Flail Chest

Published on 23/05/2015 by admin

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Flail Chest

Chapter Objectives

After reading this chapter, you will be able to:

• List the anatomic alterations of the lungs associated with a flail chest.

• Describe the causes of a flail chest.

• List the cardiopulmonary clinical manifestations associated with a flail chest.

• Describe the general management of a flail chest.

• Describe the clinical strategies and rationales of the SOAPs presented in the case study.

• Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.

Paradoxic Movement of the Chest Wall

Venous Admixture

FIGURE 21-1 Flail chest. Double fractures of three or more adjacent ribs produce instability of the chest wall and paradoxic motion of the thorax. Inset, Atelectasis, a common secondary anatomic alteration of the lungs.

Anatomic Alterations of the Lungs

A flail chest is the result of double fractures of at least three or more adjacent ribs, which causes the thoracic cage to become unstable—to flail (see Figure 21-1). The affected ribs cave in (flail) during inspiration as a result of the subatmospheric intrapleural pressure. This compresses and restricts the underlying lung area and promotes a number of pathologies, including atelectasis and lung collapse. In addition, the lung also may be contused under the fractured ribs.

A flail chest causes a restrictive lung disorder. The major pathologic or structural changes of the lungs associated with flail chest are as follows:

• Double fracture of numerous adjacent ribs

• Rib instability

• Lung volume restriction

• Atelectasis

• Lung collapse (pneumothorax)

• Lung contusion

• Secondary pneumonia

Etiology and Epidemiology

A blunt or crushing injury to the chest is usually the cause of flail chest. Such trauma may result from the following:

• Motor vehicle accidents

• Blast injury

• Direct compression by a heavy object

• Industrial accidents

OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Flail Chest

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-8) and Consolidation (see Figure 9-9)—the major anatomic alterations of the lungs associated with flail chest (see Figure 21-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Increased Respiratory Rate (Tachypnea)

Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate. These include the following:

• Stimulation of peripheral chemoreceptors (hypoxemia)

• Paradoxic movement of the chest wall

• Other mechanisms

Paradoxic Movement of the Chest Wall

When double fractures exist in at least three or more adjacent ribs, a paradoxic movement of the chest wall is seen. During inspiration the fractured ribs are pushed inward by the atmospheric pressure surrounding the chest and negative intrapleural pressure. During expiration (and particularly during forced exhalation), the flail area bulges outward when the intrapleural pressure becomes greater than the atmospheric pressure.

As a result of the paradoxic movement of the chest wall, the lung area directly beneath the broken ribs is compressed during inspiration and is pushed outward through the flail area during expiration. This abnormal chest and lung movement causes air to be shunted from one lung to another during a ventilatory cycle.

When the lung on the affected side is compressed during inspiration, gas moves into the lung on the unaffected side. During expiration, however, air from the unaffected lung moves into the affected lung. The shunting of air from one lung to another is known as pendelluft (Figure 21-2). As a consequence of the pendelluft, the patient rebreathes dead-space gas and hypoventilates. In addition to the hypoventilation produced by the pendelluft, alveolar ventilation also may be decreased by the lung compression and atelectasis associated with the unstable chest wall.

FIGURE 21-2 Lateral flail chest with accompanying pendelluft.

As a result of the pendelluft, lung compression, and atelectasis, the ratio decreases. This leads to intrapulmonary shunting and venous admixture (Figure 21-3). Because of the venous admixture, the patient’s Pao₂ and Cao₂ decrease. As this condition intensifies, the patient’s oxygen level may decline to a point low enough to stimulate the peripheral chemoreceptors, which in turn initiate an increased ventilatory rate.

FIGURE 21-3 Venous admixture in flail chest.

Other Possible Mechanisms

• Decreased lung compliance–increased ventilatory rate relationship

• Activation of the deflation receptors

• Activation of the irritant receptors

• Stimulation of the J receptors

• Pain, anxiety

Increased Heart Rate (Pulse) and Blood Pressure

Chest Assessment Findings

• Diminished breath sounds, on both the affected and the unaffected sides

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings

(Restrictive Lung Pathology)

LUNG VOLUME AND CAPACITY FINDINGS

V_T	IRV	ERV	RV
N or ↓	↓	↓	↓
VC	IC	FRC	TLC	RV/TLC ratio
↓	↓	↓	↓	N

Arterial Blood Gases

MILD TO MODERATE FLAIL CHEST

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco₂		Pao₂
↑	↓	↓ (slightly)	↓

SEVERE FLAIL CHEST

Acute Ventilatory Failure with Hypoxemia (Acute Respiratory Acidosis)

pH*	Paco₂	*	Pao₂
↓	↑	↑ (slightly)	↓

^*When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular Paco₂ level.

Oxygenation Indices *

	Do₂^†		C(a-)o₂	O₂ER
↑	↓	N	↑ (severe)	↑	↓

^*C(a-)O₂, Arterial-venous oxygen difference; DO₂, total oxygen delivery; O₂ER, oxygen extraction ratio; , pulmonary shunt fraction; , mixed venous oxygen saturation; , oxygen consumption.

^†The Do₂ may be normal in patients who have compensated to the decreased oxygenation status with (1) an increased cardiac output, (2) an increased hemoglobin level, or (3) a combination of both. When the Do₂ is normal, the O₂ER is usually normal.

Hemodynamic Indices ‡

Severe Flail Chest Disorder

CVP	RAP		PCWP	CO	SV
↑	↑	↑	↓	↓	↓
SVI	CI	RVSWI	LVSWI	PVR	SVR
↓	↓	↑	↓	↑	↓

^‡CO, Cardiac output; CVP, central venous pressure; LVSWI, left ventricular stroke work index; , mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVSWI, right ventricular stroke work index; SV, stroke volume; SVI, stroke volume index; SVR, systemic vascular resistance.

RADIOLOGIC FINDINGS

Chest Radiograph

• Increased opacity (in atelectatic areas or areas with postflail pneumonia).

• Rib fractures (may need special films—rib series—to demonstrate).

• Because of the lung compression and atelectasis associated with flail chest, the density of the lung on the affected side increases. The increase in lung density is revealed on the chest radiograph as increased opacity (i.e., whiter in appearance). The chest radiograph may also shows the rib fractures (Figure 21-4).

FIGURE 21-4 A, Chest x-ray film of a 20-year-old woman with a severe right-sided flail chest. B, Close-up of the same x-ray film, demonstrating rib fractures (arrows).

General Management of Flail Chest

In mild cases, medication for pain and routine bronchial hygiene may be the only treatments needed. In more severe cases, however, stabilization of the chest is usually required to allow bone healing and prevent atelectasis. Today, volume-controlled ventilation, accompanied by positive end-expiratory pressure (PEEP), is commonly used to stabilize a flail chest. Generally, mechanical ventilation for 5 to 10 days is adequate for sufficient bone healing to occur.

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxia, decrease the work of breathing, and decrease myocardial work. It should be noted, however, that the hypoxemia that develops in flail chest is most commonly caused by the alveolar atelectasis and capillary shunting associated with the disorder. Hypoxemia caused by capillary shunting is often refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 9-1).

Lung Expansion Therapy Protocol

Lung expansion techniques are commonly administered to offset and prevent the alveolar consolidation and atelectasis associated with flail chest (see Lung Expansion Therapy Protocol, Protocol 9-3).

Mechanical Ventilation Protocol

Because acute ventilatory failure is associated with flail chest, continuous mechanical ventilation is often required to maintain an adequate ventilatory status (see Mechanical Ventilation Protocols, Protocol 9-5, Protocol 9-6, and Protocol 9-7).

CASE STUDY

Flail Chest

Admitting History and Physical Examination

A 40-year-old obese male truck driver was involved in a serious four-vehicle accident and was taken to the emergency department of a nearby medical center, where he was found to be markedly agitated and uncooperative. He was conscious and in obvious respiratory distress. His vital signs were as follows: blood pressure 80/62, pulse 90/min, respiration rate 42/min and shallow. Bilateral paradoxic movement of the chest wall was evident.

He had a laceration of the right eyelid and deep lacerations of the right thigh with rupture of the patellar tendon. Pain and tenderness were present on palpation of the right posterior chest wall. The ribs moved inward with inspiration. The anteroposterior (AP) diameter of the chest was increased. Breath sounds were decreased bilaterally, and expiration was prolonged.

X-ray examination revealed posterolateral fractures of ribs 2 through 10 on the right and fractures of the necks of ribs 11 and 12 on the left. He had a 4+ hematuria, but his other laboratory findings were within normal limits.

The patient was intubated in the emergency department and placed on a mechanical ventilator with 3 cm H₂O PEEP, a V_T of 15 mL/kg and ventilatory rate of 12. An arterial line was placed, and the patient was taken to the operating room, where surgical repair of the eyelid and thigh was performed. In the operating room, with an Fio₂ of 1.0, the patient’s blood gas values were pH 7.48, Paco₂ 30, 23, and Pao₂ 360. The patient was transferred to the surgical intensive care unit, where the respiratory care practitioner on duty made the following assessment.

Respiratory Assessment and Plan

S N/A—patient is intubated, put on mechanical ventilator, sedated, and paralyzed (Norcuron).

O No spontaneous respirations. No paradoxic movement of chest wall on ventilator. BP 110/70, HR 100 regular, RR 12 on vent. On 100% O₂, pH 7.48, Paco₂ 30, 23, and Pao₂ 360. CXR: Bilateral rib fractures, left lung contused, no pneumothorax, no hemothorax.

• Bilateral flail chest (history, paradoxic chest movement, CXR)

• Acute alveolar hyperventilation with overoxygenation (ABG)

P Mechanical Ventilation Protocol: Decrease V_T to correct acute alveolar hyperventilation and maintain patient on controlled ventilation per protocol until chest wall is stable. Wean oxygen per Ventilator Protocol (decreased to Fio₂ 0.4). Alert charge nurse (to request increased sedation and muscle paralysis) if the patient begins to inhale above preset mechanical ventilation rate. Routine ABG monitoring and continuous Sao₂ monitoring. Careful chest assessment and auscultation to monitor for secondary pneumothorax and pneumonia.

Over the next 72 hours, the patient was kept intubated and ventilated with an Fio₂ of 0.4 and a mechanical ventilation rate of 12/min. However, his hospital course was stormy. Aggressive fluid volume resuscitation with intravenous fluids at the rate of 10 mL/hour was given. His sputum rapidly became thick and yellow. Lung Expansion Therapy Protocol was increased to a PEEP of 5 cm H₂O. On the second day, a right pneumothorax was demonstrated and a chest tube was inserted. A persistent air leak was present.

The next day, his pulse rose to 160/min and the pulmonary artery catheter showed evidence of left ventricular failure. His blood pressure was 142/82. His rectal temperature was 99.2° F. His ventilator rate was 12 breaths/min, with a PEEP of 10 cm H₂O. Auscultation revealed bilateral crackles. On an Fio₂ of 0.7, his ABGs were as follows: pH 7.37, Paco₂ 38, 23, and Pao₂ 58. He was rapidly diuresed, and his cardiac function improved dramatically. His Swan-Ganz catheter failed to “wedge.” Over the next few days, the chest x-ray film showed dense infiltrates in both lungs, and it was difficult to maintain adequate oxygenation, even with high inspired oxygen concentrations. His sputum was yellow and thick. Whenever his Sao₂ dropped below 90%, he became restless and agitated. At this time, the respiratory assessment was as follows:

Respiratory Assessment and Plan

S N/A—intubated, sedated, and paralyzed.

O Afebrile. HR 160 regular, BP 142/82, RR 12 (on vent). Right chest tube shows air leak. Crackles bilaterally. CXR: Fractures appear in line; bilateral dense infiltrates. ABG on an Fio₂ of 0.7: pH 7.37, Paco₂ 38, 23, and Pao₂ 58. Sputum thick, yellow.

• Persistent bilateral flail chest (CXR)

• Bilateral dense infiltrates suggest atelectasis vs pulmonary edema vs ARDS vs pneumonia (CXR)

• Adequate alveolar ventilation with moderate hypoxemia on present ventilator settings; oxygenation continues to worsen (ABG)

• Thick, yellow bronchial secretions (sputum)

• Pneumonia possible (despite normal temperature)

• Bronchopleural fistula on right side (chest tube bubbles)

P Mechanical Ventilation Protocol and Lung Expansion Therapy Protocol. Increase PEEP to 12 cm H₂O. Oxygen therapy per protocol (increase Fio₂ to 0.8). Institute Bronchopulmonary Hygiene Therapy Protocol and Aerosolized Medication Protocol (in-line med. neb. with 2.0 mL premixed albuterol, followed by direct instillation of acetylcysteine q4h, and suction prn. Obtain sputum for Gram stain and culture). Assist physician in the replacement of the Swan-Ganz catheter to optimize fluid therapy. Continue Sao₂ monitoring.

During the patient’s first week of hospitalization, his BUN increased to 60 mg% and his creatinine to 1.9 mg%. Liver function values remained within normal limits. The abnormal BUN and creatinine gradually returned to normal during the second week. The patient was slowly but successfully weaned off the ventilator over the next 2 weeks.

Discussion

This complicated case demonstrates the care of the traumatized patient with multiorgan failure. In this case the second organ system affected was the cardiovascular system, probably secondary to fluid overload. Initial therapy included chest wall rest and internal fixation with mechanical ventilation. By the time of the second assessment, the more classic clinical manifestations of pulmonary parenchymal change secondary to flail chest had developed. The clinical scenarios of Atelectasis (see Figure 9-8) and/or Alveolar Consolidation (see Figure 9-9) were well established, with oxygen-refractory pulmonary capillary shunting clearly in evidence.

Later, when what appeared to be acute respiratory distress syndrome (ARDS) supervened, PEEP was added, both for its effect on the ARDS and to stabilize the chest wall. Although these problems were dramatic enough, the therapist alertly noted the thick yellow bronchial secretions and added acetylcysteine and vigorous suctioning to deal with this problem. Aerosolized Bronchodilator Therapy (in this case albuterol) must always be given before or concurrently with acetylcysteine because the latter agent may cause bronchospasm if given alone. The ordering of a sputum Gram stain and culture was appropriate.

Clearly, a patient this ill should be assessed at least once—possibly more—per shift. Because this patient was hospitalized for 40 days, more than 120 such assessments were found in his chart! As we reviewed his case, this certainly did not seem to be excessive.

Related

Clinical Manifestations _ Assessment of Respiratory Disease