Pulmonary hemorrhage in association with negative pressure edema in an intubated patient

Negative pressure pulmonary edema due to upper airway obstruction following extubation is a well-recognized problem. However, frank pulmonary hemorrhage as a manifestation of upper airway obstruction is uncommon. We report a case of significant pulmonary hemorrhage and negative pressure pulmonary edema in an intubated patient. Bronchoscopy showed a collection of blood in the right lower lobe of the lungs, suggesting a localized source of bleeding. There have been two previously reported cases of pulmonary hemorrhage after upper airway obstruction. One suggested that the bleeding was due to damage to the pulmonary capillaries, the other that it was due to disruption of the bronchial vessels. We feel that in our case there was some indication that the pulmonary bleeding was a result of bronchial vessel damage. A number of factors might have been involved in its development, including negative pulmonary pressure, recent respiratory tract infection, and positive airways pressure (due to coughing).     

Negative-pressure pulmonary edema presented with concomitant spontaneous pneumomediastinum: Moore meets Macklin

Negative-pressure pulmonary edema is an unusual complication mainly associated with general anesthesia. It is caused by excessive negative intrathoracic pressure following a deep inspiration against an acute airway obstruction. The resultant decreased intrathoracic pressure amplifies venous return to the right heart and increases pulmonary capillary wedge pressure that can be further amplified by massive sympathetic discharge due to hypoxia. The combination of increased venous return and pulmonary capillary wedge pressure favours the shift of fluid into the pulmonary interstitium with resultant pulmonary edema. Conversely, spontaneous pneumomediastinum (SP) results from alveolar rupture following an excessive positive intrathoracic pressure. The air leaks out of the alveoli and along the perivascular space toward the mediastinum. We experienced a case of negative pulmonary edema which presented in association with SP. Pneumomediastinum is probably caused by an excessive positive intrathoracic pressure for a subsequent expiration against a closed airway. In the present case, both complications resolved with conservative management.     

Acute pulmonary capillary leak syndrome during elective surgery under general anesthesia

A 75-year-old previously healthy man presented for elective resection of rectal cancer under general anesthesia. Six days before the operation, he had a high-grade fever, and elevated leukocyte count and C-reactive protein concentration, but this was resolved by an intravenous antibiotic. His condition was well controlled before the operation. Soon after the operation started, severe hypoxemia emerged, with low arterial pressure. Fiberoptic bronchoscopy demonstrated a massive amount of plasma-like edema fluid; the total amount of suctioned fluid was approximately 800 ml at the end of the surgery. This acute pulmonary edema appeared to be due to increased permeability rather than pulmonary congestion as indicated by chest radiography, pulmonary artery occlusion pressure, echocardiogram, and the protein-rich edema fluid. Elevated concentrations of the proinflammatory cytokines, interleukin (IL)-6 and IL-8, in both plasma and the pulmonary edema fluid, suggested a possible role of systemic and pulmonary inflammation in the development of this acute pulmonary capillary leak. According to the “two-hit” hypothesis, the bacterial infection preceding the operation may have primed the immune cells, and the following surgical stress may have then triggered rapid progression of acute respiratory distress syndrome. We should keep in mind that, especially following sepsis, sudden massive pulmonary capillary leak can occur during elective surgery, even though the patient’s condition is well controlled.     

Stress failure of the blood-gas barrier

The blood-gas barrier must be extremely thin because oxygen and carbon dioxide cross the alveolar-capillary membrane by passive diffusion, and the diffusion resistance is proportional to thickness. Despite its remarkable size (harmonic mean thickness approximately 0.6 microm) the membrane must be immensely strong, because maintenance of its integrity is fundamental for pulmonary gas exchange. The basement membrane is probably the principal anatomical structure providing the strength of the blood-gas barrier. Experimental studies have demonstrated that wall stress of the capillaries can become very high when perfusion pressure is increased to 5.2 kPa (39 mmHg) or more, which was associated with breaks of the capillary endothelium, the alveolar epithelium, or both. These values are potentially reached or exceeded in different cardiac or pulmonary diseases, or in healthy humans subjected to heavy exercise. Stress failure of pulmonary capillaries may play a role in neurogenic pulmonary oedema, high-altitude pulmonary oedema, re-expansion pulmonary oedema, and some forms of the adult respiratory distress syndrome. Increased alveolar pressure due to lung inflation potentiates damage of the blood-gas barrier, suggesting that increases in capillary transmural pressure and transpulmonary pressure are equivalent in terms of their effects on capillary wall stress. These data may have importance for the management of patients with acute respiratory failure requiring mechanical ventilation.     

Malignant hypertension with a rare complication of pulmonary alveolar hemorrhage

A 34-year-old Japanese male was admitted to Okayama University Hospital with severe hypertension, rapidly progressive renal failure, blurred vision, dyspnea and hemoptysis. Clinical diagnosis of malignant hypertension was given and antihypertensive therapy and hemodialysis were immediately started. Renal biopsy was performed on the sixth day in hospital to examine the underlying disease, such as microscopic form of polyarteritis, since the complaint of hemoptysis and pulmonary alveolar hemorrhage was noted by computed tomography of the lungs. Typical pathological changes of malignant hypertension, i.e. fibrinoid necrosis of the afferent arterioles and proliferative endoarteritis at the interlobular arteries were observed. There was no evidence of active necrotizing glomerulonephritis and crescent formation. Renal function was gradually recovered and pulmonary hemorrhage completely disappeared by treatment with antihypertensive agents. The authors report a case of malignant hypertension with a rare complication of pulmonary alveolar hemorrhage and speculate that it may be related to vascular injuries at the alveolar capillary level caused by malignant hypertension.     

Pathophysiology of pulmonary edema following experimental brain death in the chacma baboon

Systemic and pulmonary hemodynamics have been studied during the induction of brain death in the chacma baboon. In 11 animals brain death was induced by acute intracranial hypertension. Continuous recording of blood flow through both the pulmonary artery and the aorta was obtained by electromagnetic flow meters placed around these vessels. Mean arterial, central venous, pulmonary arterial, and left atrial pressures were recorded continuously. Systemic and pulmonary vascular resistances were calculated. During the agonal period marked sympathetic activity occurred, with significant increases in circulating catecholamines and systemic vascular resistance. The great increase in systemic resistance resulted in acute left ventricular failure. Mean left atrial or pulmonary capillary wedge pressure rose above the mean pulmonary arterial pressure in 9 animals. As the systemic vascular resistance rose, a significant difference between pulmonary artery and aortic blood flows occurred, leading to blood pooling within the lungs. A mean of 72% of the total blood volume of the animal accumulated within these organs. The increase of left atrial pressure to levels higher than pulmonary artery pressure indicated a state of pulmonary capillary blood flow arrest. This, associated with the blood pooling within the lungs, almost certainly resulted in disruption of the anatomic integrity of the pulmonary capillaries (blast injury); 4 animals developed pulmonary edema, with alveolar septal interstitial hemorrhage.     

Emergency pneumonectomy for penetrating and blunt trauma

Emergency pneumonectomy for penetrating and blunt trauma has an attendant high mortality. Patients with major lung injuries presenting with prolonged shock followed by control of bleeding, resuscitation with or without aortic cross-clamping and pneumonectomy have had uniformly unsatisfactory results. From 1972 to 1982, eight patients at the University of Louisville Hospital underwent emergency pneumonectomy. All patients underwent expeditious evaluation, resuscitation, and thoracotomy with pneumonectomy. Three patients died of exsanguination (2 patients had major associated intra-abdominal injuries). Three other patients died due to pulmonary edema and right ventricular failure 2 to 3 hours after hemorrhage had been controlled and intravascular volume restored. Aortic cross-clamping was employed in four patients due to persistent hypovolemia with 100 per cent mortality. Of the two surviving patients, one presented with stable blood pressure and had pneumonectomy for tracheobronchial disruption, while the other had pneumonectomy for tangential laceration of the lung at the hilum. Pulmonary edema and right ventricular failure were responsible for mortality following emergency pneumonectomy and control of hemorrhage and restoration of blood volume. The addition of aortic cross-clamping did not seem to alter survival and may, indeed, hinder therapy due to increased vascular afterload and increased heart failure and pulmonary edema.     

Acute renal failure due to over-infusion in a child with bilateral obstruction of the pyeloureteral junction]

A 2-year-old boy was hospitalized with the chief complaint of oliguria and dyspnea. Bilateral hydronephrosis and obstruction of the pyeloureteral junction were detected by ultrasonography. Pulmonary edema was also found on chest radiographs. The clinical diagnosis was acute post renal failure due to bilateral pyeloureteral obstruction and pulmonary edema due to overtransfusion. After we performed bilateral percutaneous nephrostomy, the patient recovered from renal failure and pulmonary edema. Both nephrostomies were removed after we confirmed a non-obstructing pattern using the Whitaker test.     

Delayed presentation: negative pressure pulmonary hemorrhage

Negative pressure pulmonary hemorrhage (NPPH) is a rare, life-threatening complication that develops after an acute upper airway obstruction. A 26 year old, healthy African-American man with no underlying lung disease developed negative pressure pulmonary edema and subsequently NPPH during recovery from general anesthesia for elective spine surgery. Diagnostic bronchoscopy confirmed an alveolar source of the bleeding. Clinical improvement was quick with supportive care in the medical intensive care unit.     

Unilateral pulmonary edema following acute subglottic edema

Presented here is a case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A 3-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was later found to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.     

A thromboxane analog increases pulmonary capillary pressure but not permeability in the perfused rabbit lung

Thromboxane has been implicated as a mediator of pulmonary hypertension and pulmonary edema in acute respiratory failure. Pulmonary edema may result from increased pulmonary capillary hydrostatic pressure or from increased pulmonary vascular permeability. We therefore studied the effects of a stable thromboxane analog, U46619, on these two parameters in the perfused rabbit lung. Pulmonary capillary pressure was measured by the double vascular occlusion method, and pulmonary vascular permeability was estimated by measurement of the pulmonary fluid filtration coefficient (Kf). U46619 infusion produced pulmonary hypertension and lung weight gain; increased both the arterial (precapillary) and venous (postcapillary) components of pulmonary vascular resistance; and increased pulmonary capillary pressure from 4.7 +/- 0.5 to 9.0 +/- 0.7 mmHg (P less than 0.01). The isogravimetric pressure (equivalent to the capillary pressure corresponding to no lung weight gain) was 4.0 +/- 0.4 mmHg before U46619 and 4.6 +/- 0.4 mmHg during U46619. Therefore, U46619 significantly increased capillary pressure above isogravimetric pressure and resulted in the development of pulmonary edema. U46619 did not affect vascular permeability as measured by Kf. We conclude that pulmonary venoconstriction resulting in increased pulmonary capillary hydrostatic pressure is the major mechanism by which thromboxane produces pulmonary edema in isolated lungs.     

Lungs: blood supply,lymphatic drainage and nerve supply

The pulmonary arteries, through their capillary plexus, are entirely concerned with alveolar gaseous exchange, while the nutrient supply of the lung parenchyma is provided by the bronchial arteries. The pulmonary vein tributaries derive partly from the capillaries of the bronchial and the pulmonary arteries. The bronchial veins drain the larger bronchi. The lymphatics of the lungs drain into the nodes lying at the bifurcations of the larger bronchi, then to the tracheobronchial nodes and then into the bronchomediastinal lymph trunk on each side. These usually drain directly into the junction of the internal jugular and subclavian veins on each side, but may drain, on the right, into the right lymph trunk and, on the left, into the thoracic duct. If the subcarinal node is the site of secondary deposits it gives the typical bronchoscopic sign of widening of the carina. The principal function of the sympathetic (T2-4) supply to the lung is bronchodilatation, while the vagus fibres act as stretch receptors.     

Biting the laryngeal mask: an unusual cause of negative pressure pulmonary edema

PURPOSE: To describe negative pressure pulmonary edema due to biting of the laryngeal mask tube at emergence from general anesthesia. CLINICAL FEATURES: A healthy patient underwent general anesthesia using a laryngeal mask airway and mechanical ventilation. During recovery, the patient strongly bit the laryngeal mask and made very forceful inspiratory efforts until the mask was removed. Five minutes later, the patient developed dyspnea and had an hemoptysis of 50 ml fresh blood. Chest radiograph showed bilateral alveolar infiltrates. Pharyngo-laryngeal examination was normal. Bronchoscopy revealed no injury but diffuse pink frothy edema fluid. Clinical examination and chest radiograph became normal after 12 hr of nasal oxygen therapy confirming airway obstruction as the most available cause of this pulmonary edema. CONCLUSION: Airway obstruction due to biting of a laryngeal mask tube may result in negative pressure pulmonary edema.     

Pulmonary manifestations of the clinical syndrome of acute glomerulonephritis and lung hemorrhage

The pulmonary manifestations at the time of initial diagnosis were reviewed in 45 patients with the clinical syndrome of acute glomerulonephritis and lung hemorrhage. Initial pulmonary radiographic appearances encompassed a wide variety of abnormalities, and alveolar hemorrhage could not be reliably differentiated from other causes of pulmonary infiltration. The diseases underlying the syndrome included antiglomerular basement membrane (anti-GBM) disease (8/45), a systemic vasculitis (25/45), and idiopathic glomerulonephritis with idiopathic lung hemorrhage (12/45). A variety of acute pulmonary complications were seen, the most common being acute respiratory failure (13/45). Mortality directly due to pulmonary disease was uncommon (3/45 died from fulminant lung hemorrhage). Most deaths were from extrapulmonary manifestations of the underlying disease or infection. Follow-up studies in 22 patients 6 months after initial presentation indicated that although respiratory symptoms (3/22) or pulmonary radiologic abnormalities (5/22) were uncommon, the majority of patients had residual abnormalities on pulmonary function testing (16/22). Thus, the syndrome of alveolar hemorrhage with nephritis is associated with several distinct categories of underlying disease process. The initial chest radiograph is of limited value in differential diagnosis. Although a variety of acute and chronic respiratory complications may be anticipated and contribute significantly to morbidity, mortality is predominantly due to extrapulmonary progression of disease or infection complicating immunosuppressive therapy.     

Intermediate results with correction of tetralogy of Fallot with absent pulmonary valve using a new approach.

OBJECTIVE: The intermediate results achieved with a new technique for primary repair of tetralogy of Fallot with absent pulmonary valve syndrome are reported. METHOD: Apart from correction of tetralogy of Fallot, this approach includes translocation of the pulmonary artery anterior to the aorta and away from the tracheobronchial tree. Since November 1998 this technique has been employed in three symptomatic newborns and three infants with a diagnosis of tetralogy of Fallot with absent pulmonary valve. The median age at surgery was 37 days (range 14-256 days). The median weight at operation was 3.4 kg (range 2.9-4 kg). All patients had severe respiratory problems and congestive heart failure with cyanosis. RESULTS: There was no early or late death during the follow-up (median 27 months). One patient required redo due to failure to thrive as a consequence of right ventricle volume overload. Valved conduit was inserted to pulmonary position. Respiratory symptoms disappeared or were significantly reduced in all patients. Postoperative computed tomographic scan showed no compression of trachea and main bronchi, pulmonary artery was away from tracheobronchial tree in all patients. Patients are doing well with adequate growth. CONCLUSIONS: The new technique described here has a potential to reduce or eliminate bronchial compression by pulmonary artery. Translocation of pulmonary artery anterior to the aorta takes the dilated pulmonary artery away from the trachea and bronchial tree. This approach was found to be technically feasible and can be useful especially in symptomatic newborns and infants.     

The morphology of smoke inhalation injury in sheep

Pulmonary injury resulting from inhalation of chemical and particulate products of incomplete combustion is one of the principal determinants of mortality following burn injury. In this study, the histopathology of inhalation injury was examined in sheep. Mild, moderate, or severe smoke injury was produced in anesthetized sheep by insufflation with various doses of ambient temperature smoke, generated by burning polyethylene, wood pulp, and nonwoven cellulose pads. A total of 64 sheep were exposed and evaluated at times ranging from 15 minutes to 4 weeks after exposure. Morphologic changes in the lungs were studied using light microscopy and both transmission and scanning electron microscopy. The primary, dose-responsive injury observed was acute cell membrane damage in the trachea and bronchi leading to edema, progressive necrotic tracheobronchitis with pseudomembrane formation, and airway obstruction. These inflammatory and occlusive effects were followed by congestion, alveolar space edema, atelectasis, and bronchopneumonia. Morphologic changes occurring in the alveolar epithelium following high smoke dosage included intracellular edema in type-I cells, changes in the membrane-bound vacuoles of type-II cells, and septal thickening caused by interstitial edema. No capillary endothelial changes were observed.     

Prevention of pulmonary insufficiency through prophylactic use of PEEP and rapid respiratory rates.

This study evaluated the effectiveness of prophylactic positive end-expiratory pressure (PEEP) rapid respiratory rates (RRR), and high tidal volume (HTV) in prevention of congestive atelectasis. Measurements of pulmonary hemodynamics, mechanics, gas exchange, functional residual capacity (FRC), pathology, and cinemicroscopy were performed in 45 anesthetized dogs subjected to hemorrhagic hypotension. Randomly, the animals received control ventilation, HTV (20 ml. per kilogram), RRR (32 breaths per minute), or PEEP (5 cm. of water). Carbon dioxide was added as needed to maintain normocapnia. Control and HTV animals showed characteristic changes of congestive atelectasis (capillary congestion, stasis, interstitial edema, periarterial hemorrhage, alveolar edema, and hemorrhage). These microscopic and cinemicroscopic changes were prevented by PEEP and RRR and correlated with decreased physiological shunting (PEEP 10 percent, RRR 13 percent, HTV 22 percent; p less than 0.01) in the postshock phase. PEEP increased FRC by 40 percent (p less than 0.02) and reduced the pulmonary artery--small pulmonary vein gradient (PA-SPV), suggesting a direct effect on the capillary bed. RRR did not affect FRC but minimized the SPV-LA gradient. This effect on the pulmonary venules theoretically could be mediated by stimulating lymphatic flow, thereby decreasing interstitial edema. Thus PEEP and RRR are beneficial when used prophylactically but may work by widely differing mechanisms.     

Negative-pressure pulmonary edema (NPPE)

Negative-pressure pulmonary edema (NPPE) is a clinical entity of anaesthesiologic relevance, perioperatively caused by obstruction of the conductive airways (upper airway obstruction, UAO) due to laryngospasm in approx. 50% of the cases, its early recognition and treatment by the anaesthesist is mandatory. NPPE, also addressed as post-obstructive pulmonary edema (POPE) presents in most cases as a complex of symptoms with rapid onset, consisting of acute respiratory failure with dyspnea, tachypnea, and strained respiratory efforts. Additional signs are paradoxe ventilation, pink frothy sputum, stridor, and severe agitation. UAO produce extreme reduction of intrathoracic pressure during spontaneous ventilation, consecutively causing increase in venous return to the right ventricle and in intrathoracic blood volume, resulting in elevated hydrostatic pressures and interstitial transudation of fluids. Partially due to largely differing criteria used for diagnosis, opinions about incidence and prevalence of NPPE are unhomogenous in medical literature. It has been shown that generation of NPPE is not only limited to patients being intubated and ventilated, but occurs also in patients requiring higher fractions of oxygen.     

腹腔镜-胆道手术后-急性肺损伤

报道1例56岁男性患者,在全身麻醉下行腹腔镜胆囊切除及胆总管切开取石术,术毕发生急性肺损伤,出现严重低氧血症.后经面罩双水平正压通气(bilevel positive airway pressure,BiPAP)呼吸支持及抗炎治疗3 d康复.患者低氧血症明显但无明显呼吸窘迫、双肺弥漫性浸润明显而听诊除呼吸音较弱外无明显...     

Macroscopic and histological findings in the healing process of inhalation injury

Although many investigators reported the diagnostic and therapeutic value of bronchoscopy in the early stage of inhalation injury, few findings in the late stage of inhalation injury have been reported. We investigated histopathological changes of in trachea and bronchi after inhalation injury. Five survivors with inhalation injury underwent bronchoscopic examinations combined with biopsies from the early stage to the late stage. Although the bronchotracheal membranes improved to near normal under the bronchoscopic findings in the late or recovery stage, invasion of inflammatory cells and the capillary dilatation in the subepithelial region were still remarkable histologically. Goblet cells also increased on the surface of mucous membranes. In cases of the inhalation injury with severe burn, pulmonary edema, bronchial edema and secretions tended to be prolonged. Results suggested that continuous secretions in the respiratory tracts sometimes cause airway obstruction. Bronchoscopic and histologic findings in the healing process of inhalation injury predict long-term pulmonary functional outcome. Moreover, the aggressive pulmonary toilet seemed to be effective in removing foreign particles and accumulated secretions which also cause the inflammatory response and the obstruction in inhalation injury.