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• W4238610617 abstract "Clinicopathologic ConferenceClinicopathologic Conference John R. L. Froude, MB, BS, MRCP David B. Lewall, and MD, FRCP(C) Theodore M. Bailey, IIIMD, FCAP John R. L. Froude Internist, Department of Medicine Search for more papers by this author , David B. Lewall Chairman, Department of Radiology Search for more papers by this author , and Theodore M. Bailey, III Pathologist, Director, Sections of Microbiology and Serology Department of Pathology and Laboratory Medicine King Faisal Specialist Hospital and Research Centre Search for more papers by this author Published Online:1 Jan 1982https://doi.org/10.5144/0256-4947.1982.55SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutCASE PRESENTATIONA 42-year-old married Saudi Arabian woman with three children was referred to the King Faisal Specialist Hospital and Research Centre because of fever with malaise and breathlessness of six weeks' duration.She had been treated at another hospital for one month where her symptoms gradually worsened until she was breathless on minimal exertion. There was neither orthopnea nor paroxysmal nocturnal dyspnea. She had a dry cough, occasionally producing small amounts of white sputum.Over the two weeks prior to admission, she had had intermittent episodes of stabbing, left-sided chest pain that was sometimes aggravated by deep breathing.At the other hospital, she had received courses of cefazolin sodium, ampicillin, and trimethoprim and sulfamethoxazole (Septra®). No other clinical information was available although she was not thought to have been on steroids or anti-tuberculous drugs. She was not taking the contraceptive pill.The patient had no significant medical history nor was there illness in her family or personal contacts. She thought that she had lost some weight but was not sure. Her bowel habits, micturition, and menses were normal. She was not aware of any allergies.On examination, the patient was yanosed and breathless. Her respiratory rate was 32/min at rest. She had a fever of 39.6°C. Height was 152 cm, weight 53 kg, and blood pressure 120/70 mmHg both lying and sitting. Her pulse was 110/min in sinus rhythm and neck veins were flat. The apical impulse was unremarkable. There was no parasternal heave. The pulmonary second sound was accentuated. There were no murmurs.The patient's trachea was central and chest movement was symmetrical and full. A few crackles that were not cleared by coughing were heard at the left base of the lung. There was neither a pleural nor a pericardial rub.Mouth and fauces were normal. The abdomen was soft and neither her liver nor her spleen could be felt.Her discs and retinae were normal. There were no neurological signs.There was no lymphadenopathy. The thyroid felt normal. Breast and vaginal examinations were normal. There was neither edema nor calf tenderness on examination of the legs.Initial investigations showed hemoglobin 12.2 g/dl; white cell count 8300/cmm; 35% lymphocytes; 52% polymorphonuclear leukocytes; 8% monocytes; 4% eosinophils; and platelets 210,000/cmm. The erythrocyte sedimentation rate was 60 mm in the first hour. Urinalysis showed a trace of protein with no sugar, no bilirubin, and no cells. Chest radiograph showed miliary mottling. A tuberculin skin test (5 units [TU]) showed 10 mm induration.Arterial blood gases, breathing room air with the patient sitting at rest were PO2 44 mmHg; PCO2 30 mmHg; pH 7.44; and HCO3 20meq/1-1. The electrocardiogram showed right axis deviation with occasional ectopic beats. The SMAC-20™ blood analysis showed glucose 90mg/dl; blood urea nitrogen 18mg/dl; creatinine 1 mg/dl; sodium 136meq/l; potassium 4.4meq/l; chloride 104meq/l; uric acid 3 mg/dl; calcium 9.2 mg/dl. Inorganic phosphorous was 2.5 mg/dl; total protein 6.9 g/dl; albumin 3.5 g/dl; cholesterol 170mg/dl; total bilirubin 0.4mg/dl; direct bilirubin 0.2mg/dl. Alkaline phosphatase was 180U/L, SGPT 246 U/L; lactic dehydrogenase 1275 U/L; and creatine phospho-kinase 150 U/L.Other investigations giving negative results were blood cultures repeated three times, febrile agglutinins, cold agglutinins, smear for malaria parasites, and hepatitis antigen. Sputum tested for gram stain showed neither fungal elements nor bacterial pathogens. Sputum tested three times, by normal procedures, for acid-fast bacilli was negative each time.Prothrombin time was 13 seconds (control, 12 seconds), and partial thromboplastin time was 30 seconds (control, 32 seconds). Tests for antinuclear antibody was negative and ACTH Cortisol stimulation test was normal. Plasma Cortisol was 180ng/ml in the morning and 200ng/ml at midnight (normal range, 20 to 90 ng/ml morning; 70 to 250ng/ml midnight).The patient was admitted to the intensive care unit and treated with six liters per minute of oxygen via a nasal cannula. Her arterial PO2 rose to 70mmHg. Nafcillin and gentamicin were given intravenously, and isoniazid, rifampin, and etham-butol were given orally.On the second hospital day a liver biopsy was performed. On the third day a tracheal aspirate revealed a pure growth of Pseudomonas aeruginosa. Her hemoglobin, white cell count, platelet count, and SMAC-20™ blood analysis for that day were as before. Intravenous carbenicillin was added to her antibiotic regimen.While the first dose was being given, the patient became bluer, confused, and restless, and the arterial blood gases on six liters of oxygen via nasal cannula showed PO2 of 20mmHg, PCO2 of 27mmHg, and pH of 7.32. An endotracheal tube was inserted and the patient was artificially ventilated. The arterial PO2 rose to 50mmHg.Examination at this time was as before. There were no added sounds audible in the lung. Her neck veins remained flat and no pericardial or pleural rub was heard. Examination of the legs showed neither swelling nor calf tenderness. Her complete blood count and SMAC-20™ blood analysis remained unchanged as did her electrocardiogram and chest radiograph. Later the same day, a lung scan and pulmonary angiogram were performedDavid B. Lewall, MD:The chest radiograph taken on admission demonstrates a fine, miliary pattern throughout both lungs. Figure 1. The nodules are slightly over one millimeter in diameter, on the average, and they are uniformly distributed through both lungs. The remarkable uniformity of size and distribution is characteristic of miliary tuberculosis and it excludes many other possibilities such as silicosis. Other possibilities in the differential diagnosis are blood-borne mycoses and, rarely, blood-borne bacterial infections.1Figure 1. Posterior anterior radiograph of the chest (localized view of left lung). There is a diffuse miliary pattern. No other abnormality was present.Download FigureThe interval between the dissemination of the tubercle bacilli and the appearance on the chest radiograph of the miliary pattern is about six weeks. Thus, we can assume that the disease has been present for over a month.John R. L. Froude, MD:The history, together with the clinical and laboratory findings, suggest a progressive, febrile disease of recent onset associated with liver dysfunction and culminating in hypoxemic respiratory failure. In a previously healthy young adult who has failed to improve with conventional antibiotic treatment, disseminated tuberculosis is a very likely cause of the illness even before seeing the chest radiograph. Furthermore, tuberculosis is a common disease in Saudi Arabia. As it is readily curable with triple chemotherapy, treatment should not be delayed even in the absence of a definitive diagnosis, especially as diagnostic tests remain positive for several weeks.2 Systemic mycoses, lymphoma, and disseminated cancer should be considered in the differential diagnosis, but they are extremely unlikely in this clinical setting and I do not propose to discuss them further.I think this patient has disseminated tuberculosis, a disease with a 20 to 30 percent mortality rate even at the present time.3Patients with diabetes, previous gastrectomy, carcinoma, pregnancy, and those on steroid therapy have a predisposition to this infection. None of these conditions apply to our patient which improves the prognosis.Examination of this patient gave few clues. Choroidal tubercles were not seen, they rarely are, and splenomegaly was absent. A recent report from the United States found splenomegaly in 12 of 100 patients with disseminated tuberculosis.2 Its value as a clinical sign is lessened here as malaria and schistosomiasis are endemic in parts of Saudi Arabia.The positive tuberculin test indicates previous infection with the tubercle bacillus. In adults, disseminated tuberculosis follows reactivation of a primary infection with hematogenous dissemination. It is important to realize that the tuberculin test is negative in up to 40 percent of these patients.4 When correctly administered, using active reagent, a negative test indicates impaired cellular immunity and implies a worse prognosis.5Confirmation of the diagnosis depends on the demonstration or culture of the acid-fast bacillus. Sputum smears are negative in 66 percent of cases and, although cultures are much more often positive, the organism takes four to six weeks to grow and treatment should not be delayed.6As might be expected in this disseminated disease, the bacteria have been recovered from many body tissues and fluids. Gastric washings, urine, cerebrospinal fluid, bone marrow biopsy, and, where appropriate, aspiration of skin abscesses and lymph nodes and pleural biopsy may all be useful in providing diagnostic material.As the patient has impaired liver function, liver biopsy is a convenient way of making the diagnosis, quickly. At least 80 percent of people with disseminated tuberculosis have granulomatous hepatitis and 60 percent of these have abnormal liver function tests. Characteristically, the pattern is of an alkaline phosphatase greater than 150U/L with moderate or no SGOT and SGPT elevation. An elevated serum bilirubin is present in a minority of cases.7Many conditions cause granulomatous hepatitis. When seen with miliary mottling, however, the diagnosis of disseminated tuberculosis is strongly suggested even if the tubercle bacillus has not been demonstrated. Additional histological features can make the diagnosis more certain but I leave it to Dr Bailey to comment on this.Adrenal failure has been excluded in this patient as the plasma Cortisol and ACTH stimulation test results are normal. Although rare, adrenal failure must be looked for and promptly treated. Inappropriate antidiuretic hormone secretion is well described in disseminated tuberculosis but is excluded here because of the normal serum sodium.I would now like to concentrate on the respiratory problem in more detail.The patient presented with severe arterial hypoxemia and a PO2 of 45 mmHg. Alveolar capillary block syndrome has been documented in disseminated tuberculosis and the abnormalities in lung function may persist after many months of successful chemotherapy and long after the chest radiograph has returned to normal.4In disseminated tuberculosis, hypoxemic respiratory failure is the most common cause of death, which may occur unexpectedly.4 We have seen patients deteriorate with superadded pneumonia, pulmonary edema, and pulmonary infarction.Did this woman have pneumonia? An ill patient in the hospital for a month receiving antibiotics is very much at risk of nosocomial pneumonia and we know the patient's trachea was colonized by Pseudomonas. She was promptly given antibiotics. This treatment runs the risk of selecting more resistant organisms, yet is justifiable in such an ill patient in whom pneumonia cannot be excluded. The normal white count, the negative blood cultures, and the absence of infiltrates on the chest radiographs make active pneumonia unlikely.This patient has a history of recurrent pleuritic chest pain which is reported in up to 25 percent of patients with miliary mottling on chest radiographs.3 In addition, she had a loud pulmonary component to the second sound and right axis deviation on the electrocardiograph. There is also a clinical impression that the hypoxemia is out of proportion to the radiographic changes. This, together with the high lactose dehydrogenase, raises the possibility of pulmonary infarction especially in an ill patient bedridden for a month.Her abrupt deterioration with profound hypoxemia while breathing oxygen makes it very likely that the patient had a recent pulmonary embolus. She was fortunate to be in an intensive care unit where prompt treatment saved her life.Would Dr Lewall discuss the lung scan and the pulmonary angiogram?Dr Lewall:A perfusion lung scan was performed with macroaggregates of albumin injected intravenously. On the right lateral view there is a defect of perfusion which corresponds to the medial basal segment of the right lower lobe. Figure 2. This examination was followed by a selective right pulmonary angiogram which demonstrates a long, filling defect with lumen of the opacified branch of the pulmonary artery. Figure 3. Other similar lesions were demonstrated in other parts of the lungs. Thus, pulmonary emboli are confirmed.Figure 2. Right lateral view of lung scan. There is a perfusion defect corresponding to the medial basal segment of the right lower lobe, (arrows).Download FigureFigure 3. Coned view from right pulmonary angiogram. There is a serpiginous filling defect representing an embolus in the pulmonary artery.Download FigureTheodore M. Bailey, III, MD:The low-power view of the liver biopsy demonstrates the extensive involvement of the hepatic parenchyma by multiple small nodular granulo-mata composed of lymphocytes, epithelioid histiocytes, and multinucleated giant cells. Figure 4. Some of the granulomata show central caseation necrosis. Figure 5. The hepatic parenchyma un-involved by granulomatous lesions shows mild nonspecific reactive changes consisting of variability of nuclear size, prominent nucleoli, and scattered binucleate forms. There is no evidence of hepatocellular degeneration, inflammation, or necrosis.Figure 4. Low-power view of the liver biopsy showing the extensive involvement of the hepatic parenchyma by multiple, small, nodular granulomata. Magnified 64 times. Periodic Acid Schiff stain.Download FigureFigure 5. View of a granuloma showing caseation necrosis. Magnified 250 times. Hematoxylin and eosin stain.Download FigureThe list of disorders that cause hepatic granulo-mata is ever increasing and quite impressive. A partial list of the better known causes included infective agents such as tuberculosis, atypical mycobacteria, brucellosis, histoplasmosis, schistosomiasis, leprosy, syphilis, tularemia, Q-fever, and cytomegalovirus. Noninfective causes include berylliosis and reactions to drugs such as the sulfonamides, phenylbutazone, and allopurinol. Hodgkin's disease has also been reported to cause hepatic granulomata as have diseases of uncertain etiology including Wegener's granulomatosis, primary biliary cirrhosis, chronic active hepatitis, ulcerative colitis, regional enteritis, and sarcoidosis.8,9A major problem in the histological evaluation of hepatic granulomata is that there are really few morphological characteristics that help differentiate among the various causes. This differential must be sorted out by a combination of clinical history, physical examination, radiographic findings, serological tests, culture and complete examination of the biopsy material by routine and special stains. It is also most helpful to have an understanding of what causes hepatic granulomata in a given patient population.9,10Over the last two years at King Faisal Specialist Hospital and Research Centre, we examined 32 liver biopsies showing granulomatous hepatitis. Of these, 20 were from patients with strong clinical histories of tuberculosis. Sixteen of the 20 biopsies contained noncaseating granulomata and only one was positive for acid-fast bacilli on special stain. The remaining four contained caseating granulomata only one of which was positive for acid-fast bacilli on special stain. The other causes of hepatic granulomata in our series included schistosomiasis (one), brucellosis (two), Hodgkin's disease (five), and undetermined (four). None of these granulomata showed caseation necrosis. To date, we have not seen a case of sarcoidosis involving the liver.In this patient's biopsy, some of the granulomata showed central caseation necrosis. Central caseation necrosis does occur in hepatic miliary tuberculosis. In our patient population, if caseation necrosis is present and even if acid-fast bacilli special stains are negative, I feel the diagnosis is tuberculosis until proven otherwise. This is not to say that the presence of hepatic granuloma with caseation necrosis is pathognomonic of tuberculosis; it is not. Caseation necrosis has been seen in syphilis, brucellosis, tularemia, Q-fever, histoplasmosis, and Wegener's granulomatosis. Realistically, caseation necrosis in these diseases is rare but we see these diseases in our patient population so this differential diagnosis must be kept in mind when evaluating hepatic granulomata.10–12In this case, special stains demonstrated acid-fast bacilli. Evaluation of liver biopsies in patients ultimately proven to have tuberculosis has yielded some relatively consistent findings. In patients with isolated pulmonary tuberculosis, 31 percent were shown to have hepatic granulomata. In those with documented pulmonary and extra-pulmonary tuberculosis (exclusive of miliary involvement) 70 to 80 percent have hepatic granulomata. Over 90 percent of the patients with miliary tuberculosis will have hepatic granulomata. However, special stains for acid-fast bacilli will demonstrate the organisms in only about ten percent of cases.9–12In conclusion, this liver biopsy shows miliary involvement by tuberculous granulomata. This case also demonstrates that the liver biopsy is a valuable tool in cases of suspected tuberculosis not yet proven by other methods. Sputum cultures on this patient have been negative to date.Dr Froude:In summary, disseminated tuberculosis is a serious disease that is common in Saudi Arabia and, once suspected, should be treated with anti-tuberculous drugs even in the absence of a proven diagnosis.Liver biopsy is a convenient method of demonstrating granulomatous hepatitis which often occurs and is strong supporting evidence of the diagnosis. Finally, patients with disseminated disease are at risk of superadded infections and pulmonary emboli. This lady slowly improved and left the intensive care unit three weeks later having been treated with heparin, antituberculous drugs, and oxygen. She was discharged six weeks later, afebrile with a PO2 of 70mmHg breathing room air at rest.I leave Dr Lewall the last word to comment on her follow-up chest radiograph.Dr Lewall:A follow-up radiograph demonstrates complete clearing of the miliary pattern in the lungs. Figure 6. Clearing of miliary tuberculosis occurs much more rapidly than clearing of nonhematogenous tuberculosis; clearing is usually complete.13 There is generally a detectable response to therapy by one month and in most instances the chest radiograph returns to normal within four months.14 Clearing is faster in young patients than in old. It is noteworthy that the primary source of tuberculous infection is not usually found either radiologically or at autopsy.Figure 6. Chest radiograph showing complete clearing of the miliary pattern.Download FigureFinal Diagnosis: Disseminated tuberculosis with multiple pulmonary emboli.ARTICLE REFERENCES:1. Fraser RG, Pare JAP: Diagnosis of Diseases of the Chest. Philadelphia, WB Saunders Co. 1977 vol 1 p 220. Google Scholar2. Slavin RE, Walsh TJ, Pollack AD, et al.: Late generalized tuberculosis: a clinical pathologic analysis and comparison of 100 cases in the preantibiotic and antibiotic eras . Medicine 59 (5): 352–661980. Google Scholar3. Gelb AF, Leffier C, Brewin A, et al.: Miliary tuberculosis . Amer Rev Resp Dis 108: 1327–331973. Google Scholar4. Sahn SA, Neff TA: Miliary tuberculosis . Am J Med 56: 494–5041974. Google Scholar5. Biehl JP: Miliary tuberculosis. A review of 68 adult patients admitted to a municipal general hospital . Am Rev Resp Dis 77: 6051958. Google Scholar6. Munt PW: Miliary tuberculosis in the chemotherapy era: with a clinical review in 69 American adults . Medicine 51: 139–551972. Google Scholar7. Haex AJC, Van Beek C: Tuberculosis and Aspiration Liver Biopsy: Its Clinical Significance in Diagnosis and Therapy. Haarlem, Netherlands, Erven F. Bohn Co. 1955 p 106. Google Scholar8. MacSween RNM, Anthony PP, Scheuer PJ: Pathology of the Liver. New York, Churchill-Livingstone; 1979. Google Scholar9. Fauci AS: Granulomatous hepatitis. In: Mandell GL, Douglas RG, Bennett JE, eds: Principles and Practice of Infectious Disease. New York, Wiley Medical; 1979 pp 1070–75. Google Scholar10. Klatskin G: Hepatic granulomata: problems in interpretation . Ann NY Acad Sci 278: 427–321976. Google Scholar11. Korn RJ, Kellow WF, Heller P, et al.: Hepatic involvement in extra-pulmonary tuberculosis . Am J Med 27: 60–711959. Google Scholar12. Cucin RL, Coleman M, Eckardt JJ, et al.: The diagnosis of miliary tuberculosis: utility of peripheral blood abnormalities, bone marrow and liver needle biopsy . J Chronic Dis 26: 355–611973. Google Scholar13. Massaro D, Katz S: Rapid clearing in hematogenous pulmonary tuberculosis . Arch Intern Med 113: 5731964. Google Scholar14. Biehl JP: Miliary tuberculosis. A review of sixty-eight adult patients admitted to a municipal general hospital . Am Rev Tuberc 77: 6051958. Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 2, Issue 1January 1982 Metrics History Published online1 January 1982 KeywordsTuberculosisPulmonary embolismmiliaryInformationCopyright © 1982, Annals of Saudi MedicinePDF download" @default.
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