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John T Huggins

Publications and source records attributed to John T Huggins.

10 recordsLinked to original sources
PubMed2007

Characteristics of trapped lung: pleural fluid analysis, manometry, and air-contrast chest CT.

STUDY OBJECTIVES: To review the pleural fluid characteristics, pleural manometry, and radiographic data of patients who received a diagnosis of trapped lung in our pleural diseases service. DESIGN: Retrospective case series. METHODS: The procedure records of 247 consecutive patients who underwent pleural manometry at the Medical University of South Carolina between October 2002 and November 2005 were reviewed. Eleven patients in whom a diagnostic pneumothorax was introduced were identified. Manometry data, radiographic findings, pleural fluid analysis, final clinical diagnosis, and information regarding the initial pleural insult were retrieved from the medical record. RESULTS: All 11 patients had a clinical diagnosis of trapped lung. The causes of trapped lung were attributed to coronary artery bypass graft surgery, uremia, thoracic radiation, pericardiotomy, spontaneous bacterial pleuritis and repeated thoracentesis, and complicated parapneumonic effusion. Mean pleural fluid pH was 7.30, pleural fluid lactate dehydrogenase (LDH) was 124 IU/L, and pleural fluid total protein was 2.9 g/dL. Pleural fluid was paucicellular with mononuclear cell predominance. Pleural space elastance was increased in all cases and ranged from 19 to 149 cm H(2)O/L of pleural fluid removed. All demonstrated abnormal visceral pleural thickness on air-contrast chest CT. CONCLUSIONS: Trapped lung is a clinical entity characterized by the presence of a restrictive visceral pleural peel that was first described in 1967. The pleural fluid is paucicellular, LDH is low, and protein may be in the exudative range. The elevated total pleural fluid protein may be related to factors other than active pleural inflammation or malignancy and does not exclude the diagnosis.

Clinical Protocols↗
PubMed2006

Pleural manometry.

The goals of therapeutic thoracentesis are to remove the maximum amount of pleural fluid to improve dyspnea and to facilitate the diagnostic evaluation of large pleural effusions. Pleural manometry may be useful for immediately detecting an unexpandable lung, which may coexist when any pleural fluid accumulates. Pleural manometry may improve patient safety when removing large amounts of pleural fluid. The basics of pleural space mechanics are discussed as they apply to the normal pleural space and to pleural effusion associated with expandable and unexpandable lung. This article also discusses the instrumentation required to perform bedside manometry, how manometry may decrease the risk of re-expansion pulmonary edema when large amounts of fluid are removed, and the diagnostic capabilities of manometry.

Animals↗
PubMed2006

Pleural effusions in a series of 181 outpatients with sarcoidosis.

OBJECTIVES: Pleural effusion (PE) is considered to be a rare manifestation of pulmonary sarcoidosis. We performed thoracic ultrasonography prospectively in consecutive outpatients with sarcoidosis to determine the frequency of PEs caused by sarcoidosis and to define their pleural fluid characteristics. DESIGN: Consecutive outpatients aged >/= 18 years with biopsy-proven sarcoidosis underwent ultrasonography. SETTING: University hospital, outpatient sarcoidosis clinic. RESULTS: One hundred eighty-one outpatients were enrolled into the study. The subjects were predominately African-American and female. Most were between 30 and 60 years of age. The Scadding radiograph stages were fairly evenly distributed across all five stages (0 through 4). Five (2.8%) of 181 patients were found to have pleural fluid. Two patients had a unilateral left-sided PE, and three patients had bilateral PEs. Pleural fluid analysis (PFA) was performed in four patients. The PFA showed a lymphocyte-predominant exudate using protein criterion in only two patients, which is consistent with sarcoidosis-related PE; one patient underwent pleural biopsy, which was consistent with the diagnosis of sarcoidosis. A sarcoidosis-related PE was seen in 1 of 9 patients (11.1%) who had an exacerbation of pulmonary sarcoidosis compared to 1 of 172 patients (0.6%) who did not have an exacerbation (p < 0.4). CONCLUSION: PEs are rare in outpatients with sarcoidosis, even when a sensitive technique, such as ultrasonography, is used. The frequency of PEs was 2.8% (5 of 181 patients) with only 2 of the 181 PEs (1.1%) caused by sarcoid pleural involvement. PE in patients with sarcoidosis should not be assumed to be related to sarcoidosis. Discordance between levels of pleural fluid total protein and lactate dehydrogenase may be a characteristic finding in patients with sarcoid PE. An exacerbation of pulmonary sarcoidosis was not an independent risk factor for the development of sarcoid-related PE.

Adult↗
PubMed2006

Pathophysiology of pneumothorax following ultrasound-guided thoracentesis.

STUDY OBJECTIVES: Pneumothorax following ultrasound-guided thoracentesis is rare. Our goal was to explain the mechanisms of pneumothorax following ultrasound-guided thoracentesis in a setting where pleural manometry is routinely used. METHODS: We reviewed the patient records and procedure reports of 401 patients who underwent ultrasound-guided thoracentesis. When manometry was performed, pleural space elastance was determined. A model assuming dependence of the pleural space elastic properties on respiratory system elastic properties was used to isolate cases with presumed normal pleural space elastance. Elastance outside mean +/- SD x 2 of the isolated sample was considered abnormal. Four radiographic criteria of unexpandable lung were used: visceral pleural peel, lobar atelectasis, basilar pneumothorax, and pneumothorax with ipsilateral shift. RESULTS: There were 102 diagnostic thoracenteses, 192 therapeutic thoracenteses with pleural manometry, and 73 therapeutic thoracenteses without manometry. There was one pneumothorax that occurred from lung puncture and eight unintentional pneumothoraces, all of which showed radiographic evidence of unexpandable lung. Four of eight unintentional pneumothoraces had abnormal elastance; none had excessively negative pleural pressure (< -25 cm H(2)O). CONCLUSIONS: Unintentional pneumothoraces cannot be prevented by monitoring for symptoms or excessively negative pressure. These pneumothoraces were drainage related rather than due to penetrating lung trauma or external air introduction. We speculate that unintentional pneumothoraces are caused by transient, parenchymal-pleural fistulae caused by nonuniform stress distribution over the visceral pleura that develop during large-volume drainage if the lung cannot conform to the shape of the thoracic cavity in some patients with unexpandable lung. These fistulae appear to be pressure dependent, and the resulting pneumothoraces rarely require treatment. Drainage-related pneumothorax is an unavoidable complication of ultrasound-guided thoracentesis and appears to account for the vast majority of pneumothoraces occurring in a procedure service.

Biomechanical Phenomena↗
PubMed2004

Drug-induced pleural disease.

Drug-induced pleural disease is uncommon and less known to clinicians than drug-induced parenchymal lung disease. Pleural reactions from drugs manifest as pleural effusions, pleural thickening, or pleuritic chest pain, and may occur in the absence of parenchymal infiltrates. The clinician should be cognizant of the possibility of a drug-induced pleural reaction. A detailed drug history, temporal relationship between symptom onset and initiation of therapy, and pleural fluid eosinophilia should raise the suspicion of a drug-related process. We suspect that as new drugs are marketed in the United States, the number of drugs that result in pleuropulmonary toxicity will continue to increase. Moreover, if the cause of an exudative pleural effusion is not clinically obvious after pleural fluid analysis, drug therapy withdrawal should be a consideration if clinically appropriate before initiating an extensive diagnostic evaluation that may entail unnecessary economic burden and discomfort for the patient.

Anti-Infective Agents, Urinary↗
PubMed2004

Eucalyptus as a specific irritant causing vocal cord dysfunction.

BACKGROUND: Vocal cord dysfunction (VCD) is a well-recognized clinical entity that frequently mimics asthma and is characterized by inappropriate adduction of the vocal cords during inspiration. The pathogenesis of VCD has not yet been defined. The only previous report suggested that respiratory irritants may trigger paradoxical motion of the vocal cords. OBJECTIVE: To report the case of a 46-year-old woman with VCD precipitated by eucalyptus exposure. METHODS: A masked flexible fiberoptic nasolaryngoscopy was performed to confirm whether VCD occurred with eucalyptus and not with other known respiratory irritants. The patient underwent inhalation challenges consisting of water, ammonia, pine oil, and a combination of eucalyptus (dried leaves) and ammonia. Two independent observers before patient challenge could not identify eucalyptus. RESULTS: Vocal cord dysfunction occurred within minutes of exposure to eucalyptus. This is the first report to prospectively document that a specific irritant, eucalyptus, can precipitate VCD. Negative skin prick test results, total IgE level, and negative IgE eucalyptus-specific antibodies support a nonimmunologic mechanism. CONCLUSIONS: A new pathogenic mechanism for this clinical entity is supported by our observations. Furthermore, a nonimmunologic mechanism in which respiratory irritants may induce VCD is suspected. Future studies to elucidate this mechanism need to be performed in individuals with irritant-specific VCD.

Alveolitis, Extrinsic Allergic↗
PubMed2004

Causes and management of pleural fibrosis.

The development of pleural fibrosis follows severe pleural space inflammation which is typically associated with an exudative pleural effusion. The response of the mesothelial cell to injury and its ability, along with the basement membrane, to maintain its integrity, is vital in determining whether there is normal healing or pleural fibrosis. The formation of a fibrinous intrapleural matrix is critical to the development of pleural fibrosis. This matrix is the result of disordered fibrin turnover, whereby fibrin formation is up-regulated and fibrin dissolution is down-regulated. Cytokines, such as TGF-beta and TNF-alpha, facilitate the fibrin matrix formation. A complete understanding of the pathogenesis of pleural fibrosis and why abnormal pleural space remodeling occurs in some and not in others, remains unknown. Clinically significant pleural fibrosis requires involvement of the visceral pleura. Isolated parietal pleural fibrosis, as with asbestos pleural plaques, does not cause restriction or respiratory impairment. The causes of visceral pleural fibrosis include asbestos-associated diffuse pleural thickening, coronary bypass graft surgery, pleural infection (including tuberculous pleurisy), drug-induced pleuritis, rheumatoid pleurisy, uraemic pleurisy, and haemothorax. Systemic and intrapleural corticosteroids administered during the initial presentation of rheumatoid pleurisy in small series may decrease the incidence of pleural fibrosis. Several randomised control trials using corticosteroids in tuberculous pleurisy have not shown efficacy in reducing residual pleural fibrosis. Decortication is effective in treating symptomatic patients regardless of the cause of pleural fibrosis as long as chronicity has been documented and significant underlying parenchymal disease has been excluded.

Asbestosis↗
PubMed2004

Pleural manometry: technique and clinical implications.

INTRODUCTION: Pleural manometry during large-volume thoracentesis can prevent the development of excessively negative pleural pressures, which have been associated with re-expansion pulmonary edema; can diagnose an unexpandable lung; and can predict pleurodesis success. We currently perform pleural manometry simultaneously with both a vertical-column water manometer with an interposed resistive element, and a hemodynamic transducer connected to a standard physiologic system. We present the technique as well as the advantages and disadvantages of both systems in measuring pleural liquid pressures. TECHNIQUE: A flexible thoracentesis catheter is inserted in the most dependent portion of the pleural effusion. The water manometer consists of two lengths of IV tubing connected through a 22-gauge needle inserted into an injection terminal. The system is connected to the zeroing port of the pressure transducer, and both are carefully purged of air. The electronic system is zeroed at the level the thoracentesis catheter is introduced into the patient. Measurements are performed initially and after each 250 mL of fluid that is withdrawn. ACCURACY OF THE WATER MANOMETER: Forty consecutive patients who underwent therapeutic thoracentesis had pressure measurements. Pleural fluid removed ranged from 50 to 4,200 mL (mean, 1,445 mL). A total of 291 pressure measurements were acquired and analyzed. Mean pleural liquid pressure obtained by the water manometer had a strong positive correlation with the values obtained by a standard physiologic system (r = 0.97, p < 0.001). CONCLUSION: An overdamped water manometer is a valid method to measure mean pleural liquid pressure. Coughing invalidates pressure measurements with the water manometer; however, with the electronic method, periods of quiet breathing can be identified, allowing for the measurement of pleural pressure.

Adult↗
PubMedDate not supplied

Duro-pleural fistula diagnosed by beta2-transferrin.

An 81-year-old man was referred for evaluation of a chronic transudative pleural effusion that required 8 therapeutic thoracenteses over 11 months for relief of dyspnea. Extensive lumbar disk surgery had been performed 2 years prior to his onset of dyspnea. The diagnosis of duro-pleural fistula was confirmed by finding the presence of beta2-transferrin in the pleural fluid. The 'water-like' pleural fluid had a total protein of <1 gm/dl, an LDH of 92 IU/l, a glucose of 101 mg/dl, and pH of 7.55. beta2-Transferrin has a sensitivity approaching 100% and a specificity of 95% in identifying CSF leaks from head trauma. To our knowledge, this is the first report of beta2-transferrin in pleural fluid from a duro-pleural fistula.

Aged↗