiratory distress depends onthe amount of collapse and on the degree of pressure (ie, tension pneumothorax). CXR shows lung collapse and air in the pleural space(Figure 13–3). Small amounts of fluid may also be present in the pleural space. Tension pneumothorax presents in a similar manner,and late findings include shift of the mediastinum away from the involved side, distended neck veins, hypotension, and shock.

FIGURE 13–3.

Small right-sided pneumothorax.

Treatment and Diposition

Immediate thoracostomy is indicated for bilateral pneumothoraces. Unilateral tension pneumothorax, should be treated with immediateneedle decompression or throacostomy based on the clinical evaluation, do not wait for CXR confirmation.

PRIMARY SPONTANEOUS PNEUMOTHORAX

Patients that present with a first time SP that is small defined as < 20% or apical < 3 cm and minor symptoms should not be treated andcan be discharged home with close outpatient follow up. For larger first time SP > 20%, or > 3 cm apical or with major symptoms, simplemanual aspiration or catheter aspiration connected to a Heimlich valve is the preferred treatment. If a follow-up CXR demonstratespersistent lung reexpansion, the patient may be discharged with close follow-up and instructions to return if symptoms reappear. Ifaspiration fails, patients are best treated by thoracostomy tube in the emergency department before hospitalization. Patients with a firstrecurrence of primary SP should be treated as detailed below for secondary SP.

SECONDARY SPONTANEOUS PNEUMOTHORAX

An air evacuation procedure should be done and the patient should be admitted for observation and recurrence prevention treatment.Immediate insertion of a chest tube is preferred over the use of catheter aspiration to evacuate the pleural space.

TRAUMATIC PNEUMOTHORAX

Most patients with a pneumothorax secondary to chest trauma should be treated with chest tube insertion. Large bore tubes (28–36 Fr.)should be used if there is an associated hemothorax. If the patient will require positive pressure ventilation, a chest tube is mandatory. Allpatients with traumatic pneumothorax should be hospitalized.

Hydrothorax and Hemothorax (Pleural Fluid or Blood)

Clinical Findings

Fluid in the pleural space results in pulmonary collapse. Small amounts of air may be present as well. The patient shows moderatedyspnea or respiratory distress and has dullness with chest percussion of the affected side. CXR is diagnostic (Figure 13–4).

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FIGURE 13–4.

Large left-sided hemothorax.

Treatment

HYDROTHORAX

If dyspnea of acute onset is thought to be secondary to hydrothorax, immediate drainage in the emergency department is indicated. Aneedle or small-gauge catheter should be used if the fluid is watery. Viscous effusions may require tube thoracostomy. No more than 1–2 L should be removed at any one time because of the risk of expansion injury to the lung. The fluid should be sent for analysis (pH,specific gravity, cell count, glucose, protein, lactate dehydrogenase, and amylase), culture (for Mycobacterium tuberculosis and otherbacteria), and cytologic studies.

HEMOTHORAX

In hemothorax due to penetrating trauma, autotransfusion may be indicated. Otherwise, thoracentesis or tube thoracostomy (or both)should be done, followed by investigation into the source of bleeding (eg, aortic angiography, exploration) as indicated (Chapter 24).

Disposition

Hospitalization is required for all patients except those with chronic recurrent pleural effusions of known cause and without significanthypoxia or respiratory impairment.

Massive Atelectasis

Clinical Findings

Atelectasis is alveolar collapse that is not due to pneumothorax or hydrothorax. Decrease in chest motion on the affected side, dullnessto percussion, and decreased to absent breath sounds are noted. Dyspnea, tachycardia, and cyanosis may be present. The disorder isevident radiologically as an increase in density of the collapsed lung, with reduced volume of the involved hemithorax (narrowed ribinterspaces, elevated hemidiaphragm, and mediastinal shift to the side of involvement).

Treatment

In general, patients with atelectasis exhibit some degree of respiratory distress, which can be quite variable. In the rare patient withrespiratory failure, respiratory support (administration of oxygen and usually also assisted ventilation) should be initiated in theemergency department. Administration of oxygen is indicated for patients with hypoxia on pulse oximetry while the underlying cause isdetermined.

Disposition

Hospitalization is required unless the process is known to be chronic and nonprogressive.


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Loss of Functional Lung Parenchyma

A number of conditions can produce acute or chronic dyspnea through loss of functional pulmonary parenchyma.

The hallmarks of diseases causing loss of functional lung parenchyma are inspiratory rales (crackles) on physical examination, dullnessto percussion, auscultatory pitch changes (eg, egophony and bronchial breath sounds), and one or more infiltrates on CXR. Thesedisorders may be divided into those associated with (1) pulmonary edema, (2) pneumonia (including aspiration pneumonia), and (3)interstitial disease. Pulmonary contusion following blunt chest trauma is covered in Chapter 24.

In patients with dyspnea, several processes may be occurring simultaneously. For example, aspiration pneumonia may be a combinationof chemical pulmonary edema and bacterial pneumonia, with varying degrees of airway obstruction; viral pneumonias are often inter-stitial in their early phases; and cardiogenic pulmonary edema starts as interstitial edema before progressing to the alveolar filling stage.Additionally, it may be difficult to differentiate these conditions initially in the emergency department (eg, pneumonia from pulmonaryedema).

Pulmonary Edema

Clinical Findings

The clinical presentation of less severe pulmonary edema is similar to that associated with the more severe form discussed above.Patients generally are less dyspneic and have a history of symptoms and signs such as paroxysmal nocturnal dyspnea, graduallyincreasing peripheral edema, and intermittent chest pain if the pulmonary edema is cardiogenic. Noncardiogenic edema usually beginsmore abruptly and is more severe than the cardiogenic form. CXR shows cephalization (Figure 13–5).

FIGURE 13–5.

Mild-to-moderate pulmonary edema with cephalization of pulmonary vasculature.

Treatment

Give oxygen as needed. Additional treatment depends on whether the diagnosis is cardiogenic or noncardiogenic pulmonary edema(Chapters 33 and 35). A trial of BiPap may obviate the need for endotracheal intubation. However, intubation may be required ifhypoxemia cannot be corrected.

Disposition

Many patients with dyspnea from acute pulmonary edema require hospitalization. Some patients with chronic or recurrent pulmonaryedema (usually cardiogenic) can potentially be managed on an outpatient basis.

Pneumonia


Clinical Findings

Patients with pneumonia generally give a history of fever and cough; dyspnea is a secondary or late symptom. Production of purulent




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sputum and pleuritic chest pain are common. Physical examination usually shows a febrile patient with localized rales and dullness onpercussion, often associated with signs of consolidation (egophony, bronchial breath, and vocal sounds). In children, fever and coughare the only constant symptoms.

CXR (Figure 13–6) shows one or more infiltrates, except in patients with early pneumonia or concomitant dehydration, in whomobservation and rehydration over 4–6 hours generally will make the infiltrates visible on X-ray. Immunosuppressed patients may alsohave pneumonia without infiltrates.

FIGURE 13–6.

Radiographic appearance of a right lower lobe pneumonia.

Patients with AIDS may develop pneumonia due to Pneumocystis carinii. Despite cough, fever, dyspnea, and hypoxemia (or an elevatedalveolar-arterial PO2 gradient calculated from arterial blood gas data), the clinical findings may be few and X-ray findings extremelysubtle or normal. However, typical X-ray findings, if present, are a diffuse heterogeneous alveolar or interstitial infiltrate.

Treatment

Begin antibiotics promptly based on the clinical situation; community acquired, or health care associated pneumonia. See Chapter 42 fora more extensive discussion of evaluation and treatment of pneumonia.

Disposition

Hospitalization is warranted for all seriously ill patients, for very young or very old patients, for patients with significant concurrentillnesses, for unreliable patients, and for patients with pneumonia of unknown cause. Patients with Pneumocystis pneumonia should beadmitted.

Adolescents and young adults with mild viral, mycoplasmal, or pneumococcal pneumonia usually can be managed on an outpatient basis(Chapter 42).

Diffuse Interstitial Pulmonary Disease


Clinical Findings

Most patients with interstitial pulmonary disease have a history of chronic dyspnea, are aware of their diagnosis, and come to theemergency department because of recent worsening of symptoms. If the patient has not sought medical attention previously, interstitialpulmonary disease may be suspected if the physical examination shows diffuse “dry” rales, the CXR shows interstitial infiltrates, andarterial PCO2 and PO2 are low.

Treatment

Supportive care is the only treatment recommended in the emergency department.




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Disposition

Hospitalization should be considered for all newly diagnosed patients and for patients with known interstitial disease with significantrecent increase in dyspnea or hypoxemia.

Aspiration

Clinical Findings

Aspiration may present clinically as pneumonia without obvious prior aspiration or as respiratory distress with obvious aspiration (vomitusin mouth and on clothing and elsewhere). This latter presentation is more common in patients with altered mental status.

Treatment

Supportive care should be given immediately in all cases. If obvious aspiration has occurred, clearing the airway is the most importantemergency measure. This is best accomplished with a large-bore, hard-tipped suction device. Endotracheal intubation for better airwaycontrol and pulmonary toilet should be considered, as should emergency bronchoscopy.

Disposition

Hospitalize all patients. The patient's initial status is not a reliable guide to the need for hospitalization, because pulmonary function mayworsen progressively for 24–72 hours after aspiration.

Airway Disease

Obstruction to airflow (airway obstruction) is a principal manifestation of all types of airway disease.

Upper Airway Obstruction

Lesions of the oropharynx, larynx, or trachea may occlude the airway sufficiently to cause dyspnea.

Clinical Findings

Upper airway obstruction usually causes pronounced stridor (obstruction of inspiratory airflow equal to or greater than expiratory airflow),which may be accentuated by forced ventilatory efforts. The stridor may be accompanied by intercostal, suprasternal, or supraclavicularretractions or other signs of increased respiratory effort. The diagnosis can be made with lateral soft-tissue X-rays of the neck. In somecases, fiberoptic laryngoscopy is helpful.

Causes of upper airway obstruction include foreign bodies, tonsillar hypertrophy, croup, epiglottitis, anaphylaxis with laryngeal edema,retropharyngeal abscess, and tumors. If epiglottitis is suspected, obtain a lateral neck X-ray before attempting to visualize the upperairway directly (Chapter 32). Young children may aspirate small objects (eg, beads, coins, or peanuts) that lodge in the trachea or main-stem bronchus. Wheezing may be mistaken for bronchospastic disease. An expiratory CXR is diagnostic, showing unilateralhyperexpansion on the affected side due to the ball-valve effect of the obstructing object (which may not be visible).

Treatment

A foreign body should be removed if present. Anaphylaxis with laryngeal edema requires immediate subcutaneous or intramuscularinjection of epinephrine, 0.5–1.0 mg (0.5–1.0 mL of 1:1000 solution). Alternatively, give 0.1–0.2 mg (1–2 mL of 1:10,000 solution)intravenously. Repeat in 3–10 minutes as needed (Chapter 11). Additionally, administration of diphenhydramine, 25–50 mgintramuscularly or intravenously, or selective histamine blockers such as famotidine, 20 mg intravenously, will block further histaminerelease. Discharged patients should receive diphenhydramine, 25 mg orally every 6 hours for 24–48 hours, to prevent recurrence.

Surgical cricothyrotomy may be emergently required if obstruction progresses. Occasionally patients with hereditary angioedema (due toC1q esterase inhibitor deficiency) will present with signs and symptoms similar to those of allergic anaphylaxis. These patients areaffected little by epinephrine and require C1q esterase inhibitor replacement (or fresh-frozen plasma if C1q esterase inhibitor isunavailable).

Children with epiglottitis (Chapter 50) should not receive direct or indirect laryngoscopy in the emergency department, because laryngealspasm may precipitate complete obstruction. They should be carefully intubated in the operating room with surgeons present who canperform an emergency tracheostomy if needed. Adults with epiglottitis are less prone to sudden airway obstruction but should beadmitted and monitored closely. Both children and adults should receive intravenous antibiotics.

Disposition

Patients with dyspnea from documented or suspected upper airway obstruction require hospitalization unless the problem is chronic,mild, and nonprogressive or is due to a foreign body that can be removed in the emergency department. Successfully treated upperairway obstruction due to anaphylaxis may recur when epinephrine wears off. Therefore, a 4–6-hour period of observation (or










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hospitalization) is advisable.

Asthma, Chronic Obstructive Pulmonary Disease

(See also Chapter 33). In these disorders, expiratory airflow tends to be reduced proportionately more than the inspiratory flow. Patientswith dyspnea caused by these types of airway disease usually have a history of respiratory symptoms and are aware of their diagnosis.

Clinical Findings

Cough is commonly a feature, although sputum production is variable. Most of these patients have wheezing on auscultation, which isaccentuated during forced expiration. Other findings are similar to those discussed earlier in this chapter.

Treatment

The therapy discussed under treatment of severe forms of these disorders is also of value in less severe presentations.

Disposition

Hospitalization is indicated for patients with severe or rapidly worsening dyspnea that does not respond to a few hours of treatment in theemergency department. Patients with asthma who are discharged home should receive corticosteroid therapy: oral for those withmoderate symptoms, and oral or inhaled for those with minor symptoms.

Pulmonary Vascular Disease

Dyspnea from pulmonary vascular disease may be one of the most difficult diagnostic problems confronting the emergency physician.The manifestations of pulmonary vascular disease are extremely varied in character and severity, and there is a significant risk oflabeling patients with these illnesses as hysterical personalities or malingerers.

Acute Pulmonary Embolism


Clinical Findings

Patients with acute pulmonary embolism and infarction usually have dyspnea, tachypnea, pleuritic chest pain, tachycardia, hypoxemia,and hypocapnia. Low-grade fever, cough, hemoptysis, and wheezing may also be present. Pulmonary infiltrates, occasionally witheffusion, may be seen on X-ray.

Patients with embolization without infarction have similar manifestations but often without pulmonary infiltrates, fever, and hemoptysis. Inmassive pulmonary embolization, crushing anterior chest pain, dyspnea, severe hypoxemia, syncope, shock, and cardiac arrest arecommon. Patients with right-sided endocarditis and other causes of septic pulmonary embolization usually have high fever and rigorsassociated with symptoms of embolization; the CXR often shows multiple, scattered infiltrates that frequently cavitate after several daysof illness.

Diagnosis

Progressive, noninvasive evaluation strategies that consider specific risk factors and physical findings (Wells Criteria) have replacedinvasive methods of diagnosis. Serum d-dimer, venous lower extremity Doppler ultrasound, spiral CT, CT angiography, and ventilation–perfusion scanning have significantly decreased the need for conventional pulmonary angiography in suspected pulmonary embolism.

Treatment

Give oxygen. Give morphine as necessary for pain. Treat shock if present. Heparin should be started (unless contraindicated) ifembolization is strongly suspected. For adults, give a bolus of 80 units/kg followed by an infusion of 18 units/kg/h adjusting the rate tomaintain the prothrombin time at 1.5–2 times control values. Selected patients may be appropriate for low-molecular-weight heparintherapy (enoxaparin sodium, 1 mg/kg subcutaneously every 12 hours or fondaparinux 5 mg SQ for < 50 kg patient, 10 mg SQ for > 100kg patient, and 7.5 mg SQ for all others). Thrombolytic therapy should generally be reserved for patients with moderate to severe rightventricular dysfunction. See Chapter 33 for further discussion on management.

Disposition

Patients with suspected or documented pulmonary embolization almost always require hospitalization.

Miscellaneous Conditions

Pleurisy

Clinical Findings








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Pleurisy and pleuritic pain from any cause may produce a sensation of dyspnea. Even conditions such as rib fractures that producepleuritic pain in the absence of significant underlying pulmonary parenchymal abnormalities may cause splinting and atelectasis sufficientto produce hypoxemia. When pleural fluid forms, the pain and friction rub may lessen or disappear. Pleurisy is often part of a viralsyndrome (which may occasionally be accompanied by pericarditis). Fever, myalgias, headache, nasal congestion, or flu-like symptomsmay be present. A CXR is required to exclude underlying lung disease, pleural effusion, or pneumothorax.

Treatment

Other than measures for relief of pain, therapy must be directed toward the underlying lesions.

Disposition

Hospitalization is required if the patient is severely hypoxemic (arterial PO2 ≤ 60 mm Hg as a new finding), if parenteral analgesia isrequired for pain relief, or if the underlying disease requires hospital treatment.

Metabolic Acidosis

Clinical Findings

Metabolic acidosis (eg, diabetic ketoacidosis, salicylate overdose) can produce secondary hyperventilation that may be taken fordyspnea or respiratory distress. Arterial blood gas analyses usually show a normal or high PO2, marked hypocapnia (PCO2 of 10–20mm Hg), and metabolic acidosis (low serum bicarbonate concentration).

Treatment and Disposition

Treatment depends on the underlying condition. Patients almost always require hospitalization for management of the underlying causeof metabolic acidosis (Chapter 44).

Neurologic Hyperventilation

Primary central nervous system disease can produce a variety of abnormal breathing patterns, including central hyperventilation andCheyne–Stokes respiration, any of which could be mistaken for respiratory distress. Cheyne–Stokes respiration may also occur when thecirculation is slowed, as in heart failure.

Clinical Findings

The diagnosis is based on finding obvious neurologic or cardiac disease consistent with the respiratory pattern. The arterial PO2 isusually normal; PCO2 may be low or high.

Treatment

No treatment of the respiratory condition is required.

Disposition

Disposition depends on the underlying disease.

Psychogenic Hyperventilation and Pulmonary Neurosis

Clinical Findings

Patients with psychogenic hyperventilation usually present with a history of acute dyspnea and anxiety, often precipitated by personal orenvironmental factors. Hyperventilation to the point of tetany is diagnostic. Lightheadedness (due to cerebral vasoconstriction) andcircumoral or limb paresthesias are often present. Another helpful feature is that the dyspnea often improves with exercise. Patients canbe calmed enough to speak, whereas in organic dyspnea, patients may not be capable of speech. There are usually no abnormalities onthe screening database other than a low arterial PCO2, normal or high arterial PO2, and elevated pH. Most of these patients can bediagnosed in the emergency department as having neuroses, but the possibility of pulmonary vascular disease must be considered.

Treatment

There is no specific treatment. Reassurance is usually helpful. Patients with symptomatic hypocapnia (circumoral tingling, carpopedalspasm, tetany) or marked respiratory alkalosis (pH > 7.55) should breathe into an airtight bag for several minutes to relieve hypocapnia.

Disposition

The patient should be referred to a pulmonary clinic or internist for complete evaluation and reassurance.

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Management of severe respiratory distress.

The radiographic appearance of severe pulmonary edema.

Small right-sided pneumothorax.

Large left-sided hemothorax.

Mild-to-moderate pulmonary edema with cephalization of pulmonary vasculature.

Radiographic appearance of a right lower lobe pneumonia.









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