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Laryngospasm-Induced Pulmonary Edema
Laryngospasm-Induced Pulmonary Edema* Freebie N. Jackson, M.D.;t Virginia Rowlariil,M.D.;t and GuenterCorssen, M.D.§
Laryngospasm developed in a 33-year-old womao folowlog attempted endotracheal intuiJatioL Followinl establislunent of the airway, the patient developed palmonary edema which was SDCCellfnlly treated by conveatlonal
means. The .eqaeace of events..._... Chat JarnaCIIIpMIII predplblted the deftlopment .. the ............,. edenla in this patient.
The etiologies of pulmonary edema are myriad. Acute upper airway obstruction is rarely mentioned, however, among the possible precipitating causes. this potential complication must be recognized and treated promptly to minimize delayed morbidity and mortality among survivors of acute upper airway obstruction. We report a case of laryngospasm complicated by the development of pulmonary edema and comment on the pathophysiologic consequence of acute upper airway obstruction leading to this complication.
Immediately, the patient developed apparent laryngospasm, and attempts to administer positive pressure oxygen by facial maslc were met with marked resistance to airflow. No breath sounds were present on physical eumiDation, and the patient became increasingly cyanotic. She was immediately treated with intravenous aminophylline and epinephrine; within three minutes, she could again be ventilated by maslc, at which time arterial blood gas levels revealed Po2, 56 mm Hg; Pco2 , 91 mm Hg; pH, 7.10; and Hco3, 28 mEq/L. Several minutes later, while receiving supplemental oxygen at 8 L/min via mask, repeat arterial blood gas levels showed Po2, 161 mm Hg; Pco2, 72 mm Hg; pH, 7 .32; and Hco3, 35 mEq/L (patient received 44 mEq sodium bicarbonate intravenously). Blood pressure was continuously monitored during the episode, and no hypotension was noted. The patient remained alert and awake during the event without apparent emesis or aspiration. Immediately following the clearing of her airway, auscultation revealed normal breath sounds. During the ensuing 20 minutes, the patient became increasingly dyspneic with the development of diffuse rales and wheezes without stridor. Cardiac eumiDation revealed a sinus tachycardia without murmur or S3 gallop, a pulsus paradoxus of 40 mm Hg, and ECG demonstrated a supraventricular tachy-
A 33-year-old multiparous Mexican-American woman was admitted at full term with spontaneous rupture of membranes on March 21, 1979. She bad received prenatal care without neurologic symptoms, enjoyed a normal weight gain, normal blood pressure readings, and showed no proteinuria on urinalysis. Her admission examination revealed blood pressure of 130/100 mm Hg supine and 130178 mm Hg lying on her left side, pitting pedal edema, and an otherwise normal physical examination results. A dipstick urinalysis was positive for protein; however, two repeat urinalyses showed no protein. Blood chemistry samples drawn two days postpartum showed the foJlowing values: albumin, 3.1 gm/100 ml; blood urea nitrogen, 7 mg/100 ml; and creatinine, 0.8 mg/100 ml. She was treated with magnesium sulfate in conventional doses for 24 hours during which time she had a normal vaginal delivery of a healthy male infant Her immediate postpartum course was uneventful. On the second postpartum day, the patient was scheduled for an elective bilateral tubal ligation and received the following intramuscular premedications; atropine, 0.4 mg; meperidine, 50 mg; and hydroxyzine, 25 mg. Ninety minutes later, endotracheal intubation was attempted after induction of anesthesia with 250 mg of thiopental sodium and 100 mg of succinylcholine, preceded by 3 mg of curare, all administered intravenously. Due to the patient's unusual body habits (obesity, short neck), the vocal cords could not be visualized, and two blind attempts at intubation were unsuccessful. •From the Departments of Medicine and Anesthesiology, Maricopa County General Hospital, Phoenix. tMedical Resident, Department of Medicine. :tAssociate Chief of Pulmonary Medicine. §Chairman, Department of Anesthesia; Professor Emeritus, University of Alabama. Manuscript received October 1; revision accepted January 31.
CHEST, 78: 6, DECEMBER, 1980
F'lcUBE 1. Portable anteroposterior chest roentgenogram demonstrates diffuse, bilateral alveolar infiltration.
LARYNGOSPASM-INDUCED PULMONARY OEMA 811
F'ICUIIE 2. Portable anteroposterior roentgenogram two days later shows clearing of alveolar illfiltration. cardia without acute ST-T changes. Approximately one hour after laryngospasm, a portable anteroposterior chest roentgenogram (Fig 1 ) demonstrated diffuse, bilateral alveolar infiltration. Repeat arterial blood gas levels revealed Po2 , 68 mm Hg; Pco2 , 33 mm Hg; pH, 7.41; and Hco3 , 26 mEq/L (8 L/min via nasal prongs). Continuous positive airway pressure (CPAP=5) em H 20 was administered via facial mask, and corticosteroids, as well as diuretics, were given intravenously. She responded well to this therapy voiding 3 Lin 36 hours, for a combined postpartum diuresis of 5 L. On the day following the acute obstructive episode, the CPAP was discontinued. A portable anteroposterior chest roentgenogram obtained two days later showed clearing of the alveolar illfiltration (Fig 2) . Arterial blood gas levels at this time were Po2 , f¥1 mm Hg; Pco, 27 mm Hg; pH, 7.50; and Hco8 , 22 mEq/L (room air). By March 26, lf¥19, the patient was asymptomatic with clear lungs on physical examination. She was discharged home and had no recurrent problems during six months of follow-up. DISCUSSION
Our patient was a previously healthy postpartum woman, who developed severe laryngospasm during attempted endotracheal intubation. Though she was treated for presumed preeclampsia, the criteria for this were not totally satisfied. A review of prenatal records did not demonstrate an abrupt weight change, prenatal and postpartum blood pressure readings were not significantly different, there were no neurologic signs or symptoms, repeat urinalyses showed no proteinuria, and blood chemistry samples showed normal renal function. Laryngospasm is a well-recognized complication of laryngeal intubation occurring in experimental animals as well as humans. This occurs via laryngeal reftexes which may cause spasm of the glottis and bronchi.1 Resolution of upper airway obstruction in our patient was followed by the development of
820 JACKSON, ROWLAND, CORSSEN
pulmonary edema. The temporal sequence strongly suggests a causal relationship between the acute obstructive episode and the subsequent onset of pulmonary edema. Although this complication of laryngospasm is recognized by anesthesiologists, 2 we found no prior case reported in the literature. The natural course of acute upper airway obstruction is death, occurring within minutes, as a consequence of profound hypoxia. Even when an airway is promptly established, survival may be jeopardized by the development of pulmonary edema. Comroe3 lists four basic causes of pulmonary edema as follows : increased pulmonary edema-increased pulmonary capillary pressure, decreased plasma colloidal osmotic pressure, increased pulmonary capillary permeability, and decreased intrathoracic pressure. Pulmonary edema occurring in connection with acute upper airway obstruction is primarily the result of decreased intrathoracic pressure, a pathogenetic mechanism which bas received relatively little emphasis in the literature. Decreased intrathoracic pressure in upper airway obstruction is generated by attempted inspiration against a closed glottis. The result is a mean negative transpulmonary pressure, which favors transudation of 8uid from the pulmonary capillaries into the interstitial space. Negative intrapleural pressure generated by an external source, as in rapid evacuation of pneumothorax or pleural effusion, may also be complicated by the development of pulmonary edema. Recently, studies of pulmonary mechanics during acute asthmatic attacks have also revealed large negative pressures during inspiration.4 It has been suggested that over-vigorous 8uid therapy may lead to increased lung water in this situation. Acute hypoxia, which developed in our patient, may have been an additional factor contributing to the development of pulmonary edema. Moss et al5 have produced noncardiogenic pulmonary edema in experimental animals solely by cerebral perfusion with hypoxic blood. A postulated mechanism is altered hypothalamic function leading to autonomically-mediated pulmonary vascular constriction, capillary hypertension, and interstitial edema formation. Our patient's prompt response to treatment, including CPAP, supplemental oxygen, diuretics, and steroids, was gratifying. Considering the potentially serious consequences of untreated pulmonary edema, patients who recover from acute upper airway obstruction should be closely monitored for the development of this complication. The primary pathogenetic mechanism for pulmonary edema in this situation is believed to be decreased intrathoracic pressure. CHEST, 78: 6, DECEMBER, 1980
I Blanc VF, Tremblay NAG: The complications o( tracheal intubation: a new clarification with a review oE the literature." Anesth Analg 1924; 53:202-13. 2 Keating J: Anesthetic accidents. 2nd ed. Chicago: Year Book Medical Publishers,l961:105. 3 Comroe JH: The Lung: clinical physiology and pulmonary
function tests. 2nd ed. Chicago: Year Book Medical Publishers, 1962. 4 Stalcup SA, .~llins RB: Mechanical forces producing pulmOnarY 8dema fn acute asthma. Engl J Med lf117; 2f11:592-6 5 Moss G, Stanton C, Stein AA: The centrineurogenic etiology of acute respiratory distress syndrome. Am J Surg 1973; 126:39-41.
American Medical Research Expedition to Everest Two treks to the expedition base camp of Mt. Everest are being arranged especially for physicians with an interest in high altitude medicine and physiology. The treks last 25 days and are scheduled for September, 1981. They will be led by Drs. Charles Houston and Gil Roberts. Further details about the treks may be obtained &om Mountain Travel, 1398 Solano Avenue, Albany, California 94706.
19th Annual Seminar, lmageology 1981 The Department of Radiology, Mount Sinai Medical Center, Miami Beach, will present the 19th Annual Seminar, January 25-30 at the Sheraton Bal Harbor Hotel, Miami Beach. Dr. Manuel Viamonte, Jr. is the program director. For further information, contact Ms. Lucy R. Kelley, c/o Miami Seminars, PO Box 343762, Coral Gables, Florida 33134.
Basic Echocardiography The Division of Diagnostic Ultrasound of Thomas Jefferson University Hospital,
will present a course on Basic Echocardiography, February 2-6. Dr. Barry B. Goldberg
is the course director. For information, please contact Ms. Kathy Bonner, Education Secretary, Division of Diagnostic Ultrasound, 1015 Walnut Street, Philadelphia 19107.
CHEST, 78: 6, DECEMBER, 1980
WYNGOSPu.INDUCU PUUIOURY DEliA 121
Laryngospasm developed in a 33-year-old womao folowlog attempted endotracheal intuiJatioL Followinl establislunent of the airway, the patient developed palmonary edema which was SDCCellfnlly treated by conveatlonal
means. The .eqaeace of events..._... Chat JarnaCIIIpMIII predplblted the deftlopment .. the ............,. edenla in this patient.
The etiologies of pulmonary edema are myriad. Acute upper airway obstruction is rarely mentioned, however, among the possible precipitating causes. this potential complication must be recognized and treated promptly to minimize delayed morbidity and mortality among survivors of acute upper airway obstruction. We report a case of laryngospasm complicated by the development of pulmonary edema and comment on the pathophysiologic consequence of acute upper airway obstruction leading to this complication.
Immediately, the patient developed apparent laryngospasm, and attempts to administer positive pressure oxygen by facial maslc were met with marked resistance to airflow. No breath sounds were present on physical eumiDation, and the patient became increasingly cyanotic. She was immediately treated with intravenous aminophylline and epinephrine; within three minutes, she could again be ventilated by maslc, at which time arterial blood gas levels revealed Po2, 56 mm Hg; Pco2 , 91 mm Hg; pH, 7.10; and Hco3, 28 mEq/L. Several minutes later, while receiving supplemental oxygen at 8 L/min via mask, repeat arterial blood gas levels showed Po2, 161 mm Hg; Pco2, 72 mm Hg; pH, 7 .32; and Hco3, 35 mEq/L (patient received 44 mEq sodium bicarbonate intravenously). Blood pressure was continuously monitored during the episode, and no hypotension was noted. The patient remained alert and awake during the event without apparent emesis or aspiration. Immediately following the clearing of her airway, auscultation revealed normal breath sounds. During the ensuing 20 minutes, the patient became increasingly dyspneic with the development of diffuse rales and wheezes without stridor. Cardiac eumiDation revealed a sinus tachycardia without murmur or S3 gallop, a pulsus paradoxus of 40 mm Hg, and ECG demonstrated a supraventricular tachy-
A 33-year-old multiparous Mexican-American woman was admitted at full term with spontaneous rupture of membranes on March 21, 1979. She bad received prenatal care without neurologic symptoms, enjoyed a normal weight gain, normal blood pressure readings, and showed no proteinuria on urinalysis. Her admission examination revealed blood pressure of 130/100 mm Hg supine and 130178 mm Hg lying on her left side, pitting pedal edema, and an otherwise normal physical examination results. A dipstick urinalysis was positive for protein; however, two repeat urinalyses showed no protein. Blood chemistry samples drawn two days postpartum showed the foJlowing values: albumin, 3.1 gm/100 ml; blood urea nitrogen, 7 mg/100 ml; and creatinine, 0.8 mg/100 ml. She was treated with magnesium sulfate in conventional doses for 24 hours during which time she had a normal vaginal delivery of a healthy male infant Her immediate postpartum course was uneventful. On the second postpartum day, the patient was scheduled for an elective bilateral tubal ligation and received the following intramuscular premedications; atropine, 0.4 mg; meperidine, 50 mg; and hydroxyzine, 25 mg. Ninety minutes later, endotracheal intubation was attempted after induction of anesthesia with 250 mg of thiopental sodium and 100 mg of succinylcholine, preceded by 3 mg of curare, all administered intravenously. Due to the patient's unusual body habits (obesity, short neck), the vocal cords could not be visualized, and two blind attempts at intubation were unsuccessful. •From the Departments of Medicine and Anesthesiology, Maricopa County General Hospital, Phoenix. tMedical Resident, Department of Medicine. :tAssociate Chief of Pulmonary Medicine. §Chairman, Department of Anesthesia; Professor Emeritus, University of Alabama. Manuscript received October 1; revision accepted January 31.
CHEST, 78: 6, DECEMBER, 1980
F'lcUBE 1. Portable anteroposterior chest roentgenogram demonstrates diffuse, bilateral alveolar infiltration.
LARYNGOSPASM-INDUCED PULMONARY OEMA 811
F'ICUIIE 2. Portable anteroposterior roentgenogram two days later shows clearing of alveolar illfiltration. cardia without acute ST-T changes. Approximately one hour after laryngospasm, a portable anteroposterior chest roentgenogram (Fig 1 ) demonstrated diffuse, bilateral alveolar infiltration. Repeat arterial blood gas levels revealed Po2 , 68 mm Hg; Pco2 , 33 mm Hg; pH, 7.41; and Hco3 , 26 mEq/L (8 L/min via nasal prongs). Continuous positive airway pressure (CPAP=5) em H 20 was administered via facial mask, and corticosteroids, as well as diuretics, were given intravenously. She responded well to this therapy voiding 3 Lin 36 hours, for a combined postpartum diuresis of 5 L. On the day following the acute obstructive episode, the CPAP was discontinued. A portable anteroposterior chest roentgenogram obtained two days later showed clearing of the alveolar illfiltration (Fig 2) . Arterial blood gas levels at this time were Po2 , f¥1 mm Hg; Pco, 27 mm Hg; pH, 7.50; and Hco8 , 22 mEq/L (room air). By March 26, lf¥19, the patient was asymptomatic with clear lungs on physical examination. She was discharged home and had no recurrent problems during six months of follow-up. DISCUSSION
Our patient was a previously healthy postpartum woman, who developed severe laryngospasm during attempted endotracheal intubation. Though she was treated for presumed preeclampsia, the criteria for this were not totally satisfied. A review of prenatal records did not demonstrate an abrupt weight change, prenatal and postpartum blood pressure readings were not significantly different, there were no neurologic signs or symptoms, repeat urinalyses showed no proteinuria, and blood chemistry samples showed normal renal function. Laryngospasm is a well-recognized complication of laryngeal intubation occurring in experimental animals as well as humans. This occurs via laryngeal reftexes which may cause spasm of the glottis and bronchi.1 Resolution of upper airway obstruction in our patient was followed by the development of
820 JACKSON, ROWLAND, CORSSEN
pulmonary edema. The temporal sequence strongly suggests a causal relationship between the acute obstructive episode and the subsequent onset of pulmonary edema. Although this complication of laryngospasm is recognized by anesthesiologists, 2 we found no prior case reported in the literature. The natural course of acute upper airway obstruction is death, occurring within minutes, as a consequence of profound hypoxia. Even when an airway is promptly established, survival may be jeopardized by the development of pulmonary edema. Comroe3 lists four basic causes of pulmonary edema as follows : increased pulmonary edema-increased pulmonary capillary pressure, decreased plasma colloidal osmotic pressure, increased pulmonary capillary permeability, and decreased intrathoracic pressure. Pulmonary edema occurring in connection with acute upper airway obstruction is primarily the result of decreased intrathoracic pressure, a pathogenetic mechanism which bas received relatively little emphasis in the literature. Decreased intrathoracic pressure in upper airway obstruction is generated by attempted inspiration against a closed glottis. The result is a mean negative transpulmonary pressure, which favors transudation of 8uid from the pulmonary capillaries into the interstitial space. Negative intrapleural pressure generated by an external source, as in rapid evacuation of pneumothorax or pleural effusion, may also be complicated by the development of pulmonary edema. Recently, studies of pulmonary mechanics during acute asthmatic attacks have also revealed large negative pressures during inspiration.4 It has been suggested that over-vigorous 8uid therapy may lead to increased lung water in this situation. Acute hypoxia, which developed in our patient, may have been an additional factor contributing to the development of pulmonary edema. Moss et al5 have produced noncardiogenic pulmonary edema in experimental animals solely by cerebral perfusion with hypoxic blood. A postulated mechanism is altered hypothalamic function leading to autonomically-mediated pulmonary vascular constriction, capillary hypertension, and interstitial edema formation. Our patient's prompt response to treatment, including CPAP, supplemental oxygen, diuretics, and steroids, was gratifying. Considering the potentially serious consequences of untreated pulmonary edema, patients who recover from acute upper airway obstruction should be closely monitored for the development of this complication. The primary pathogenetic mechanism for pulmonary edema in this situation is believed to be decreased intrathoracic pressure. CHEST, 78: 6, DECEMBER, 1980
I Blanc VF, Tremblay NAG: The complications o( tracheal intubation: a new clarification with a review oE the literature." Anesth Analg 1924; 53:202-13. 2 Keating J: Anesthetic accidents. 2nd ed. Chicago: Year Book Medical Publishers,l961:105. 3 Comroe JH: The Lung: clinical physiology and pulmonary
function tests. 2nd ed. Chicago: Year Book Medical Publishers, 1962. 4 Stalcup SA, .~llins RB: Mechanical forces producing pulmOnarY 8dema fn acute asthma. Engl J Med lf117; 2f11:592-6 5 Moss G, Stanton C, Stein AA: The centrineurogenic etiology of acute respiratory distress syndrome. Am J Surg 1973; 126:39-41.
American Medical Research Expedition to Everest Two treks to the expedition base camp of Mt. Everest are being arranged especially for physicians with an interest in high altitude medicine and physiology. The treks last 25 days and are scheduled for September, 1981. They will be led by Drs. Charles Houston and Gil Roberts. Further details about the treks may be obtained &om Mountain Travel, 1398 Solano Avenue, Albany, California 94706.
19th Annual Seminar, lmageology 1981 The Department of Radiology, Mount Sinai Medical Center, Miami Beach, will present the 19th Annual Seminar, January 25-30 at the Sheraton Bal Harbor Hotel, Miami Beach. Dr. Manuel Viamonte, Jr. is the program director. For further information, contact Ms. Lucy R. Kelley, c/o Miami Seminars, PO Box 343762, Coral Gables, Florida 33134.
Basic Echocardiography The Division of Diagnostic Ultrasound of Thomas Jefferson University Hospital,
will present a course on Basic Echocardiography, February 2-6. Dr. Barry B. Goldberg
is the course director. For information, please contact Ms. Kathy Bonner, Education Secretary, Division of Diagnostic Ultrasound, 1015 Walnut Street, Philadelphia 19107.
CHEST, 78: 6, DECEMBER, 1980
WYNGOSPu.INDUCU PUUIOURY DEliA 121