Subcutaneous and mediastinal emphysema. Pathophysiology, diagnosis, and management.

Subcutaneous emphysema and pneumomediastinum occur frequently in critically ill patients in association with blunt or penetrating trauma, soft-tissue infections, or any condition that creates a gradient between intra-alveolar and perivascular interstitial pressures. A continuum of fascial planes connects cervical soft tissues with the medlastinum and retroperitoneum, permitting aberrant air arising in any one of these areas to spread elsewhere. Diagnosis is made in the appropriate clinical setting by careful physical examination and inspection of the chest roentgenogram. While the presence of air in subcutaneous or mediastinal tissue is not dangerous in itself, prompt recognition of the underlying cause is essential. Certain trauma-related causes may require surgical intervention, but the routine use of chest tubes tracheostomy, or mediastinal drains is not recommended.

Multiple plasmacytomas with thoracic and biliary involvement.

The course of a patient who had nonsecretory multiple myeloma was characterized by extraosseous plasmacytomas that were initially limited to pleural lesions with effusion and subcutaneous masses. Subsequently, we noted the development of obstructive jaundice caused by a mass at the head of the pancreas, which was diagnosed by abdominal ultrasound and responded to radiation therapy, and bilateral pulmonary nodules, which were visualized by fiberoptic bronchoscopy. Forceps biopsy of an endobronchial lesion showed plasmacytoma similar in histologic features to her original osseous lesions. The pulmonary nodules responded to cyclophosphamide and prednisone. During her course, she had three forms of intrathoracic myeloma: rib lesions extending into pulmonary tissue, pleural disease, and multiple endobronchial masses. The biliary and pulmonary manifestations of plasmacytomas are rarely seen. Diagnosis by noninvasive procedures and rapid response to conservative therapy were important in this patient's care.

Decreased hypoxic ventilatory drive in the obesity-hypoventilation syndrome.

Most patients with extreme obesity do not exhibit alveolar hypoventilation, but an intriguing minority do. The mechanism(s) of this phenomenon remain unknown. A disorder in ventilatory control has been suggested as a major factor in the pathogenesis of the obesity-hypoventilation syndrome. Accordingly, hypoxic and hypercapnic ventilatory drives were measured in 10 patients with the typical symptoms of the syndrome: obesity, hypersomnolence, hypercapnia, hypoxemia, polycythemia and cor pulmonale. Hypoxic ventilatory drive, measured as the shape parameter A, averaged 21.9 +/- 5.35, approximately one-sixth that in normal controls, A = 126 +/- 8.6 (P less than 0.01). The ventilatory response to hypercapnia also was markedly reduced, the slope of the response averaging 0.51 +/- 0.005, or about one-third the normal value of 1.83 +/- 0.13 (P less than 0.01). This decreased responsiveness in hypoxic and hypercapnic ventilatory drive was consistent throughout the group. The depression in ventilatory drive found in the obesity-hypoventilation syndrome may be causally related to the alveolar hypoventilation manifested by these patients.

Legionnaires' disease. Clinical and pulmonary histopathologic features of a sporadic case.

The pulmonary histopathologic features in a sporadic case of Legionnaires' disease are shown. The changes include acute bronchitis with focal ulceration and diffuse acute interstitial pneumonitis. These changes are not those seen with typical bacterial pneumonia but are similar to changes seen when viruses, rickettsiae, chlamydiae, or Mycoplasma pneumoniae organisms are the infecting agents.

Cardiac asystole during an hypoxic drive study in a normal subject.

A healthy 31-year-old man who had previously sojourned to an altitude of 5,000 meters with no detrimental effect developed sudden cardiac asystole during a progressive hypoxic ventilatory response ( HVR ) test. At the moment of asystole, his alveolar PO2 (PAO2) was 41 mm Hg and his arterial oxygen saturation (SaO2) was 81 percent. Cardiopulmonary resuscitation was initiated, and after 20 seconds of asystole and apnea, he recovered normal sinus rhythm and spontaneous respiration. A subsequent ECG and cardiac enzyme levels were normal. During testing, he demonstrated depressed ventilation in response to hypoxia and a slowing of the heart rate. Careful observation of heart rate and breath-by-breath ventilation during HVR tests may predict this potentially fatal complication.

Severe precocious emphysema in intravenous methylphenidate (Ritalin) abusers.

Intravenous (IV) drug abuse is known to cause pulmonary tale granulomatosis. Reports have documented a syndrome of pulmonary vascular sclerosis in long-term IV methylphenidate users. Although this would be expected to produce restrictive lung disease, we hereby report six patients who have severe obstructive lung disease. All had used IV methylphenidate for at least four years. One of these patients died of progressive respiratory insufficiency and the others are clinically disabled. Their symptoms and airflow obstruction are more severe than those of most patients with chronic obstructive pulmonary disease. In these individuals, we cannot say that precocious obstructive lung disease is not due to a combination of smoking and other factors, nor can we be certain that methylphenidate is the offending agent. However, this cluster of cases among methylphenidate abusers suggests that long-term IV exposure to this drug might lead to early severe obstructive lung disease.

A comparison of spirometric values with subjects in standing and sitting positions.

Spirograms obtained from 235 subjects in standing and sitting positions revealed small differences for the forced vital capacity (FVC) and forced expiratory volume in one second (FEV1). No statistically significant differences were found for the mean forced expiratory flow during the middle half of the FVC (FEF25-75%, or maximal midexpiratory flow) and FEV1/FVC. Sitting values were, on the average, higher for determinations greater than FVC of 2.14 L, FEV1 of 1.68 L, FEF25-75% of 2.16 L/sec, and FEV1/FVC of 75.7 percent. On the average, subjects with less than these values performed slightly better in the standing position.

Carbon dioxide excretion via bronchopleural fistulas in adult respiratory distress syndrome.

Expired gas and gas leaked via thoracostomy tubes was collected in nine patients with the adult respiratory distress syndrome (ARDS) and bronchopleural fistulas. Mean minute ventilation in the group was 23.9 +/- 7.5 L/min with 31 +/- 23 percent of the gas escaping via the leak. Carbon dioxide was present in the leaked gas in every patient, with the fraction of CO2 excreted via the leak highly correlated with the fraction of minute ventilation exiting via the leak (r = 0.86, p less than 0.005). Mean concentration of CO2 in leaked gas was 1.3 +/- 0.5 percent. We conclude that some of the gas leaked via a bronchopleural fistula in such patients participated in gas exchange.

Persistent bronchopleural air leak during mechanical ventilation. A review of 39 cases.

Bronchopleural fistula (BPF), or bronchopleural air leak, is regarded as an ominous complication of ventilator management in acute respiratory failure, but data on its natural course and prognosis are lacking. We reviewed all instances of mechanical ventilation at a major trauma center during a four-year period, and found that 39 of the 1,700 mechanically-ventilated patients developed BPF lasting at least 24 hrs. Overall mortality in these 39 patients was 67 percent, and this was higher when BPF developed late in the illness (16 of 17, or 94 percent, when mean onset was hospital day 13), than when it occurred within 24 hours of admission (ten of 22, or 45 percent, p = 0.002). Survival in patients with chest trauma (12 of 27, 44 percent), most of whom had air leaks on or just after admission, was better than in those with other primary diagnoses (one of 12, 8 percent, p less than 0.005). All eight patients whose maximum air leak exceeded 500 ml per breath died, whereas 13 of 30 with smaller maximum leaks survived (p less than 0.05). Despite leaks as large as 900 ml per breath, however, conventional ventilator adjustments permitted avoidance of severe respiratory acidosis (pH less than 7.30) in all but two patients. We conclude that the occurrence of BPF during mechanical ventilation identifies patients with high mortality, but that unmanageable respiratory acidosis from this complication is rare.

Prediction of successful ventilator weaning using airway occlusion pressure and hypercapnic challenge.

We studied eleven patients during 14 attempts at weaning from mechanical ventilation to determine whether central ventilatory drive, measured as airway occlusion pressure 0.1 s after onset of inspiration (P 0.1), during spontaneous breathing before and during a brief hypercapnic challenge, could accurately predict the success or failure of the attempt. All patients were recovering from acute respiratory failure and could breathe spontaneously for 20 minutes on a T-piece but were judged clinically to be marginal weaning candidates. Minute ventilation (VI) and P 0.1 were measured while breathing spontaneously and were repeated during a hypercapnic challenge that raised end-tidal PCO2 approximately 10 mm Hg. Seven of the 14 weaning attempts were unsuccessful, requiring reinstitution of mechanical ventilation. Although the failure group had lower mean maximum inspiratory force and higher spontaneous respiratory rate, no threshold value separated the failure from the success group. Ventilation increased more during hypercapnic challenge in those patients whose weaning attempt was successful, but overlap of results between the two groups rendered this test inaccurate for predicting weaning success. In contrast, successfully weaned patients had greater augmentation of P 0.1 during hypercapnia, expressed as the ratio of P 0.1 during CO2-stimulated to P 0.1 during baseline values, than did those who failed weaning (p less than 0.005). This ratio succeeded, and was thus both specific and sensitive as a predictor of successful weaning from mechanical ventilation in these patients.

Total lung capacity. An insensitive measure of impairment in patients with asbestosis and chronic obstructive pulmonary disease?

The total lung capacity (TLC) is frequently used as a measure of respiratory impairment in patients with asbestosis. Because asbestosis and chronic obstructive pulmonary disease (COPD) exert opposite effects on the TLC, it may be an insensitive measure of impairment in patients with both abnormalities. To assess this, we compared asbestos-exposed patients with functional evidence of COPD and radiographic evidence of interstitial fibrosis (group 1) to those with interstitial fibrosis alone (group 2). Despite the two groups being comparable in degree of radiographic "fibrosis," no case of restrictive impairment (reduced TLC) was identified among those with both interstitial fibrosis and COPD (group 1), compared to 33 percent of those with interstitial fibrosis alone (group 2). In addition, those patients with both interstitial fibrosis and COPD, compared to those with interstitial fibrosis alone, were found to have greater impairment as measured by alveolar-arterial oxygen difference and diffusing capacity. We conclude that the TLC is an insensitive measure of impairment due to asbestosis in patients with the common setting of coexistent asbestosis and COPD.

Prolonged respiratory paralysis in wound botulism.

Two patients had wound botulism with longer duration of respiratory paralysis than previously described. Each sustained extensive trauma to soft tissues and grossly contaminated wounds when thrown from a vehicle in a rural area. Progressive muscular weakness and respiratory distress occurred 8 and 13 days after injury, in the presence of infected wounds and clinical and laboratory findings characteristic of botulism. Spontaneous vital capacity and inspiratory effort served as bedside indicators of ventilatory function throughout 11 weeks of ventilatory support in each case and paralleled other clinical assessments of progress and recovery. Wound botulism may result in neuromuscular paralysis for a prolonged period. These cases illustrate the primary role of scrupulous nursing and respiratory care throughout such a period of ventilatory insufficiency.

Variability of arterial blood gas values in stable patients in the ICU.

To establish guidelines for the interpretation of changes in arterial blood gas (ABG) values, we studied 29 clinically stable ICU patients for spontaneous variability in PaO2, PaCO2 and pH. ABGs were sampled six times over a 50-minute period, during which all patients received a fixed FIO2 of 0.5 via endotracheal tube and underwent no therapeutic interventions. Each sample was analyzed in duplicate with careful attention to method of collection and measurement. The range separating the lowest and highest PaO2 varied from 1 to 45 mm Hg (16.2 +/- 10.9 mm Hg [mean +/- SD] ). For PaCO2 this range was from 1 to 8 mm Hg (3.0 +/- 1.9 mm Hg). Coefficient of variation for PaO2 and PaCO2 averaged 5.1 +/- 3.2 percent (mean +/- SD) and 3.0 +/- 1.5 percent respectively. pH varied within 0.03 +/- 0.02 units. Percentage change in PaO2 between sequential intrapatient samples averaged 5.3 +/- 2.8 percent (mean +/- SD) and 7.1 +/- 7.9 percent over ten- and 50-minute intervals, respectively. Various clinical features were analyzed by multiple regression analysis for their relation to PaO2 variation. Only leukocyte count and mean arterial oxygen content were statistically significant associations (p less than 0.05), but together explained less than 35 percent of the variation observed. Because considerable spontaneous variation occurs, even in stable patients, clinicians should base therapeutic decisions on trends in PaO2 values rather than on isolated changes interpreted without appropriate clinical correlation.

Prospective evaluation of amiodarone pulmonary toxicity.

Reports of pulmonary infiltrates in patients taking amiodarone, initiated the study of 69 patients for pulmonary toxicity using serial chest roentgenograms (CXRs), pulmonary function tests (PFTs), and symptoms before and during therapy. Mean PFTs did not significantly change from their baseline normal values, but 10 percent of patients had a greater than or equal to 15 percent fall in total lung capacity, and 28 percent a greater than or equal to 15 percent fall in diffusion capacity (DCO) following treatment. Initial abnormalities in pulmonary function or CXR were predictive of risk of developing pulmonary toxicity. Degree of exposure to amiodarone (dose plus duration) correlated only weakly with development of pulmonary toxicity, which could occur in patients taking relatively small doses of the drug. Pulmonary complications of amiodarone are common, in most cases reversible, and often confused with congestive heart failure or pneumonia. Patients should be evaluated before treatment by assessing symptoms, CXRs, and DCO. Patients with initial abnormalities in these parameters, particularly both CXR and DCO abnormalities, should be considered for alternative therapy.

Influence of body size and gender on control of ventilation.

Hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses are influenced by both metabolic activity and hormonal factors. By studying 67 subjects of both sexes, including those at the extremes of stature, we examined the influence of gender, CO2 production (VCO2), O2 consumption (VO2), body surface area (BSA), and vital capacity (VC) on resting ventilation (VE), HVR, and HCVR. We measured resting VE, VO2, and VCO2 and then performed isocapnic progressive hypoxic and hypercapnic ventilatory responses. The effect of stature was reflected in higher VE and metabolic rate (both P less than 0.001) in tall men compared with short men that was ablated by correction for BSA. Perhaps because their heights vary less than those of the men, tall women were not statistically distinguishable from short women in any of these measured parameters. Tall men tended to have greater hypoxic chemosensitivity than short men but this was not significantly different (P = 0.07). Gender affected the control of ventilation in a number of ways. Men had higher VE (P less than 0.05) and metabolic rate (P less than 0.001) than women. Even after correction for BSA men still had higher metabolic rates. Women had higher VE/VCO2 than men (P less than 0.05) and lower resting end-tidal Pco2 (PETCO2) values (P less than 0.05). Both A, the shape parameter of the hyperbolic HVR curve, and HVR determined from mouth occlusion pressure (AP) were greater in women than in men, although only AP reached statistical significance. However, corrections of A for BSA (P less than 0.05), VCO2 (P less than 0.01), and VC (P less than 0.001) amplified these differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Monitoring hemodynamics in the critically ill.

Intelligent, safe patient management based on hemodynamic monitoring requires that the right measurements be made, that the data so generated be accurate, and that the clinician's judgment and understanding of their use be appropriate. This article discusses the catheterization of systemic and pulmonary arteries, with an emphasis on the purposes to be served by monitoring rather than on specific measurements, techniques, or devices.

Pneumothorax and barotrauma.

This article discusses pneumothorax and barotrauma from the viewpoints of both the intensivist/pulmonologist and the emergency room physician because both groups of clinicians frequently encounter these potentially life-threatening conditions. The discussion focuses primarily on pneumothorax and barotrauma as they occur in adults rather than in neonates and children.

Complications of mechanical ventilation. A bedside approach.

Instead of cataloging complications reported to occur during mechanical ventilation, the authors have discussed the potential causes for several common scenarios in the management of ventilated patients. These include the new development of hypotension, acute respiratory distress (fighting the ventilator), repeated sounding of the ventilator's high-pressure alarm, hypoxemia, blood from the endotracheal tube, and the problem of diagnosing VAP. In the course of considering likely explanations for this group of circumstances for which the clinician is consulted or called to the bedside, virtually all reported ventilator-associated complications must be discussed. This new approach to an important aspect of ICU care may aid in clinical problem-solving and reduce the likelihood that a diagnosis will be missed or inappropriate measures taken in the absence of a systematic, pathophysiology-based approach.

Effects of pulmonary function of oral high frequency oscillation in normal and asthmatic subjects.

High frequency jet devices are not only used as 'internal percussors' to aid clearance of pulmonary secretions, but are also a mode of ventilatory support. As physical stimuli can cause bronchospasm in asthmatic individuals, we hypothesized that direct airway vibration may induce bronchospasm. To ascertain whether an airway vibration jet device could cause bronchoconstriction, we exposed eight asthmatic and six normal subjects to 5 min of jet-induced airway vibration or placebo treatment with cross-over at 3 h. Subjects breathed spontaneously for 5 min through an open mouthpiece into which either jet (10 Hz, 25 psi) or sham pulsations (same device, pressure vented to room at compressor) were delivered in a double-blind, random order. A constant-volume body plethysmography measured functional residual capacity and specific airway conductance (SGAW) and a water seal spirometer measured forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC). These pulmonary function measurements were taken before and at 5, 10, 20, 30, 60, 90 and 120 min after each exposure. In the normal subjects there was no significant change in any pulmonary function. There was not statistically significant change in the pulmonary function in the asthmatic patients. However, the oral high frequency oscillator induced a clinical asthmatic attack in one asthmatic patient. In this one patient, the FEV1 fell 35% from its initial value at 5 min following exposure to a maximum of 49% decline from initial value at 1 h following exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Complications associated with mechanical ventilation.

A constellation of adverse effects and complications may be associated with mechanical ventilation, although in many instances the causal role of the ventilator itself has not been established. Complications occur with greater frequency than is generally appreciated, and tend to be under-reported in the medical literature. Among the potential adverse physiologic effects of positive-pressure ventilation are decreased cardiac output, unintended respiratory alkalosis, increased intracranial pressure, gastric distension, and impairment of hepatic and renal function. Failure of the ventilator to cycle, of safety alarms to function properly, and of inspired gas to be properly heated or humidified are examples of equipment-related complications. Perhaps most feared among medical complications occurring during mechanical ventilation are pneumothorax, bronchopleural fistula, and the development of nosocomial pneumonia; these entities may owe as much to the impairment of host defenses and normal tissue integrity as to the presence of the ventilator per se. Finally, a variety of avoidable "misadventures," due primarily to lapses of understanding and communication among the physicians, nurses, and respiratory care practitioners managing the ventilated patient, can adversely affect comfort, morbidity, and ultimate outcome.