Negative Pressure Pulmonary Edema Research Articles

Negative Pressure Pulmonary Edema

Negative Pressure Pulmonary Edema

Negative pressure pulmonary edema following cervical disc hernia surgery

Negative pressure pulmonary edema following cervical disc hernia surgery

Negative pressure pulmonary edema.

Negative pressure pulmonary edema.

Clinical Features of Patients with Diffuse Alveolar Hemorrhage due to Negative-Pressure Pulmonary Edema.

Diffuse alveolar hemorrhage (DAH) with negative-pressure pulmonary edema (NPPE) is an uncommon yet life-threatening condition. We aimed at describing the circumstances, clinical, radiological, and bronchoscopic features, as well as the outcome of patients with NPPE-related DAH. We performed a retrospective, observational cohort study, using data prospectively collected over 35years in an intensive care unit (ICU). Of the 149 patients admitted for DAH, we identified 18 NPPE episodes in 15 patients, one admitted four times for recurrent NPPE-related DAH. The patients were primarily young, male, and athletic. The NPPE setting was postoperative (n=12/18, 67%) or following generalized tonic-clonic seizures (n=6/18, 33%). Hemoptysis was almost constant (n=17/18, 94%), yet rarely massive (>200cc, n=1/18, 6%), with anemia observed in 10 (56%) episodes. The DAH triad (hemoptysis, anemia, and pulmonary infiltrates) was observed in 50% of episodes (n=9/18), and acute respiratory failure in 94% (n=17/18). Chest computed tomography revealed diffuse bilateral ground glass opacities (n=10/10, 100%), while bronchoscopy detected bilateral hemorrhage (n=12/12, 100%) and macroscopically bloody bronchoalveolar lavage, with siderophage absence in most (n=7/8, 88%), indicating acute DAH. While one episode proved fatal, the other 17 recovered rapidly, with a mean ICU stay lasting 4.6 (2-15)days. Typically, the evolution was rapidly favorable under supportive care. NPPE-related DAH is a rare life-threatening condition occurring primarily after tonic-clonic generalized seizure or generalized anesthesia. Clinical circumstances are a key to its diagnosis. Early diagnosis and recognition likely allow for successful management of this potentially serious complication, whereas ictal-DAH appears ominous in epileptic patients.

Negative Pressure Pulmonary Oedema after Sedation in a Patient Undergoing Pacemaker Implantation

Negative pressure pulmonary oedema (NPPE) is a manifestation of upper airway obstruction and is seen after extubation postoperatively. The large negative intrathoracic pressure generated by forced inspiration against an obstructed airway is thought to be the principal mechanism involved. It is a dangerous and potentially fatal condition with a multifactorial pathogenesis. The Authors report a case of negative pressure pulmonary oedema occurring periprocedurally while undergoing permanent pacemaker implantation under local anaesthesia and light sedation due to upper airway obstruction caused by falling back of the tongue. Key words: Negative pressure pulmonary oedema, Sedation, permanent pacemaker implantation, Upper airway obstruction.

Negative Pressure Pulmonary Edema: A Rare Complication Following Extubation

Negative Pressure Pulmonary Edema: A Rare Complication Following Extubation

A Case of 10p-Syndrome That Caused Negative Pressure Pulmonary Edema after Extubation during Dental Treatment under General Anesthesia

A Case of 10p-Syndrome That Caused Negative Pressure Pulmonary Edema after Extubation during Dental Treatment under General Anesthesia

食事中の喉頭異物が原因で発症した陰圧性肺水腫の1症例

食事中の喉頭異物が原因で発症した陰圧性肺水腫の1症例

Postoperative negative pressure pulmonary edema following repetitive laryngospasm even after reversal of neuromuscular blockade by sugammadex: a case report.

Laryngospasm, an occlusion of the glottis, can occur at any time during anesthesia, and is associated with serious perioperative complications such as hypoxia, hypercabia, aspiration, bronchospasm, arrhythmia, prolonged recovery, cardiac collapse, and eventually catastrophic death. Importantly, postoperative negative pressure pulmonary edema (NPPE) is a rare, but well described life-threatening complication related to acute and chronic upper airway obstruction. Sugammadex well known for affirmatively reducing the postoperative pulmonary complications associated with residual neuromuscular blockade may have an indirect role in triggering the negative intrathoracic pressure by raising a rapid and efficacious respiratory muscle strength in acute upper airway obstruction. Herein, we report a case of postoperative NPPE following repetitive laryngospasm even after reversal of rocuronium-induced neuromuscular blockade using sugammadex.

Endoskopik Sinüs Cerrahisi Sonrası Gelişen Negatif Basınçlı Akciğer Ödemi

Endoskopik Sinüs Cerrahisi Sonrası Gelişen Negatif Basınçlı Akciğer Ödemi

Clinical analysis of 9 patients with acute laryngitis and negative pressure pulmonary edema

Objective To investigate the clinical characteristics and treatment of negative pressure pulmonary edema (NPPE) with acute laryngitis in children, and to monitor the change of inflammatory factors. Methods The data of 9 cases with NPPE and acute laryngitis in Pediatric Intensive Care Unit of Xuzhou Children′s Hospital from August 2010 to March 2015 were analyzed.Ten children of acute laryngitis without NPPE in our hospital were selected as the control group.The changes of the TNF-α and IL-6 between the 2 groups were compared before and after treatment . Results (1) All the 9 children in NPPE group were associated with third degree laryngeal obstruction.The onset of NPPE in 8 cases varied from 8 minutes to half an hour following relief of obstruction, and 1 child with NPPE occurred 2 hours after relief of obstruction.Four of the 9 children had pink frothy pulmonary secretions but the other 5 children did not.NPPE chest radiograph showed diffuse interstitial and alveolar infiltrates.All these patients received these therapeutic measures including mechanical ventilation, retaining high positive end expiratory pressure(PEEP)(5-8 cmH2O, 1 cmH2O=0.098 kPa), glucocorticoids, limiting the fluid input volume to 60-80 mL/(kg·d). Three of the 9 cases were treated with diuretics.The disappearance of rales on chest auscultation varied from 6 hours to 30 hours.Duration of mechanical ventilation was less than 48 hours, and all the children were cured.(2) The levels of TNF-α and IL-6 in NPPE group were significantly higher than those in the control group before treatment [(369.16±48.19) ng/L vs (281.77±45.59) ng/L, (30.39±9.60) ng/L vs (20.43±4.80) ng/L, P<0.05]. After 48-hour treatment, the levels of TNF-α and IL-6 in both groups significantly decreased compared with before treatment (all P<0.01); and the levels of TNF-α and IL-6 in NPPE group were (281.10±47.45) ng/L and (20.04±5.87) ng/L, respectively, which were also significantly higher than those in the control group(P<0.05). Conclusions NPPE is manifested by rapid onset of respiratory distress rapidly after relief of the airway obstruction.Imaging suggested edema change. The prognosis will be good if early support of breath and limiting the fluid input volume are applied properly.The inflammatory response is one of the possible mechanisms of NPPE. Key words: Acute laryngitis; Negative pressure pulmonary edema; Child

Clinical analysis of nine children with acute laryngitis complicated with negative pressure pulmonary edema and changes of inflammatory factors

Objective To investigate the clinical characteristics and treatment of children with acute laryngitis complicated with negative pressure pulmonary edema(NPPE), and the changes of inflammatory factors were monitored. Methods Data of 9 cases with acute laryngitis complicated with NPPE in pediatric intensive care unit from August 2010 to March 2015 were analyzed.The levels of TNF-α and IL-6 of 8 cases were detected at admission and checked again forty-eight hours after therapy.Ten children of acute laryngitis without NPPE were selected as disease control group, and ten healthy children as normal control group. Results (1)The onset of NPPE varied from 8 minutes to 2 hours following relief of obstruction, and presented with acute respiratory distress, decreased oxygen saturation, tachycardia, rales on chest auscultation.All these patients received therapeutic measures including mechanical ventilation, limiting the fluid input volume.The disappearance of rales on chest auscultation varied from 6 hours to 30 hours.Duration of mechanical ventilation was less than 48 hours, and all the children were cured.(2)Compared with the children of disease control group and normal control group, in acute phase the plasma levels of TNF-α and IL-6 in children with NPPE were significantly higher(P<0.01). The indicators of NPPE group significantly decreased after 48 hours therapy(P<0.01). Conclusion NPPE is manifested by rapid onset of respiratory distress after relief of the airway obstruction.The symptoms resolve rapidly if early support of breath and limiting the fluid input volume are applied properly.The inflammatory response is one of the possible mechanisms of NPPE. Key words: Acute laryngitis; Negative pressure pulmonary edema; Children

Laringeal maske kullanımı sırasında negatif basınçlı pulmoner ödem: Olgu sunumu

Negative pressure pulmonary edema (NPPE), a non-cardiogenic pulmonary edema, develops due to airway obstruction. Young, healthy, male patients, who have a lot of muscle mass that can lead to produce high negative intra-pleural pressure (athletes pulmonary edema syndrome, APS), are under the risk of developing NPPE. Usually, NPPE develops after extubation in patients who undergo endotracheal intubation however; there are some case reports showing that it can develop after laryngeal mask application (LMA) even in a less manner. The most possible reasons lead to airway obstruction during LMA use are biting of laryngeal mask tube, misplacement of tube, and laryngospasm. This case report presents a patient who undergoes LMA and develops NPPE due to laryngospasm during recovery from anesthesia.

An anesthetic management of negative pressure pulmonary edema

Negative pressure pulmonary edema (NPPE) is one of the common complications of upper airway obstruction seen by anesthesiologist during either in induction or emergence sometimes both. Patients who have experienced NPPE are generally healthy without comorbidities. NPPE is a result of marked decrease in intrathoracic pressure caused by ventilator efforts against a closed glottis resulting in disruption of normal intravascular Starling mechanism, leading to transudation of intravascular protein, and fluids into the pulmonary interstitium. The onset of NPPE is usually rapid and without prompt recognition and intervention, the outcome can be fatal. This case report is of a 40-year-old female adult, who underwent right-sided percutaneous nephrolithotomy for stone in the right kidney otherwise uncomplicated surgical procedure.

Takotsubo cardiomyopathy precipitated by negative pressure pulmonary oedema following total thyroidectomy.

‘Takotsubo cardiomyopathy (TCM)’ or ‘stress cardiomyopathy’ is a reversible cardiomyopathy that is precipitated by intense emotional or physical stress. This syndrome is characterised by symptoms mimicking acute coronary syndrome with transient systolic dysfunction associated with regional wall motion abnormalities, which extend beyond a single coronary vascular bed in the absence of obstructive coronary vascular disease. The presentation of TCM and myocardial infarction is similar with sudden onset of chest pain, breathlessness as well as abnormalities in both the electrocardiogram and cardiac enzymes. It is difficult to differentiate between the two until cardiac catheterisation establishes the diagnosis. We report a case of TCM in a post-menopausal female, precipitated by negative pressure pulmonary oedema following total thyroidectomy in whom timely cardiac catheterisation established the diagnosis and influenced the management. Heightened awareness of this unique cardiomyopathy is essential to have a high index of suspicion in at-risk population for the prompt diagnosis of stress-related cardiomyopathy syndromes occurring in the perioperative period.

Acute Postoperative Negative Pressure Pulmonary Edema as Complication of Acute Airway Obstruction: Case Report

Acute postoperative negative pressure pulmonary edema (NPPE) is a respiratory complication due to acute airway obstruction (UAO) that occurs shortly after extubation of patients who underwent general anesthesia (incidence 0.05 to 0.1% ). Usually, this complication develops in healthy young patients, capable of generating high negative intrathoracic pressures(NIP), which is the catalyst in the pathophysiological cascade of acute pulmonary edema.Commonly presents as acute respiratory distress that requires immediate intervention. We report a case of postoperative NPPE occurred immediately after tracheal extubation in an adult patient, who underwent a minor elective orthopedic surgery under general anesthesia(GA). After extubation, UAO due to laryngospasm was observed and the patient started desaturating rapidely. Application of positive pressure via face mask ventilation (FiO2 100%) was unsuccessful in providing effective ventilation so we decided to reintubate the patient. Soon after reintubation, there were bilateral pulmonary rales and pink frothy secretion inside the tracheal tube, compatible with NPPE. Treatment was rapidly instituted with diuretic, corticosteroid and ventilator support with added PEEP. Pulmonary edema resolved completely near after 8 hours later without any complications in the intensive care unit.

Negative pressure pulmonary oedema: an alarming complication of general anaesthesia in a young healthy male

Negative pressure pulmonary oedema: an alarming complication of general anaesthesia in a young healthy male

食物窒息による陰圧性肺水腫の一例

食物窒息による陰圧性肺水腫の一例

A case of negative pressure pulmonary edema caused by upper airway occlusion due to bilateral recurrent laryngeal nerve paralysis after total thyroidectomy

A case of negative pressure pulmonary edema caused by upper airway occlusion due to bilateral recurrent laryngeal nerve paralysis after total thyroidectomy

Bit‐induced asphyxia in the racehorse as a cause of sudden death

SummaryThe prevention of sudden death requires removal of its cause and this is unknown. The author's hypothesis is that bit‐induced asphyxia, partial or complete, is a cause of sudden death. Antemortem data on bit‐induced asphyxia were compared with post mortem data on sudden deaths to explore a possible cause‐and‐effect relationship. Causal categories from sudden death necropsy data were reclassified. Those causing a horse to fall (cardiopulmonary failures) were considered primary effects and those resulting from a fall (CNS trauma and haemorrhagic shock) secondary effects. Cardiac failure from negative pressure pulmonary oedema caused by bit‐induced obstruction of the nasopharynx was consistent with the hypothesis. In 1988, asphyxia from recurrent laryngeal neuropathy was posited as a cause of exercise‐induced pulmonary haemorrhage (EIPH). It is now suggested that the bit is another cause of asphyxia; EIPH is a sign of negative pressure pulmonary oedema which, in turn, causes cardiac failure and sudden death. By breaking the airtight lip‐seal at exercise, a bit dissipates negative pressure in the oral compartments, destabilises the soft palate and obstructs the nasopharynx. Bitted rein pressure, kinking the airway and rendering parts of it flaccid, is a further cause of asphyxia. The data comparison supports a unifying hypothesis on 4 problems currently considered idiopathic; that the bit is an ultimate cause of palatal instability, dynamic collapse of the upper respiratory tract, EIPH and sudden death. Bitless training and racing trials are recommended as a means of demonstrating that bitless racing is possible, preferable and predicted to reduce the prevalence of all 4 problems.