Miliary Tuberculosis and Adult Respiratory Distress Syndrome JON S. HUSEBY, M.D.; and LEONARD D. HUDSON, M.D.; Seattle, Washington
Three patients with miliary tuberculosis developed the adult respiratory distress syndrome. In two patients this complication developed despite treatment with antituberculous drugs. The third patient developed the syndrome, but miliary tuberculosis was not suspected. The presence of disseminated intravascular coagulation in all three cases suggests a possible pathophysiologic relation. Miliary tuberculosis should be considered in patients presenting with adult respiratory distress syndrome of unknown cause.
DEFINITIVE CARE for the adult respiratory distress syn-
drome may depend on recognizing a treatable cause. We present here the cases of three patients who developed adult respiratory distress syndrome as a complication of miliary tuberculosis. Case Reports PATIENT 1
A 58-year-old black woman was admitted to the hospital with shortness of breath, which had gradually increased through 1 week, and confusion of 1 day's duration. She had moderate respiratory distress, cyanosis, and a slightly stiff neck. Her supine blood pressure was 80/60 mm Hg; pulse rate, 150/min; temperature, 39 °C; and respiratory rate, 46/min. There was no evidence of congestive heart failure. A chest roentgenogram at admission showed a pattern of diffuse small nodular lesions (Figure 1) compatible with miliary tuberculosis. Arterial blood gas studies (room air breathing) included Pao2 of 41 mm Hg; Paco2, 33 mm Hg; and pH, 7.55. Other laboratory values at admission included leukocyte count, 6500/mm3; hematocrit, 44%; and platelet count, 33 000/mm3. Lumbar puncture showed an opening pressure of 100 mm of HzO; the cerebrospinal fluid (CSF) contained 34 erythrocytes and 12 polymorphonuclear neutrophils per mm3. The CSF glucose was 41 mg/dl with a simultaneous blood glucose of 235; the CSF protein was 46 mg/dl. Sputum showed acid-fast bacilli on smear and later was positive for Mycobacterium tuberculosis on culture. Blood and CSF cultures were sterile. Miliary tuberculosis was diagnosed, and treatment was started in the intensive care unit with isoniazid, 300 mg, rifampin, 600 mg, and streptomycin, 1 g daily. Assisted ventilation was started with a volume-cycled respirator. The pulmonary wedge pressure (Swan-Ganz pulmonary artery catheter) was 6 mm Hg. Sixteen hours after admission, the Pao2 on an inspired oxygen fraction (F1O2) of 0.7 was 74 mm Hg, and the chest roentgenogram showed bilateral diffuse infiltrates consistent with pulmonary edema (Figure 2). At this time the pulmonary wedge pressure was 5 mm Hg. The Pa02 increased to 184 • From the Respiratory Disease Divisions, Harborview Medical Center and Seattle United States Public Health Service Hospital; and the Respiratory Disease Division, Department of Medicine, University of Washington; Seattle, Washington.
mm Hg with 15 cm of H2O positive end-expiratory pressure on an F1O2 of 0.7. Intravenous steroid therapy was started. The patient's condition and oxygenation improved during the next 3 days. On the fifth hospital day her mental status deteriorated and hypotension developed. Diffuse bleeding was noted. Complete coagulation studies, not obtained before, showed prothrombin time of 17.8 sec (control, 12.5); partial thromboplastin time, 116 sec (controls 39); fibrinogen, 54 mg/dl; fibrin degradation products greater than 40 fig/ml; and platelet count, 22 000/mm3. Cephalothin and gentamicin therapies were started because of the possibility of sepsis, although all blood cultures subsequently were sterile. Persistent complications up until death included hypotension treated with dopamine and fluid administration, gangrene of both hands and feet, and rising blood urea nitrogen and creatinine levels despite good urinary output. There was no further resolution in the hypoxemia despite a relatively clear chest roentgenogram on the last hospital day. Bilateral tension pneumothoraces occurred terminally. Autopsy showed miliary tuberculosis. Granulomas with marked central necrosis associated with acid-fast bacilli were seen in the lungs, kidneys, spleen, liver, and adrenal glands. Pulmonary edema fluid and diffuse hyaline membranes were present. Except for mild coronary atherosclerosis, the heart was normal. PATIENT 2
A 63-year-old Filipino man was admitted to the hospital with fever (38.6 °C), sweating, and shaking chills. Chest and cardiac findings were normal. A chest roentgenogram at admission showed a diffuse finely nodular infiltrate compatible with miliary tuberculosis. Hema-
Figure 1 . Admission chest roentgenogram from Patient 1 consistent with miliary tuberculosis.
Annals of Internal Medicine 85:609-611, 1976
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Figure 2. Chest roentgenogram from Patient 1 16 h after admission showing diffuse infiltrates consistent with pulmonary edema. Pulmonary wedge pressure was 5 mm Hg.
tocrit was 42%; leukocyte count, 8200/mm3; platelet count, 120 000/mm3; alkaline phosphatase, 214 IU (normal, 85); total bilirubin, 2.5 mg/dl; serum glutamic oxalacetic transaminase (SGOT), 161 U; lactate dehydrogenase (LDH), 166 U; and prothrombin time, 100% activity. Intermediate purified protein derivative (PPD), second strength PPD, and mumps skin tests were negative, Blood, urine, and sputum cultures were sterile. Several sputa were negative on smear for acid-fast bacilli. A liver biopsy showed caseating granulomas and acid-fast bacilli. Treatment was started with isoniazid, 300 mg, ethambutol, 1500 mg, and streptomycin, 1 g daily. Three days later the patient developed progressive dyspnea without chest pain, cough, or hemoptysis. He was bleeding from the gums and from venipuncture sites. His neck veins were flat while supine. Chest and cardiac findings were normal except for tachypnea and tachycardia. Electrocardiogram findings were normal. Chest roentgenogram showed diffuse bilateral alveolar infiltrates with an unchanged heart size. Gram's stain of the sputum showed a few leukocytes and no bacteria. Arterial blood gas studies (room air breathing) included Pao2 of 45 mm Hg; Paco2, 16 mm Hg; HCOa, 8 meq/litre; and pH, 7.32. Central venous pressure was zero. A coagulation profile showed prothrombin time of 21 sec (control, 13.5); partial thromboplastin time, 123 sec (control, 38); thrombin time, 27 sec (control, 21); fibrinogen, 135 mg/dl; and platelet count, 49 000/mm3. The Pao2 (100% oxygen by mask) decreased to 37 mm Hg. Endotracheal intubation was done and assisted ventilation started with a volume respirator. The central venous pressure increased to 9 cm of H 2 0 with intravenous sodium bicarbonate and saline, but urine output diminished. During the next day the patient's oxygenation deteriorated; on an Fi02 of 1.0, the Pao2 fell from 144 to 34 mm Hg. Fifteen hours after intubation, the patient developed recurrent episodes of supraventricular tachycardia followed by asystole and died. At autopsy, both lungs showed miliary tuberculosis with severe congestion, edema, and hyaline membranes. There were also multiple miliary caseous foci in the liver and scattered caseous nodules in the spleen and abdominal lymph nodes. No evidence of pulmonary emboli or pneumonia was found. The heart showed mild coronary atherosclerosis. PATIENT 3
A 45-year-old black man was admitted to the hospital with malaise, anorexia, and fever of 3 weeks' duration. His medical history included alcoholic hepatitis. 610
He was thin and tremulous, with scleral icterus, hepatomegaly, and a normal heart and chest; his temperature was 38 °C. Total bilirubin was 9.3 mg/dl; SGOT, 129 U; prothrombin time, 48% activity; platelet count, 123 000/mm3; hematocrit, 46%; and leukocyte count, 6300/mm3. Chest roentgenogram and electrocardiogram findings were normal. Blood, urine, and sputum cultures showed no growth. The diagnosis was alcoholic hepatitis. Twenty days after admission he became tachypneic and obtunded. Arterial blood gas studies (room air breathing) included pH of 7.35; Pao2, 60 mm Hg; and Paco2, 16 mm Hg. Chest roentgenogram showed diffuse alveolar infiltrates without cardiomegaly. The patient was transferred to the intensive care unit. The Swan-Ganz wedge pressure was 12 mm Hg. He was bleeding from his gingiva and venipuncture sites. Prothrombin time was 18% activity; thrombin time, 120 sec (control, 18); partial thromboplastin time, 131 sec (control, 40); fibrin degradation products greater than 40 /ig/ml, platelet count, 41 000/mm3; and hematocrit, 25%. Assisted ventilation was started with a volume respirator. On an Fi02 of 1.0, the Pao2 was 74 mm Hg but increased to 247 mm Hg with 15 cm of HoO positive end-expiratory pressure. Gentamicin, cephalothin, dopamine, methylprednisolone, and therapy for hepatic encephalopathy were started. One sputum smear was negative for acid-fast bacilli. His pulmonary status improved, but he developed progressive hypotension and metabolic acidosis and died 2 days after transfer to the intensive care unit. At autopsy, massive miliary tuberculosis, involving the lungs, liver, spleen, and adrenal glands, and mild alcoholic hepatitis were found. The heart was normal. Discussion
In Patients 1 and 3 a cardiogenic cause for the pulmonary edema was excluded by a normal pulmonary wedge pressure and in Patient 2 by a low central venous pressure. All three had normal hearts at autopsy. Reports of miliary tuberculosis as a cause of adult respiratory distress syndrome are unusual. A recent report described acute respiratory failure refractory to 100% oxygen in a patient thought to have a viral pneumonia ( 1 ) ; the patient died despite ventilatory support with positive end-expiratory pressure and extracorporeal membrane oxygenation. Postmortem examination showed extensive miliary tuberculosis. Even retrospectively the initial chest roentgenogram was thought to show interstitial pneumonia at the lung bases rather than the pattern of miliary tuberculosis; subsequent roentgenograms showed progressive diffuse pulmonary infiltration consistent with the adult respiratory distress syndrome. Another patient who may have had miliary tuberculosis and the adult respiratory distress syndrome was reported by Goldfine and colleagues ( 2 ) . Disseminated intravascular coagulaTable 1. Summary of Reports Describing Disseminated Intr avascular Coagulation (DIC) or Adult Respiratory Dis.tress Syndrome (ARDS), or Both, Complicating Miliary Tuberculosis* Reports
Pati ents
DIC
ARDS
n0. Rosenthal (4) Homan and co-workers (1) Goldfine and co-workers (2) Grieco and Chmel (3) Mavligit, Binder, and Crosby (5) Sahn and Neff (6) Current report
3
1I ]I 1I ]I ]I I$
+ ++ ++
—
++ ++ ++
++ + +
* + + = Documented; + = probable; — = n o evidence for diagnosis.
November 1976 • Annals of Internal Medicine • Volume 85 • Number 5
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— —
++
tion was emphasized as a complication, but a diagnosis of adult respiratory distress syndrome was suggested by severe respiratory distress, normal cardiac examination except for tachycardia, Pao2 of 32 mm Hg (3 litres of supplemental oxygen per minute), and bilateral diffuse alveolar infiltrates. Grieco and Chmel (3) allude in their review of acute disseminated tuberculosis to a patient whose initial chest roentgenogram was negative except for a Ghon complex and minimal pleural effusion but who developed physical and roentgenographic findings suggestive of pulmonary edema and died despite digoxin and diuretics. Autopsy showed extensive miliary tuberculosis. This patient may have had the adult respiratory distress syndrome. Although the mechanism by which miliary tuberculosis produces the syndrome is not known, presumably injury to alveolar capillary membranes causes increased permeability to fluid containing solutes and protein. Possible mechanisms include massive release of mycobacteria into the pulmonary circulation causing damage to the capillary endothelium, embolization of platelet-fibrin aggregates to the pulmonary capillaries with subsequent endothelial injury, or a cell-mediated hypersensitivity reaction leading to increased vascular permeability. We have no direct evidence for these possibilities. In our patients and in two of the three cases from our literature review, disseminated intravascular coagulation, itself an unusual complication, coexisted with the adult respiratory distress syndrome (see Table 1). The events accompanying disseminated intravascular coagulation, especially the embolization of tiny fibrin and platelet aggregates to the lungs, may be important mechanisms in the
syndrome; some experimental evidence supports this view (7-10). On the other hand, the syndrome and disseminated intravascular coagulation both occur in various acute illnesses; their association may simply reflect a common triggering event. ACKNOWLEDGMENTS: Received 19 February 1976; revisions accepted 26 August 1976. • Requests for reprints should be addressed to Leonard D. Hudson, M.D.; Respiratory Disease Division, Harborview Medical Center, 325 Ninth Ave.; Seattle, WA 98104. References 1. HOMAN W, HARMAN E, BRAUN NM, et al: Miliary tuberculosis
presenting as acute respiratory failure: treatment by membrane oxygenator and ventricle pump. Chest 67:366-369, 1975 2. GOLDFINE ID, SCHACHTER H, BARCLAY WR, et al: Consumption
coagulopathy in miliary tuberculosis. Ann Intern Med 71:775777, 1969 3. GRIECO MH, CHMEL H: Acute disseminated tuberculosis as a diagnostic problem. A clinical study based on twenty-eight cases. Am Rev Respir Dis 109:554-560, 1974 4. ROSENTHAL N: The blood picture in purpura. / Lab Clin Med 13:303-322, 1928 5. MAVLIGIT GM, BINDER RA, CROSBY WH: Disseminated intra-
vascular coagulation in miliary tuberculosis. Arch Intern Med 130:388-389, 1972 fe. SAHN SA, NEFF TA: Miliary tuberculosis. Am J Med 56:495505, 1974 7. BLAISDELL FW: Pathophysiology of the respiratory distress syndrome. Arch Surg 108:44-49, 1974 8. HUBER G, MASON R, PEGG C, et al: Production, reversal and
prevention of experimental hyaline membranes following disseminated intravascular coagulation (abstract). Clin Res 17:450, 1969 9. STALLONE RJ, LIM RC JR, BLAISDELL FW: The pathogenesis of
pulmonary changes following ischemia of the lower extremities. Ann Thorac Surg 7:539-549, 1969 10. NACHMAN RL, WEKSLER B, FERRIS B: Characterization of hu-
man platelet vascular permeability-enhancing activity. / Clin Invest 51:549-556, 1972
Huseby and Hudson • Miliary Tuberculosis
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Three patients with miliary tuberculosis developed the adult respiratory distress syndrome. In two patients this complication developed despite treatment with antituberculous drugs. The third patient developed the syndrome, but miliary tuberculosis was not suspected. The presence of disseminated intravascular coagulation in all three cases suggests a possible pathophysiologic relation. Miliary tuberculosis should be considered in patients presenting with adult respiratory distress syndrome of unknown cause.
DEFINITIVE CARE for the adult respiratory distress syn-
drome may depend on recognizing a treatable cause. We present here the cases of three patients who developed adult respiratory distress syndrome as a complication of miliary tuberculosis. Case Reports PATIENT 1
A 58-year-old black woman was admitted to the hospital with shortness of breath, which had gradually increased through 1 week, and confusion of 1 day's duration. She had moderate respiratory distress, cyanosis, and a slightly stiff neck. Her supine blood pressure was 80/60 mm Hg; pulse rate, 150/min; temperature, 39 °C; and respiratory rate, 46/min. There was no evidence of congestive heart failure. A chest roentgenogram at admission showed a pattern of diffuse small nodular lesions (Figure 1) compatible with miliary tuberculosis. Arterial blood gas studies (room air breathing) included Pao2 of 41 mm Hg; Paco2, 33 mm Hg; and pH, 7.55. Other laboratory values at admission included leukocyte count, 6500/mm3; hematocrit, 44%; and platelet count, 33 000/mm3. Lumbar puncture showed an opening pressure of 100 mm of HzO; the cerebrospinal fluid (CSF) contained 34 erythrocytes and 12 polymorphonuclear neutrophils per mm3. The CSF glucose was 41 mg/dl with a simultaneous blood glucose of 235; the CSF protein was 46 mg/dl. Sputum showed acid-fast bacilli on smear and later was positive for Mycobacterium tuberculosis on culture. Blood and CSF cultures were sterile. Miliary tuberculosis was diagnosed, and treatment was started in the intensive care unit with isoniazid, 300 mg, rifampin, 600 mg, and streptomycin, 1 g daily. Assisted ventilation was started with a volume-cycled respirator. The pulmonary wedge pressure (Swan-Ganz pulmonary artery catheter) was 6 mm Hg. Sixteen hours after admission, the Pao2 on an inspired oxygen fraction (F1O2) of 0.7 was 74 mm Hg, and the chest roentgenogram showed bilateral diffuse infiltrates consistent with pulmonary edema (Figure 2). At this time the pulmonary wedge pressure was 5 mm Hg. The Pa02 increased to 184 • From the Respiratory Disease Divisions, Harborview Medical Center and Seattle United States Public Health Service Hospital; and the Respiratory Disease Division, Department of Medicine, University of Washington; Seattle, Washington.
mm Hg with 15 cm of H2O positive end-expiratory pressure on an F1O2 of 0.7. Intravenous steroid therapy was started. The patient's condition and oxygenation improved during the next 3 days. On the fifth hospital day her mental status deteriorated and hypotension developed. Diffuse bleeding was noted. Complete coagulation studies, not obtained before, showed prothrombin time of 17.8 sec (control, 12.5); partial thromboplastin time, 116 sec (controls 39); fibrinogen, 54 mg/dl; fibrin degradation products greater than 40 fig/ml; and platelet count, 22 000/mm3. Cephalothin and gentamicin therapies were started because of the possibility of sepsis, although all blood cultures subsequently were sterile. Persistent complications up until death included hypotension treated with dopamine and fluid administration, gangrene of both hands and feet, and rising blood urea nitrogen and creatinine levels despite good urinary output. There was no further resolution in the hypoxemia despite a relatively clear chest roentgenogram on the last hospital day. Bilateral tension pneumothoraces occurred terminally. Autopsy showed miliary tuberculosis. Granulomas with marked central necrosis associated with acid-fast bacilli were seen in the lungs, kidneys, spleen, liver, and adrenal glands. Pulmonary edema fluid and diffuse hyaline membranes were present. Except for mild coronary atherosclerosis, the heart was normal. PATIENT 2
A 63-year-old Filipino man was admitted to the hospital with fever (38.6 °C), sweating, and shaking chills. Chest and cardiac findings were normal. A chest roentgenogram at admission showed a diffuse finely nodular infiltrate compatible with miliary tuberculosis. Hema-
Figure 1 . Admission chest roentgenogram from Patient 1 consistent with miliary tuberculosis.
Annals of Internal Medicine 85:609-611, 1976
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Figure 2. Chest roentgenogram from Patient 1 16 h after admission showing diffuse infiltrates consistent with pulmonary edema. Pulmonary wedge pressure was 5 mm Hg.
tocrit was 42%; leukocyte count, 8200/mm3; platelet count, 120 000/mm3; alkaline phosphatase, 214 IU (normal, 85); total bilirubin, 2.5 mg/dl; serum glutamic oxalacetic transaminase (SGOT), 161 U; lactate dehydrogenase (LDH), 166 U; and prothrombin time, 100% activity. Intermediate purified protein derivative (PPD), second strength PPD, and mumps skin tests were negative, Blood, urine, and sputum cultures were sterile. Several sputa were negative on smear for acid-fast bacilli. A liver biopsy showed caseating granulomas and acid-fast bacilli. Treatment was started with isoniazid, 300 mg, ethambutol, 1500 mg, and streptomycin, 1 g daily. Three days later the patient developed progressive dyspnea without chest pain, cough, or hemoptysis. He was bleeding from the gums and from venipuncture sites. His neck veins were flat while supine. Chest and cardiac findings were normal except for tachypnea and tachycardia. Electrocardiogram findings were normal. Chest roentgenogram showed diffuse bilateral alveolar infiltrates with an unchanged heart size. Gram's stain of the sputum showed a few leukocytes and no bacteria. Arterial blood gas studies (room air breathing) included Pao2 of 45 mm Hg; Paco2, 16 mm Hg; HCOa, 8 meq/litre; and pH, 7.32. Central venous pressure was zero. A coagulation profile showed prothrombin time of 21 sec (control, 13.5); partial thromboplastin time, 123 sec (control, 38); thrombin time, 27 sec (control, 21); fibrinogen, 135 mg/dl; and platelet count, 49 000/mm3. The Pao2 (100% oxygen by mask) decreased to 37 mm Hg. Endotracheal intubation was done and assisted ventilation started with a volume respirator. The central venous pressure increased to 9 cm of H 2 0 with intravenous sodium bicarbonate and saline, but urine output diminished. During the next day the patient's oxygenation deteriorated; on an Fi02 of 1.0, the Pao2 fell from 144 to 34 mm Hg. Fifteen hours after intubation, the patient developed recurrent episodes of supraventricular tachycardia followed by asystole and died. At autopsy, both lungs showed miliary tuberculosis with severe congestion, edema, and hyaline membranes. There were also multiple miliary caseous foci in the liver and scattered caseous nodules in the spleen and abdominal lymph nodes. No evidence of pulmonary emboli or pneumonia was found. The heart showed mild coronary atherosclerosis. PATIENT 3
A 45-year-old black man was admitted to the hospital with malaise, anorexia, and fever of 3 weeks' duration. His medical history included alcoholic hepatitis. 610
He was thin and tremulous, with scleral icterus, hepatomegaly, and a normal heart and chest; his temperature was 38 °C. Total bilirubin was 9.3 mg/dl; SGOT, 129 U; prothrombin time, 48% activity; platelet count, 123 000/mm3; hematocrit, 46%; and leukocyte count, 6300/mm3. Chest roentgenogram and electrocardiogram findings were normal. Blood, urine, and sputum cultures showed no growth. The diagnosis was alcoholic hepatitis. Twenty days after admission he became tachypneic and obtunded. Arterial blood gas studies (room air breathing) included pH of 7.35; Pao2, 60 mm Hg; and Paco2, 16 mm Hg. Chest roentgenogram showed diffuse alveolar infiltrates without cardiomegaly. The patient was transferred to the intensive care unit. The Swan-Ganz wedge pressure was 12 mm Hg. He was bleeding from his gingiva and venipuncture sites. Prothrombin time was 18% activity; thrombin time, 120 sec (control, 18); partial thromboplastin time, 131 sec (control, 40); fibrin degradation products greater than 40 /ig/ml, platelet count, 41 000/mm3; and hematocrit, 25%. Assisted ventilation was started with a volume respirator. On an Fi02 of 1.0, the Pao2 was 74 mm Hg but increased to 247 mm Hg with 15 cm of HoO positive end-expiratory pressure. Gentamicin, cephalothin, dopamine, methylprednisolone, and therapy for hepatic encephalopathy were started. One sputum smear was negative for acid-fast bacilli. His pulmonary status improved, but he developed progressive hypotension and metabolic acidosis and died 2 days after transfer to the intensive care unit. At autopsy, massive miliary tuberculosis, involving the lungs, liver, spleen, and adrenal glands, and mild alcoholic hepatitis were found. The heart was normal. Discussion
In Patients 1 and 3 a cardiogenic cause for the pulmonary edema was excluded by a normal pulmonary wedge pressure and in Patient 2 by a low central venous pressure. All three had normal hearts at autopsy. Reports of miliary tuberculosis as a cause of adult respiratory distress syndrome are unusual. A recent report described acute respiratory failure refractory to 100% oxygen in a patient thought to have a viral pneumonia ( 1 ) ; the patient died despite ventilatory support with positive end-expiratory pressure and extracorporeal membrane oxygenation. Postmortem examination showed extensive miliary tuberculosis. Even retrospectively the initial chest roentgenogram was thought to show interstitial pneumonia at the lung bases rather than the pattern of miliary tuberculosis; subsequent roentgenograms showed progressive diffuse pulmonary infiltration consistent with the adult respiratory distress syndrome. Another patient who may have had miliary tuberculosis and the adult respiratory distress syndrome was reported by Goldfine and colleagues ( 2 ) . Disseminated intravascular coagulaTable 1. Summary of Reports Describing Disseminated Intr avascular Coagulation (DIC) or Adult Respiratory Dis.tress Syndrome (ARDS), or Both, Complicating Miliary Tuberculosis* Reports
Pati ents
DIC
ARDS
n0. Rosenthal (4) Homan and co-workers (1) Goldfine and co-workers (2) Grieco and Chmel (3) Mavligit, Binder, and Crosby (5) Sahn and Neff (6) Current report
3
1I ]I 1I ]I ]I I$
+ ++ ++
—
++ ++ ++
++ + +
* + + = Documented; + = probable; — = n o evidence for diagnosis.
November 1976 • Annals of Internal Medicine • Volume 85 • Number 5
Downloaded From: http://annals.org/pdfaccess.ashx?url=/data/journals/aim/19515/ by a University of California San Diego User on 03/20/2017
— —
++
tion was emphasized as a complication, but a diagnosis of adult respiratory distress syndrome was suggested by severe respiratory distress, normal cardiac examination except for tachycardia, Pao2 of 32 mm Hg (3 litres of supplemental oxygen per minute), and bilateral diffuse alveolar infiltrates. Grieco and Chmel (3) allude in their review of acute disseminated tuberculosis to a patient whose initial chest roentgenogram was negative except for a Ghon complex and minimal pleural effusion but who developed physical and roentgenographic findings suggestive of pulmonary edema and died despite digoxin and diuretics. Autopsy showed extensive miliary tuberculosis. This patient may have had the adult respiratory distress syndrome. Although the mechanism by which miliary tuberculosis produces the syndrome is not known, presumably injury to alveolar capillary membranes causes increased permeability to fluid containing solutes and protein. Possible mechanisms include massive release of mycobacteria into the pulmonary circulation causing damage to the capillary endothelium, embolization of platelet-fibrin aggregates to the pulmonary capillaries with subsequent endothelial injury, or a cell-mediated hypersensitivity reaction leading to increased vascular permeability. We have no direct evidence for these possibilities. In our patients and in two of the three cases from our literature review, disseminated intravascular coagulation, itself an unusual complication, coexisted with the adult respiratory distress syndrome (see Table 1). The events accompanying disseminated intravascular coagulation, especially the embolization of tiny fibrin and platelet aggregates to the lungs, may be important mechanisms in the
syndrome; some experimental evidence supports this view (7-10). On the other hand, the syndrome and disseminated intravascular coagulation both occur in various acute illnesses; their association may simply reflect a common triggering event. ACKNOWLEDGMENTS: Received 19 February 1976; revisions accepted 26 August 1976. • Requests for reprints should be addressed to Leonard D. Hudson, M.D.; Respiratory Disease Division, Harborview Medical Center, 325 Ninth Ave.; Seattle, WA 98104. References 1. HOMAN W, HARMAN E, BRAUN NM, et al: Miliary tuberculosis
presenting as acute respiratory failure: treatment by membrane oxygenator and ventricle pump. Chest 67:366-369, 1975 2. GOLDFINE ID, SCHACHTER H, BARCLAY WR, et al: Consumption
coagulopathy in miliary tuberculosis. Ann Intern Med 71:775777, 1969 3. GRIECO MH, CHMEL H: Acute disseminated tuberculosis as a diagnostic problem. A clinical study based on twenty-eight cases. Am Rev Respir Dis 109:554-560, 1974 4. ROSENTHAL N: The blood picture in purpura. / Lab Clin Med 13:303-322, 1928 5. MAVLIGIT GM, BINDER RA, CROSBY WH: Disseminated intra-
vascular coagulation in miliary tuberculosis. Arch Intern Med 130:388-389, 1972 fe. SAHN SA, NEFF TA: Miliary tuberculosis. Am J Med 56:495505, 1974 7. BLAISDELL FW: Pathophysiology of the respiratory distress syndrome. Arch Surg 108:44-49, 1974 8. HUBER G, MASON R, PEGG C, et al: Production, reversal and
prevention of experimental hyaline membranes following disseminated intravascular coagulation (abstract). Clin Res 17:450, 1969 9. STALLONE RJ, LIM RC JR, BLAISDELL FW: The pathogenesis of
pulmonary changes following ischemia of the lower extremities. Ann Thorac Surg 7:539-549, 1969 10. NACHMAN RL, WEKSLER B, FERRIS B: Characterization of hu-
man platelet vascular permeability-enhancing activity. / Clin Invest 51:549-556, 1972
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![[A case of miliary tuberculosis (miliary TB) accompanied with adult respiratory distress syndrome (ARDS) in a patient with Cushing's syndrome].](/assets/img/hold.png)
