Laryngospasm is a serious event that can result in partial or complete upper airway obstruction. It is a common complication during recovery phase of anaesthesia, resulting from acute irritation of the vocal folds. We report a rare case of laryngospasm secondary to a multinodular goitre that settled after treatment. We postulate that the enlarged thyroid gland can lead to direct irritation of the laryngeal nerve as possible cause of repeated episodes of laryngospasm in this patient. To our knowledge, this is the first reported case of a multinodular goitre as the underlying cause of laryngospasm.
Airway Obstruction ; Laryngismus ; Goitre, Nodular

Pulmonary edema that follows upper airway obstruction may occur in a variety of clinical situations. Post anesthetic laryngospasm has been implicated as the most frequent cause of this syndrome. Risk factors for development of post laryngospasm pulmonary edema include difficult intubation; nasal, oral, or pharyngeal surgical site; and obesity with obstructive apnea. We report a case that developed acute bilateral pulmonary edema after laryngospasm induced by failed intubation.
Airway Obstruction ; Apnea ; Intubation* ; Laryngismus ; Obesity ; Pulmonary Edema* ; Risk Factors

BACKGROUND: Because desflurane can cause airway irritability when used to induce anesthesia, drugs aimed at reducing airway irritability. This study investigated the possible differences between lidocaine and alfentanil on the decrease in the airway irritability during desflurane inhaled induction. METHODS: 75 patients (25 in each groups) were assigned randomly to induce anesthesia with inhaled desflurane. The breathing circuit was primed with desflurane 6% in 50% O2 and 50% N2O. After pretreatment with 2% lidocaine (1 mg/kg), or alfentanil (10microgram/kg), or saline (7 ml) intravenously 2 minutes before inducing anesthesia, each patient breathed the gas mixture through a tight fitting facemask. The time to loss of consciousness, cough, laryngospasm, excitatory movement and hemodynamics were checked before and after inhalation. RESULTS: The time to loss of consciousness, cough and excitatory movement were lower significantly between in the control group and other groups, but there was no difference between the 2% lidocaine and alfentanil groups. The blood pressure and heart rate were lower in the alfentanil group, but the heart rate was similar. CONCLUSIONS: These results explain that intravenous 2% lidocaine appears to be useful. However, Intravenous alfentanil can also reduce the airway irritability and stabilize the hemodynamics significantly when desflurane is used to induce anesthesia.
Alfentanil* ; Anesthesia ; Blood Pressure ; Cough ; Heart Rate ; Hemodynamics* ; Humans ; Inhalation ; Laryngismus ; Lidocaine* ; Respiration ; Unconsciousness

BACKGROUND: This study was performed to compare responses to the insertion of an intubating laryngeal mask airway (ILMA) and to the intubation of an endotracheal tube according to insertion time when used with sevoflurane and without muscle relaxant. METHODS: We used 50% N2O-O2-8% sevoflurane and a 10% topical lidocaine spray. Forty-eight patients were randomized into four groups according to insertion time (each, n = 12). The ILMA was inserted at 3, 4, 5, and 6 minutes after sevoflurane induction and intubation was performed at 1 minute after ILMA insertion. Responses to intubation, such as vital signs, jaw relaxation, coughing, biting, movements, and laryngospasm were compared according to ILMA insertion time. RESULTS: At 3 minutes, overall responses to insertion and intubation were worse than at 4, 5, and 6 minutes (P < 0.05). At 4, 5, and 6 minutes, responses to the insertion of the ILMA and the intubation of endotracheal tube were satisfactory. CONCLUSIONS: Insertion of ILMA at 4 minutes after sevoflurane induction proved satisfactory, and this could be applied in clinical practice.
Cough ; Humans ; Intubation ; Intubation, Intratracheal* ; Jaw ; Laryngeal Masks* ; Laryngismus ; Lidocaine ; Relaxation ; Vital Signs

There are many predisposing factors for acute pulmonary edema, Pulmonary edema in well recognized complication of acute airway obstruction, especially in small children, but rarely seen in adults. We present a case of noncardiogenic pulmonary edema that developed in adult following removal of endotracheal intubation after esophagoscopy, The sequence of events suggest that laryngospasm precipitated the development of the pulmonary edema in this patient.
Adult ; Airway Obstruction ; Causality ; Child ; Esophagoscopy* ; Humans ; Intubation, Intratracheal ; Laryngismus ; Pulmonary Edema*

BACKGROUND: Because desflurane can cause airway reactivity, the use of opioids are aimed at its reduction. This study was designed to evaluate the effect of continuous remifentanil infusion on the airway reactivity during desflurane inhalation. METHODS: 108 adult ASA physical status class I patients were enrolled in this study. The patients were divided into four groups.The breathing circuit was primed with 8 vol% desflurane in 3 L/min each of N2O and O2. Anesthesia was induced with 0.2 mg/kg of intravenous etomidate. After 2 minutes, either 20 ml/hr saline, or 0.15, 0.25 or 0.35g/kg/min remifentanil, groups S, R1, R2 and R3, respectively, was infused. Each patient inhaled the gas mixture through a tight fitting facemask. During this period, the coughing, secretions, breathing hold, laryngospasms, excitatory movements and hemodynamics were measured. RESULTS: The coughing, spasms, secretions and excitatory movements were significantly lower in the remifentanil than the saline infusion group (P 0.05). However, the breathing hold was significantly higher in group R3 (P 0.001). The mean arterial pressure and heart rate were more stable in groups R1 and R2. CONCLUSIONS: These results demonstrate that groups R1 and R2 had significantly reduced airway reactivity, with stabilize hemodynamics, during desflurane inhalation.
Adult ; Analgesics, Opioid ; Anesthesia ; Arterial Pressure ; Cough ; Etomidate ; Heart Rate ; Hemodynamics ; Humans ; Inhalation* ; Laryngismus ; Respiration ; Spasm

Pulmonary Edema is a complication of acute upper airway obstruction secondary to laryngospasm. This serious complication is treated promptly to minimize the delayed morbidity and mortality among the patients. Acute pulmonary edema followed the event in minutes to hours and required ventilatory assistance to maintain oxygenation. All patients eventually respond to fluid restriction diuretics and steroids. We present a case of pulmonary edema that occured in a 37 years old healthy adult after extubation caused by a laryngospasm.
Adult ; Airway Obstruction ; Diuretics ; Edema ; Humans ; Laryngismus ; Larynx ; Lung ; Mortality ; Oxygen ; Pulmonary Edema* ; Spasm ; Steroids

The etiology of pulmonary edema are myriad. Pulmonary edema is a complication of acute upper airway obstruction secondary to laryngospasm. When pulmonay edema occurs, it usually follows relief of the obstruction. Acute pulmonary edema must be treated promptly among the patients who recover from acute upper airway obstruction. The treatments are fluid restriction, diuretics, steroids, ventilatory assistance to maintain oxygenation. Ventilatory assistance is important and has various methods, but we chosed intrapulmonary percussive ventilation (IPV). It is of benefit to adequate oxygenation without ventilatory induced lung linjury (VILI), easy removal of secretion, intratracheal nebulization with bronchodilator, and patient's comfortness. We present a case of noncardiogenic pulmonary edema that occured in an adult patient following extubation of the trachea caused by a laryngospasm.
Adult ; Airway Obstruction* ; Diuretics ; Edema ; Humans ; Laryngismus ; Lung ; Oxygen ; Pulmonary Edema* ; Steroids ; Trachea ; Ventilation*

Acute pulmonary edema associated with intense laryngospasm during or after anesthesia seems to be a rare complication. Although emergency reestablishment of the airway may avert fatal hypoxia, subsequent morbidity may follow from the delayed effects of the obstruction. We recently observed a 16-year-old, 5kg boy, with inguinal hernia who developed laryngospasm and pulmonary edema following a herniorrhaphy and he had no evidence of cardiac enlargement or cardiovascular disease.
Adolescent ; Anesthesia ; Anoxia ; Cardiovascular Diseases ; Emergencies ; Hernia, Inguinal ; Herniorrhaphy ; Humans ; Laryngismus* ; Male ; Pulmonary Edema*

The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm. Although the reaction is not IgE-mediated, patients can also present with anaphylactic hypersensitivity reactions, including hypotension, after exposure to COX-1 inhibiting drugs. All patients with AERD have underlying nasal polyps and intractable sinus disease which may be difficult to treat with standard medical and surgical interventions. This review article focuses on the management of AERD patients with a particular emphasis on aspirin desensitization and continuous treatment with aspirin.
Aspirin ; Asthma ; Bronchial Spasm ; Cyclooxygenase 1 ; Humans ; Hypersensitivity ; Hypotension ; Laryngismus ; Nasal Polyps