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Acute postobstructive pulmonary edema: Case presentation and review
ORIGINAL
RESEARCH
Acute Postobstructive Pulmonary Edema: Case Presentation and Review Steve Talbert, RN, MSN’
1.
University of Kentucky Hospital Air Medical Service, Lexington, Ky.
Address for correspondence and reprints: Steve Talbert, RN, MSN, University of Kentucky Hospital Air Medical Service, 800 Rose St., Room HA038, Lexington, KY 40536 Copyright Associates
0 1998
1067-991
W98/$5.00
Reprint
by the Air Medical
Journal
+ 0
no. 7411 J9248l
Air Medical Journal
17:3
July-September
Case Presentation An outlying hospital requested air medical transport of a &year-old boy experiencing partial upper airway obstruction with associated respiratory distress. Four days before this episode, his pediatrician diagnosed him with strep throat and mononucleosis. Treatment included penicillin G injections and oral amoxicillin. His parents returned him to the emergency department after his respiratory distress worsened. He was admitted for observation and given racemic epinephrine nebulizer treatments, dexamethasone, cefotaxime, and albuterol syrup. He became more combative and restless, and his oxygen saturations (SpOz)fell to 88%. When the flight crew arrived, the patient’s respiratory status had improved. Physical examination revealed tachypnea, retractions, and stridor. He was awake and alert and followed commands. His SpOzincreased to 94%; oxygen was being administered through a nonrebreather mask at 15 L/minute. The patient was moved to the aircraft and transported to Children’s Hospital. His respiratory status improved somewhat in transport as his SpOzincreased to 100%. He was admitted directly to the pediatric intensive care unit (PICU). Initial evaluation by the pediatric intensivist revealed significant tons&r hypertrophy with exudate. Admission chest radiograph demonstrated pulmonary edema. The patient continued to exhibit respiratory distress. Otolaryngology and anesthesia professionals were consulted, 1998
and the patient was taken emergently to the operating room (OR) for airway management, bronchoscopy, and removal of massively hypertrophied and inflamed tonsils and adenoids. The OR course was uneventful, and the patient was taken to the postanesthesia care unit (PACU) after surgery. The patient was extubated in the PACU. However, his oxygen saturations began to drop, and he again became tachypneic. A repeat chest radiograph showed increased interstitial fluid consis tent with postobstructive pulmonary edema (see Figure 1). The patient was reintubated and returned to the PICU. The patient’s pulmonary edema was treated with ventilatory support, furosemide, steroids, antibiotics, and judicious fluid management (3/4 mainte nance). He remained intubated for 24 hours. After successful extubation, the patient’s recovery was uncomplicated. He remained on oral antibiotics and a tapering dose of steroids. He was discharged to home on postoperative day 3 in good condition. Discussion Acute postobstructive pulmonary edema (APOPE) is a complication of both partial and complete obstruction of the upper airway and occurs in approximately 12%of all obstruction cases.Yhe condition has been associated with a number of etiologies, including epiglottitis, tonsillar and adenoid hypertrophy, laryngospasm, hanging, strangulation, and intubation.1,57 Although APOPE is 111
typically a self-limiting event that resolves withii 24 hours, one reported fatality was noted in the literature.2 APOPE is more common in young, healthy individuals because they are physically capable of generating significantly more negative intrathoracic pressure.lbs Its onset may be rapid or delayed for up to 4 hours.’ Pathophysiology The pathophysiology of APOPE is multifactorial.1~289 The three mechanisms widely accepted as contributing to the development of APOPE are intrathoracic pressure changes, hypoxia, and sympathetic nervous system activation. Intrathoracic pressure changes. Changes in intrathoracic pressure caused by upper airway obstruction lead to fluid shifts into the pulmonary interstitial space. A victim of partial or complete acute obstruction of the upper airway must create significantly more negative intrathoracic pressures to move an adequate volume of air past the obstruction and into the lungs. Inspiration against an obstruction (Mueller maneuver) has been shown to have a negative impact on the hemodynamic statelo and damage alveoli, capillaries, and the alveolarcapillary membrane. WJ~Intra-alveolar and, consequently, pulmonary interstitial pressures are significantly negative at the same time that pulmonary vessel hydrostatic pressure is increased (as a result of left ventricular dysfunction and increased pulmonary blood volume), creating a large pressure gradient favoring fluid movement into the interstitial space. Furthermore, damaged alveolar and capillary membranes cause further fluid &ii into the interstitium. Negative intrathoracic pressure impairs left ventricular function. Negative pressure pulls the myocardium outward while contractile action moves the myocardium inward. These opposing forces mean the heart must generate more active tension before it can push open the aortic valve. In essence, negative intrathoracic pressure increases after-load and myocardial oxygen demands and may result in decreased cardiac output and cardiomyopathy.1o In chronic obstruction (eg, tonsilar hypertrophy), additional forces may be involved.g Chronic obstruction increases 112
Increased interstitial with postobstructive
intrinsic positive end expiratory pressure (PEEP) and, consequently, intrathoracic pressure. Once the obstruction is relieved (eg, tonsillectomy), intrathoracic pressure suddenly decreases, resulting in a sudden increase in venous return. This increased volume is passed on to the pulmonary system, creating more intravascular hydrostatic pressure that moves fluid into the interstitial space. Figure 2 illustrates how changes in intrathoracic pressure eventually lead to the development of APOPE. Hypoxia. Alveolar hypoxia causes further disturbances in pulmonary fluid mechanics. Partial or complete airway obstruction may lead to alveolar hypoxia, either through alveolar carbon dioxide retention, resulting in decreased alveolar partial pressure of oxygen, or through atelectasis and intrapulmonary shunting.l.8.11Hypoxia results in pulmonary vasoconstriction, increased capillary hydrostatic pressure, and increased vascular permeability.” These pathophysiological consequences of hypoxia drive fluid from the intravascular space into the interstitial space.
fluid consistent pulmonary edema
Sympathetic nervous system activation. Hypoxia also stimulates sympathetic nervous system activity. Catecholamines cause systemic vasoconstriction, increased venous return, and increased afterload to the heart Pulmonary blood volume subsequently is augmented, resulting in increased pulmonary hydrostatic pressure and movement of fluid into the interstitial space.‘J1Figure 3 illustrates how hypoxia and sympathetic nervous system stimulation eventually can lead to APOPE development. Treatment As previously mentioned, APOPE generally is self-limited and will resolve within 24 to 48 hours of onset. General treatment goals are to improve oxygena tion and resolve interstitial edema. Most patients require ventilatory support and supplemental oxygen.1.8”Other interventions may include PEEP, diuretics, and fluid restriction?g Implications for Air Transport APOPE should become part of the diiferential when evaluating patients with
July-September
1998
17:3
Air Medical Journal
airway obstructions or those experiencing respiratory distress after extubation or airway obstruction resolution. The index of suspicion should be increased if the patient is young or physically fit. Carefully monitoring the patient’s respiratory status for signs of developing pulmonary edema is essential. Caring for a patient with APOPE during air transport is not significantly different than caring for any patient experiencing pulmonary edema. Initial therapy includes supplemental oxygen, morphine, and diuretics (eg, furosemide). The flight crew should be prepared to assist with ventilation and intubate if the patient’s respiratory status is sufficiently compromised. Sedation and neuromuscular blockade may be helpful with intubation or achieving adequate ventilatory support.
Changes
in lntrathoracic
Chronic Obstruction
Conclusion APOPE occurs in approximately 12% of all airway obstructions. Although usually self-limited and apt to resolve within 24 hours, APOPE can progress and cause more serious respiratory distress. Practitioners caring for patients with an hay obstruction should monitor them closely for signs of worsening respiratory function. Such monitoring is important during the acute phase of care and in the hours after relief of the obstruction. Patients who develop respiratory distress tier outpatient surgery should be evaluated for APOPE.
Pressure
Acute Obstruction
Nervous
Hypoxia and Sympathetic System Stimulation Leading
to APOPE
Alveolar Hypoxia I 4 t Pulmonary Vascular Permeability
I
1 Pulmonary Vasoconstriction
Acute Systemic Hypoxia 4 SNS Activation 4 Peripheral Vasoconstriction I + t venous R&XII
v t Pulmonary Vascular Hydrostatic Pressure.
I
4 t Afterload
t Palmonary J Vascular Vobme
1 Fluid Movement fmm Intravascular to Interstitial and Alveolar Spaces . (pulmonary Edema)
References 1. Lang S& Duncan PG, Shephard DAE, Ha HC. Pulmonary edema associated with airway obstruction. Can J Anaesth 1990;37:21@8. 2. Adolph MD, Oliver AM, Dejak T. Death from adult respiratory distress syndrome and multiorgan failure following acute upper airway obstrwtion. ENT J 1994;73:3247. k3. K&i A, Crosby ET, Lui AC. Airway and respire tory management following nonlethal hanging. Can J Anaesth 1997;44:44550. 4. Aouad M, Ashkar K. Pulmonary edema following postoperative laryngospasm. Middle East J Anesthesiol1997;14:59-63.
Air Medical Journal
17:3 July-September
5.
Eid AA, Agabani M, Grady K. Negative-pressure pulmonary edema: a cautionary tale. Cleve CIin J Med 1997$X151-4. 6. Dicpinigaitis PV, Mehta DC. Postobstructive pulmonary edema induced by endotracheal tube occlusion. Intensive Care Med 1995;21: 104850. 7. DeVane GG. Acute postobsbwtive pulmonary edema. CRNA 1995;6:110-3.
8.
Wilson GW, Bircher NG. Acute pulmonary edema developing atter laryngospasm: report of a case. J Oral MaxiIlofac Surg 1995;53:211-4.
9.
Guffin
1998
TN,
Har-El
G, Sanders
A Lucente
Nash M. Acute postobstructive pulmonary ede ma Otolaryngol Head Neck Surg 1995;112:2357. 10. Somers VK, Dyken ME, Skinner JL Autonomic and hemodynamic responses and interactions during the Mueller maneuver in humans. J Auton Nerv Syst 1993$4:253-g. 11. Ruftle J, Gleason M, Domino KB, Gersony WM. Zucker HA. Pulmonary edema and transient cardiomyopathy in a previously healthy adoles cent after general anesthesia. J Cardiothorac Vast Anesth 1994:8:46570.
FE,
113
RESEARCH
Acute Postobstructive Pulmonary Edema: Case Presentation and Review Steve Talbert, RN, MSN’
1.
University of Kentucky Hospital Air Medical Service, Lexington, Ky.
Address for correspondence and reprints: Steve Talbert, RN, MSN, University of Kentucky Hospital Air Medical Service, 800 Rose St., Room HA038, Lexington, KY 40536 Copyright Associates
0 1998
1067-991
W98/$5.00
Reprint
by the Air Medical
Journal
+ 0
no. 7411 J9248l
Air Medical Journal
17:3
July-September
Case Presentation An outlying hospital requested air medical transport of a &year-old boy experiencing partial upper airway obstruction with associated respiratory distress. Four days before this episode, his pediatrician diagnosed him with strep throat and mononucleosis. Treatment included penicillin G injections and oral amoxicillin. His parents returned him to the emergency department after his respiratory distress worsened. He was admitted for observation and given racemic epinephrine nebulizer treatments, dexamethasone, cefotaxime, and albuterol syrup. He became more combative and restless, and his oxygen saturations (SpOz)fell to 88%. When the flight crew arrived, the patient’s respiratory status had improved. Physical examination revealed tachypnea, retractions, and stridor. He was awake and alert and followed commands. His SpOzincreased to 94%; oxygen was being administered through a nonrebreather mask at 15 L/minute. The patient was moved to the aircraft and transported to Children’s Hospital. His respiratory status improved somewhat in transport as his SpOzincreased to 100%. He was admitted directly to the pediatric intensive care unit (PICU). Initial evaluation by the pediatric intensivist revealed significant tons&r hypertrophy with exudate. Admission chest radiograph demonstrated pulmonary edema. The patient continued to exhibit respiratory distress. Otolaryngology and anesthesia professionals were consulted, 1998
and the patient was taken emergently to the operating room (OR) for airway management, bronchoscopy, and removal of massively hypertrophied and inflamed tonsils and adenoids. The OR course was uneventful, and the patient was taken to the postanesthesia care unit (PACU) after surgery. The patient was extubated in the PACU. However, his oxygen saturations began to drop, and he again became tachypneic. A repeat chest radiograph showed increased interstitial fluid consis tent with postobstructive pulmonary edema (see Figure 1). The patient was reintubated and returned to the PICU. The patient’s pulmonary edema was treated with ventilatory support, furosemide, steroids, antibiotics, and judicious fluid management (3/4 mainte nance). He remained intubated for 24 hours. After successful extubation, the patient’s recovery was uncomplicated. He remained on oral antibiotics and a tapering dose of steroids. He was discharged to home on postoperative day 3 in good condition. Discussion Acute postobstructive pulmonary edema (APOPE) is a complication of both partial and complete obstruction of the upper airway and occurs in approximately 12%of all obstruction cases.Yhe condition has been associated with a number of etiologies, including epiglottitis, tonsillar and adenoid hypertrophy, laryngospasm, hanging, strangulation, and intubation.1,57 Although APOPE is 111
typically a self-limiting event that resolves withii 24 hours, one reported fatality was noted in the literature.2 APOPE is more common in young, healthy individuals because they are physically capable of generating significantly more negative intrathoracic pressure.lbs Its onset may be rapid or delayed for up to 4 hours.’ Pathophysiology The pathophysiology of APOPE is multifactorial.1~289 The three mechanisms widely accepted as contributing to the development of APOPE are intrathoracic pressure changes, hypoxia, and sympathetic nervous system activation. Intrathoracic pressure changes. Changes in intrathoracic pressure caused by upper airway obstruction lead to fluid shifts into the pulmonary interstitial space. A victim of partial or complete acute obstruction of the upper airway must create significantly more negative intrathoracic pressures to move an adequate volume of air past the obstruction and into the lungs. Inspiration against an obstruction (Mueller maneuver) has been shown to have a negative impact on the hemodynamic statelo and damage alveoli, capillaries, and the alveolarcapillary membrane. WJ~Intra-alveolar and, consequently, pulmonary interstitial pressures are significantly negative at the same time that pulmonary vessel hydrostatic pressure is increased (as a result of left ventricular dysfunction and increased pulmonary blood volume), creating a large pressure gradient favoring fluid movement into the interstitial space. Furthermore, damaged alveolar and capillary membranes cause further fluid &ii into the interstitium. Negative intrathoracic pressure impairs left ventricular function. Negative pressure pulls the myocardium outward while contractile action moves the myocardium inward. These opposing forces mean the heart must generate more active tension before it can push open the aortic valve. In essence, negative intrathoracic pressure increases after-load and myocardial oxygen demands and may result in decreased cardiac output and cardiomyopathy.1o In chronic obstruction (eg, tonsilar hypertrophy), additional forces may be involved.g Chronic obstruction increases 112
Increased interstitial with postobstructive
intrinsic positive end expiratory pressure (PEEP) and, consequently, intrathoracic pressure. Once the obstruction is relieved (eg, tonsillectomy), intrathoracic pressure suddenly decreases, resulting in a sudden increase in venous return. This increased volume is passed on to the pulmonary system, creating more intravascular hydrostatic pressure that moves fluid into the interstitial space. Figure 2 illustrates how changes in intrathoracic pressure eventually lead to the development of APOPE. Hypoxia. Alveolar hypoxia causes further disturbances in pulmonary fluid mechanics. Partial or complete airway obstruction may lead to alveolar hypoxia, either through alveolar carbon dioxide retention, resulting in decreased alveolar partial pressure of oxygen, or through atelectasis and intrapulmonary shunting.l.8.11Hypoxia results in pulmonary vasoconstriction, increased capillary hydrostatic pressure, and increased vascular permeability.” These pathophysiological consequences of hypoxia drive fluid from the intravascular space into the interstitial space.
fluid consistent pulmonary edema
Sympathetic nervous system activation. Hypoxia also stimulates sympathetic nervous system activity. Catecholamines cause systemic vasoconstriction, increased venous return, and increased afterload to the heart Pulmonary blood volume subsequently is augmented, resulting in increased pulmonary hydrostatic pressure and movement of fluid into the interstitial space.‘J1Figure 3 illustrates how hypoxia and sympathetic nervous system stimulation eventually can lead to APOPE development. Treatment As previously mentioned, APOPE generally is self-limited and will resolve within 24 to 48 hours of onset. General treatment goals are to improve oxygena tion and resolve interstitial edema. Most patients require ventilatory support and supplemental oxygen.1.8”Other interventions may include PEEP, diuretics, and fluid restriction?g Implications for Air Transport APOPE should become part of the diiferential when evaluating patients with
July-September
1998
17:3
Air Medical Journal
airway obstructions or those experiencing respiratory distress after extubation or airway obstruction resolution. The index of suspicion should be increased if the patient is young or physically fit. Carefully monitoring the patient’s respiratory status for signs of developing pulmonary edema is essential. Caring for a patient with APOPE during air transport is not significantly different than caring for any patient experiencing pulmonary edema. Initial therapy includes supplemental oxygen, morphine, and diuretics (eg, furosemide). The flight crew should be prepared to assist with ventilation and intubate if the patient’s respiratory status is sufficiently compromised. Sedation and neuromuscular blockade may be helpful with intubation or achieving adequate ventilatory support.
Changes
in lntrathoracic
Chronic Obstruction
Conclusion APOPE occurs in approximately 12% of all airway obstructions. Although usually self-limited and apt to resolve within 24 hours, APOPE can progress and cause more serious respiratory distress. Practitioners caring for patients with an hay obstruction should monitor them closely for signs of worsening respiratory function. Such monitoring is important during the acute phase of care and in the hours after relief of the obstruction. Patients who develop respiratory distress tier outpatient surgery should be evaluated for APOPE.
Pressure
Acute Obstruction
Nervous
Hypoxia and Sympathetic System Stimulation Leading
to APOPE
Alveolar Hypoxia I 4 t Pulmonary Vascular Permeability
I
1 Pulmonary Vasoconstriction
Acute Systemic Hypoxia 4 SNS Activation 4 Peripheral Vasoconstriction I + t venous R&XII
v t Pulmonary Vascular Hydrostatic Pressure.
I
4 t Afterload
t Palmonary J Vascular Vobme
1 Fluid Movement fmm Intravascular to Interstitial and Alveolar Spaces . (pulmonary Edema)
References 1. Lang S& Duncan PG, Shephard DAE, Ha HC. Pulmonary edema associated with airway obstruction. Can J Anaesth 1990;37:21@8. 2. Adolph MD, Oliver AM, Dejak T. Death from adult respiratory distress syndrome and multiorgan failure following acute upper airway obstrwtion. ENT J 1994;73:3247. k3. K&i A, Crosby ET, Lui AC. Airway and respire tory management following nonlethal hanging. Can J Anaesth 1997;44:44550. 4. Aouad M, Ashkar K. Pulmonary edema following postoperative laryngospasm. Middle East J Anesthesiol1997;14:59-63.
Air Medical Journal
17:3 July-September
5.
Eid AA, Agabani M, Grady K. Negative-pressure pulmonary edema: a cautionary tale. Cleve CIin J Med 1997$X151-4. 6. Dicpinigaitis PV, Mehta DC. Postobstructive pulmonary edema induced by endotracheal tube occlusion. Intensive Care Med 1995;21: 104850. 7. DeVane GG. Acute postobsbwtive pulmonary edema. CRNA 1995;6:110-3.
8.
Wilson GW, Bircher NG. Acute pulmonary edema developing atter laryngospasm: report of a case. J Oral MaxiIlofac Surg 1995;53:211-4.
9.
Guffin
1998
TN,
Har-El
G, Sanders
A Lucente
Nash M. Acute postobstructive pulmonary ede ma Otolaryngol Head Neck Surg 1995;112:2357. 10. Somers VK, Dyken ME, Skinner JL Autonomic and hemodynamic responses and interactions during the Mueller maneuver in humans. J Auton Nerv Syst 1993$4:253-g. 11. Ruftle J, Gleason M, Domino KB, Gersony WM. Zucker HA. Pulmonary edema and transient cardiomyopathy in a previously healthy adoles cent after general anesthesia. J Cardiothorac Vast Anesth 1994:8:46570.
FE,
113