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Advances in Prospective Payment for Pulmonary Patients
daytime hypercapnia in certain patients with obstructive sleep apnea. 4 The second question: Which pathologic events during sleep apnea affect awake ventilation? Sleep deprivation can decrease the ventilatory drive in normal humans, 10 and severe hypoxemia and hypercapnia during sleep can produce reversible awake hypercapnia in man. 11-12 Therefore, nocturnal hypoxemia, nocturnal hypercapnia, and sleep disturbances all may be important mediators of daytime hypercapnia in patients with sleep apnea. The third question: What mechanisms underlie the effect of apnea and its associated hypoxemia upon central ventilatory control? Preliminary studies suggest that severe hypoxemia during sleep apnea may greatly increase the production of adenosine and other adenosine triphosphate metabolites.":" Since adenosine and its analogues inhibit neuronal transmission," induce hypoventilation in experimental animals,":" and may modulate ventilatory depression during hypoxemia," adenosine may mediate some effects of severe hypoxemia upon the ventilatory control centers of the brain in patients with sleep apnea. Answers to these three clinically important questions may clarify the close but mysterious ties between sleep apnea and the obesity-hypoventilation syndrome. Larry]. Findley, M.D. e harlottescille, Virginia Division of Pulmonary Medicine, Department of Internal Medicine, University of Virginia. Reprint requests: Dr. Findley, University ofVirginia Medical Center, Box 225, Charlottesville22908
REFERENCES 1 Gastaut H, Tassinari, Duron B. Polygraphic study of the episodic diurnal and nocturnal (hypnic and respiratory) manifestations of the Pickwick syndrome. Brain Res 1966; 2:167-86 2 Burwell C, Robin E, Whaley R, Bickelmann A. Extreme obesity associated with alveolar hypoventilation-a Pickwickian syndrome. Am J Med 1956; 21:811-18 3 Tassinari C, Bernardina B, Cirignotta F, Ambrosetto G. Apnoeic periods and the respiratory related arousal patterns during sleep in the Pickwickian syndrome. A polygraphic study. Bull Physiopath. Resp 1972; 8:1087-1102 4 Rapoport D, Garay S, Epstein H, Goldring R. Hypercapnia in the obstructive sleep apnea syndrome; a reevaluation of the Pickwickian syndrome. Chest 1986; 89:627-35 5 Bradley 1: Rutherford R, Lue F: Moldofsky H, Grossman R, Zamel N, et al. Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea. Am Rev Respir Dis 1986; 134:920-24 6 Jones J, Wilhoit S, Findley L, Suratt P Oxyhemoglobin saturation during sleep in subjects with and without the obesityhypoventilation syndrome. Chest 1985; 88:9-15 7 Rochester D, Enson Y. Current concepts in the pathogenesis of the obesity-hypoventilation syndrome. Am J Med 1974; 57:402-20 8 Garay S, Rapoport D, Sorkin B, Epstein H, Feinberg I, Goldring R. Regulation of ventilation in the obstructive sleep apnea syndrome. Am Rev Respir Dis 1981; 124:451-57 9 Zwillich C, Sutton F, Pierson D, Creagh E, Weil J. Decreased
10 11 12 13 14 15
16 17
18
hypoxic ventilatory drive in the obesity-hypoventilation syndrome. Am J Med 1975; 59:343-48 White D, Douglas N, Pickett C, Zwillich C, \Veil J. Sleep deprivation and the control of ventilation. Am Rev Respir Dis 1983; 128:984-86 Garay S, Turino G, Goldring R. Sustained reversal of chronic hypercapnia in patients with alveolar hypoventilation syndromes. Am J Med 1981; 70:269-74 Hoeppner ~ Cockcroft D, Dosman ], Cotton D. Nighttime ventilation improves respiratory failure in secondary kyphoscoliosis. Am Rev Respir Dis 1984; 129:240-43 Findley L, Boykin M, Fallon 1: Belardinelli L. Plasma adenosine is increased in patients with sleep apnea and severe nocturnal hypoxemia. Am Rev Respir Dis 1986; 133:lSOA(abstract) Hasday ], Grum C. Nocturnal increase of urinary uric acid: creatinine ratio-a biochemical correlate of sleep-associated hypoxemia. Am Rev Respir Dis 1987; 135:534-38 Phillis], Wu E Roles of adenosine and adenine nucleotides in the central nervous system. In: Daly J, Kuroda Y, Phillis ], Shimizu H, Vi M, eds. Physiology and pharmacology of adenosine derivatives. New York:Raven Press, 1983:219-36 Eldridge F, Millhorn 0, Kiley J. Antagonism by theophylline of respiratory inhibition induced by adenosine. J Appl Physiol 1985; 59:1428-33 Lagercrantz H, Yamamoto Y, Fredholm B, Prabhakar N, von Euler C. Adenosine analogues depress ventilation in rabbit neonates. Theophylline stimulation of respiration via adenosine receptors. Ped Res 1984; 18:387-90 Millhorn D, Eldridge F, Kiley J, Waldrop L Prolonged inhibition of respiration following acute hypoxia in glomectomized cats. Respir PhysioI1984; 57:331-40
Advances in Prospective Payment for Pulmonary Patients On May 19, 1987, the Health Care Financing Administration (HCFA) published changes to the Diagnosis-Related Group (DRG) classification system proposed for Federal fiscal year 1988. 1 Two new DRGs for ventilator patients were proposed among the changes. One DRG would be for patients who have tracheostomy procedure codes and would be considered a surgical classification. The other DRC would be for nonsurgical patien ts ven tilated through endotracheal tubes. Only patients with a primary diagnosis of respiratory disease would be covered. The relative payment for these new DRGs would be great since the HCFA's analysis of 1985 billing data indicated that for all respiratory patients the average charge for those on ventilators was two to ten times greater than for other patients in the same DRCs. At Rush-Presbyterian-St. Luke's Medical Center we reviewed the annual costs of 446 Medicare patients who received care in our medical intensive care unit and determined they exceeded by over $4.7 million the actual reimbursements for similar patients under the Medicare Prospective Payment System." Each day on a ventilator added $439 for respiratory-related CHEST I 92 I 5 I NOVEMBER, 1987
n3
services to the total hospital costs," Another study we recently completed at RushPresbyterian-St. Luke's Medical Center revealed that 95 Medicare patients seen over a one-year period who required prolonged ventilator care accrued costs of $3,656,137 or $38,486 per patient. This compared to Medicare payments for patients in similar Diagnosis Related Groups of $8,421 per patient. 3 A similar study published simultaneously found that Medicare patients admitted to both tertiary care and community based hospitals found that mean costs per patient were $31,896 (charges $47,391) compared with Medicare payments for similar types of patients of $10,981. 4 HCFA should be congratulated for these proposed changes, but they nevertheless address only some of the financial bias DRGs present for ventilator patients. Of the 95 patients in our study sample, only 33 were covered by the two new DRGs HCFA proposes. The remainder of the patients did not have respiratory principal diagnoses. Cost of care for patients requiring mechanical ventilation without a primary respiratory diagnosis (ie, neurologic decrease) was not less than those with a respiratory diagnosis. The potential for abuse is also great since the payment for ventilator patients receiving a tracheostomy has a much greater reimbursement than those who need prolonged endotracheal intubation. Studies have shown that the complications of a tracheostomy are greater than those of long-term intubations by endotracheal tube." HCFA recognizes the potential for abuse and will monitor this possibility closely. 1 Despite some potential problems, this legislation has important implications for our patients. The potential for patients to be disenfranchised from medical care is less after these changes are enacted. Reimbursement for care in the intensive care unit will also more closely approximate the costs of medical care. The HCFA is to be congratulated for this move. Also, our professional societies have used their legislative influence to lobby to get needed reimbursement to prevent a bias against critical care and for patients cared for in specialized units. The Government Liaison Committee of the American College of Chest Physicians has been particularly vigorous in efforts to acquaint national legislators with current inequality in the reimbursement policies. The official journal of ACC:g Chest, has provided a national forum for data which was of assistance to HCFA as they evaluated current practices.v' These efforts are to be congratulated. Roger C. Bone, M.D., F.C.C.P.
Chicago
Ralph C. Brown Professor and Chairman, Der~tment of In~e~nal Medicine; Chief, Section of Pulmonary and Critical Care Medicine, Rush-Presbyterian-St. Luke's Medical Center. Reprint requests: Dr. Bone, Rush Medical College, 1753 West Congress Parkway, Chicago 60612
REFERENCES 1 Federal Register. 52(No 96):1880-1881, May 19, 1987 2 Butler P\V, Bone RC, Field T. Technology under Medicare diagnosis-related groups prospective payment. Implications for medical intensive care. Chest 1985; 87:229 3 Douglass PS, Rosen RL, Butler PW, Bone RC. DRG payment for chronic ventilator patients: Implications and recommendations. Chest 1987; 91:413-17 4 Gracey 0, Gillespie 0, Nobrega F, Naessens ]M, Krishan I. The financial implications of prolonged ventilator care of medicare patients under the prospective payment system: A multicenter study. Chest 1987; 91:424-27 5 Stauffer ]L, Olson DE, Petty TL. Complications and consequences of endotracheal intubation and tracheostomy-A prospective study of 150 critically ill adult patients. Am ] Med 1981; 70:65-75
The Esophagus The Neglected Chest Organ? he thoracic cavity's organs include the heart, the T lung and the esophagus. The American College of
Chest Physicians (and the journal Chest, as its official publication) are predominated by cardiologists, pulmonologists and cardiothoracic surgeons whose primary orientation is that of either the cardiac or pulmonary subsystems. However, it seems timely to remind "chest" physicians that physiology and pathology of the esophagus are important considerations because of their impact on the other thoracic organs. Coronary angiography in some patients (10 to 15 percent) with chest pain considered typical for angina will rule out important coronary artery disease. Many of these patients can eventually be proved to have esophageal disorders causing their symptoms. In some cases, an esophageal motility disorder is found,':" and on other occasions, gastroesophageal reflux is the culprit. 2 Both these disorders are eminently treatable and it is not acceptable simply to dismiss patients with the information that they do not have coronary artery disease and therefore their chest pain is not important. One follow-up study' showed that pain persists in the majority of these patients and half of them are so incapacitated that they are not able to return to work or their normal life-style. Accordingly, the cardiologist who clears the heart as the cause of chest pain must not stop but must continue the evaluation with a diagnostic evaluation of other organ systems, including the esophagus. It is also quite clear that esophageal disorders can be responsible for pulmonary disease. The patient presenting with evidence of destructive aspiration, in the absence of neurologic impairment or alcohol abuse, probably has reflux disease and should be evaluated for Editorials
REFERENCES 1 Gastaut H, Tassinari, Duron B. Polygraphic study of the episodic diurnal and nocturnal (hypnic and respiratory) manifestations of the Pickwick syndrome. Brain Res 1966; 2:167-86 2 Burwell C, Robin E, Whaley R, Bickelmann A. Extreme obesity associated with alveolar hypoventilation-a Pickwickian syndrome. Am J Med 1956; 21:811-18 3 Tassinari C, Bernardina B, Cirignotta F, Ambrosetto G. Apnoeic periods and the respiratory related arousal patterns during sleep in the Pickwickian syndrome. A polygraphic study. Bull Physiopath. Resp 1972; 8:1087-1102 4 Rapoport D, Garay S, Epstein H, Goldring R. Hypercapnia in the obstructive sleep apnea syndrome; a reevaluation of the Pickwickian syndrome. Chest 1986; 89:627-35 5 Bradley 1: Rutherford R, Lue F: Moldofsky H, Grossman R, Zamel N, et al. Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea. Am Rev Respir Dis 1986; 134:920-24 6 Jones J, Wilhoit S, Findley L, Suratt P Oxyhemoglobin saturation during sleep in subjects with and without the obesityhypoventilation syndrome. Chest 1985; 88:9-15 7 Rochester D, Enson Y. Current concepts in the pathogenesis of the obesity-hypoventilation syndrome. Am J Med 1974; 57:402-20 8 Garay S, Rapoport D, Sorkin B, Epstein H, Feinberg I, Goldring R. Regulation of ventilation in the obstructive sleep apnea syndrome. Am Rev Respir Dis 1981; 124:451-57 9 Zwillich C, Sutton F, Pierson D, Creagh E, Weil J. Decreased
10 11 12 13 14 15
16 17
18
hypoxic ventilatory drive in the obesity-hypoventilation syndrome. Am J Med 1975; 59:343-48 White D, Douglas N, Pickett C, Zwillich C, \Veil J. Sleep deprivation and the control of ventilation. Am Rev Respir Dis 1983; 128:984-86 Garay S, Turino G, Goldring R. Sustained reversal of chronic hypercapnia in patients with alveolar hypoventilation syndromes. Am J Med 1981; 70:269-74 Hoeppner ~ Cockcroft D, Dosman ], Cotton D. Nighttime ventilation improves respiratory failure in secondary kyphoscoliosis. Am Rev Respir Dis 1984; 129:240-43 Findley L, Boykin M, Fallon 1: Belardinelli L. Plasma adenosine is increased in patients with sleep apnea and severe nocturnal hypoxemia. Am Rev Respir Dis 1986; 133:lSOA(abstract) Hasday ], Grum C. Nocturnal increase of urinary uric acid: creatinine ratio-a biochemical correlate of sleep-associated hypoxemia. Am Rev Respir Dis 1987; 135:534-38 Phillis], Wu E Roles of adenosine and adenine nucleotides in the central nervous system. In: Daly J, Kuroda Y, Phillis ], Shimizu H, Vi M, eds. Physiology and pharmacology of adenosine derivatives. New York:Raven Press, 1983:219-36 Eldridge F, Millhorn 0, Kiley J. Antagonism by theophylline of respiratory inhibition induced by adenosine. J Appl Physiol 1985; 59:1428-33 Lagercrantz H, Yamamoto Y, Fredholm B, Prabhakar N, von Euler C. Adenosine analogues depress ventilation in rabbit neonates. Theophylline stimulation of respiration via adenosine receptors. Ped Res 1984; 18:387-90 Millhorn D, Eldridge F, Kiley J, Waldrop L Prolonged inhibition of respiration following acute hypoxia in glomectomized cats. Respir PhysioI1984; 57:331-40
Advances in Prospective Payment for Pulmonary Patients On May 19, 1987, the Health Care Financing Administration (HCFA) published changes to the Diagnosis-Related Group (DRG) classification system proposed for Federal fiscal year 1988. 1 Two new DRGs for ventilator patients were proposed among the changes. One DRG would be for patients who have tracheostomy procedure codes and would be considered a surgical classification. The other DRC would be for nonsurgical patien ts ven tilated through endotracheal tubes. Only patients with a primary diagnosis of respiratory disease would be covered. The relative payment for these new DRGs would be great since the HCFA's analysis of 1985 billing data indicated that for all respiratory patients the average charge for those on ventilators was two to ten times greater than for other patients in the same DRCs. At Rush-Presbyterian-St. Luke's Medical Center we reviewed the annual costs of 446 Medicare patients who received care in our medical intensive care unit and determined they exceeded by over $4.7 million the actual reimbursements for similar patients under the Medicare Prospective Payment System." Each day on a ventilator added $439 for respiratory-related CHEST I 92 I 5 I NOVEMBER, 1987
n3
services to the total hospital costs," Another study we recently completed at RushPresbyterian-St. Luke's Medical Center revealed that 95 Medicare patients seen over a one-year period who required prolonged ventilator care accrued costs of $3,656,137 or $38,486 per patient. This compared to Medicare payments for patients in similar Diagnosis Related Groups of $8,421 per patient. 3 A similar study published simultaneously found that Medicare patients admitted to both tertiary care and community based hospitals found that mean costs per patient were $31,896 (charges $47,391) compared with Medicare payments for similar types of patients of $10,981. 4 HCFA should be congratulated for these proposed changes, but they nevertheless address only some of the financial bias DRGs present for ventilator patients. Of the 95 patients in our study sample, only 33 were covered by the two new DRGs HCFA proposes. The remainder of the patients did not have respiratory principal diagnoses. Cost of care for patients requiring mechanical ventilation without a primary respiratory diagnosis (ie, neurologic decrease) was not less than those with a respiratory diagnosis. The potential for abuse is also great since the payment for ventilator patients receiving a tracheostomy has a much greater reimbursement than those who need prolonged endotracheal intubation. Studies have shown that the complications of a tracheostomy are greater than those of long-term intubations by endotracheal tube." HCFA recognizes the potential for abuse and will monitor this possibility closely. 1 Despite some potential problems, this legislation has important implications for our patients. The potential for patients to be disenfranchised from medical care is less after these changes are enacted. Reimbursement for care in the intensive care unit will also more closely approximate the costs of medical care. The HCFA is to be congratulated for this move. Also, our professional societies have used their legislative influence to lobby to get needed reimbursement to prevent a bias against critical care and for patients cared for in specialized units. The Government Liaison Committee of the American College of Chest Physicians has been particularly vigorous in efforts to acquaint national legislators with current inequality in the reimbursement policies. The official journal of ACC:g Chest, has provided a national forum for data which was of assistance to HCFA as they evaluated current practices.v' These efforts are to be congratulated. Roger C. Bone, M.D., F.C.C.P.
Chicago
Ralph C. Brown Professor and Chairman, Der~tment of In~e~nal Medicine; Chief, Section of Pulmonary and Critical Care Medicine, Rush-Presbyterian-St. Luke's Medical Center. Reprint requests: Dr. Bone, Rush Medical College, 1753 West Congress Parkway, Chicago 60612
REFERENCES 1 Federal Register. 52(No 96):1880-1881, May 19, 1987 2 Butler P\V, Bone RC, Field T. Technology under Medicare diagnosis-related groups prospective payment. Implications for medical intensive care. Chest 1985; 87:229 3 Douglass PS, Rosen RL, Butler PW, Bone RC. DRG payment for chronic ventilator patients: Implications and recommendations. Chest 1987; 91:413-17 4 Gracey 0, Gillespie 0, Nobrega F, Naessens ]M, Krishan I. The financial implications of prolonged ventilator care of medicare patients under the prospective payment system: A multicenter study. Chest 1987; 91:424-27 5 Stauffer ]L, Olson DE, Petty TL. Complications and consequences of endotracheal intubation and tracheostomy-A prospective study of 150 critically ill adult patients. Am ] Med 1981; 70:65-75
The Esophagus The Neglected Chest Organ? he thoracic cavity's organs include the heart, the T lung and the esophagus. The American College of
Chest Physicians (and the journal Chest, as its official publication) are predominated by cardiologists, pulmonologists and cardiothoracic surgeons whose primary orientation is that of either the cardiac or pulmonary subsystems. However, it seems timely to remind "chest" physicians that physiology and pathology of the esophagus are important considerations because of their impact on the other thoracic organs. Coronary angiography in some patients (10 to 15 percent) with chest pain considered typical for angina will rule out important coronary artery disease. Many of these patients can eventually be proved to have esophageal disorders causing their symptoms. In some cases, an esophageal motility disorder is found,':" and on other occasions, gastroesophageal reflux is the culprit. 2 Both these disorders are eminently treatable and it is not acceptable simply to dismiss patients with the information that they do not have coronary artery disease and therefore their chest pain is not important. One follow-up study' showed that pain persists in the majority of these patients and half of them are so incapacitated that they are not able to return to work or their normal life-style. Accordingly, the cardiologist who clears the heart as the cause of chest pain must not stop but must continue the evaluation with a diagnostic evaluation of other organ systems, including the esophagus. It is also quite clear that esophageal disorders can be responsible for pulmonary disease. The patient presenting with evidence of destructive aspiration, in the absence of neurologic impairment or alcohol abuse, probably has reflux disease and should be evaluated for Editorials