A patient with Down\u27s syndrome and sickle cell trait developed the adult respiratory distress syndrome and cerebral infarction during infection with Mycoplasma pneumoniae. The slow recovery of pulmonary function was unrelated to antimicrobial therapy. Sickle cell trait may be a risk factor for severe M. pneumoniae infection. The possible underlying mechanism for this relationship is explored, and the relationship between sickle cell trait, cold agglutinins, and the cerebral infarction is discussed

Pensler, Mark I.

Radke, Jan R.

English

Henry Ford Health System Scholarly Commons

Henry Ford Hospital Medical Journal Volume 28 Number 1 Article 12 3-1980 ARDS and Cerebral Infarction Complicating Mycoplasma Pneumonia in Sickle Cell Trait Mark I. Pensler Jan R. Radke Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal  Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Pensler, Mark I. and Radke, Jan R. (1980) "ARDS and Cerebral Infarction Complicating Mycoplasma Pneumonia in Sickle Cell Trait," Henry Ford Hospital Medical Journal : Vol. 28 : No. 1 , 60-62. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol28/iss1/12 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hosp Med Journal Vol 28, No 1, 1980 ARDS and Cerebral Infarction Complicating Mycoplasma Pneumonia in Sickle Cell Traitt Mark I. Pensler, MD* and Jan R. Radke, MD* A patient with Down's syndrome and sickle cell trait developed the adult respiratory distress syndrome and cerebral infarction during infection with Mycoplasma pneumoniae. The slow recovery of pulmonary function was unrelated to antimicrobial therapy. Sickle cell trait may N4ycoplasma pneumoniae usually causes upper respira-tory tract symptoms or a mild pneumonia (1), although severe complications (2,3) are occasionally seen. Un-usually severe cases have been reported previously in both sickle cell (4) and sickle cell-hemoglobin C disease (5,6). This report describes the clinical course of a patient with sickle cell trait who developed rising complement fixation titers to M. pneumoniae. Case Report A 21-year-old black man with Down's syndrome was admitted to Henry Ford Hospital in severe respiratory distress with a one-week history of sore throat, sneezing, and increased respiratory secre-tions. An older brother had similar symptoms. After admission, the patient developed anorexia, fever, headache, and shortness of breath followed by sudden weakness of his right side. He had no known cardiac disease. Physical examination revealed an agitated patient in marked respiratory distress. His temperature was 39.5°C, blood pressure 100/80 mm Hg, and pulse 104/minute and regular. Typical stigmata of Down's syndrome were present. The tympanic mem-branes and the carotid pulses were normal; no bruits were noted. Inspiratory crackles were heard over both lower lung fields ante-riorly and posteriorly. There was conjugate deviation of the eyes to the left. His right arm and leg exhibited flaccid hemiparesis. Submitted for publication: November 2, 1979 Accepted for publication: December 14, 1979 * Department of Internal Medicine, Division of Pulmonary Medicine, Henry Ford Hospital Address reprint requests to Dr. Pensler, Departmentof Internal Medicine, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, Ml 48202 tThis paper received the Annual In-Training Manuscript Award. be a nsk factor for severe M. pneumoniae infection. The possible underlying mechanism for this relationship is ex-plored, and the relationship between sickle cell trait, cold agglutinins, and the cerebral infarction is discussed. and the Babinski response was extensor on the right. The re-mainder of the examination was unremarkable. A chest radiograph (Fig. 1) revealed diffuse infiltrates in both lung fields. The hemoglobin was 8.3 gm% with no sickle forms noted on peripheral smear. On room air the arterial blood oxygen tension (PaOj) was 32 mm Hg, arterial blood carbon dioxide (PaCOj) was40 mm Hg, and pH 7.32. Cram stain ofthe yellowish sputum revealed numerous polymorphonuclear leukocytes but no organisms. Cerebrospinal fluid was clear, colorless, and with-out cells or organisms. Because of the progressive respiratoryfailure, the patient required ventilatory support. Pulmonary and femoral arterial catheters were inserted. Positive end expiratory pressure (PEEP) of 10 cm of water was added to help decrease inspired oxygen concentration and venous admixture. The patient received erythromycin (1 gm every 6 hours), nafcillin, and gentamycin, although only the erythromycin was continued after sputum and blood cultures were reported to be negative. A neurology consultant agreed with thediagnosisof a large infarct in the disttibution of the left middle cerebral artery. The cold agglutinin titer was 1:2,048 on day 1 and 1:131,072 on day 11. Complement fixation level for M. pneumoniae was 1:64 on day 1 and 1:512 on day 11. Hemoglobin electrophoresis revealed hemoglobin A at 65.1%, hemoglobin A2 at 2.6%, and hemoglobin S at 32.3%. The patient was anergic. Serum protein and Immunoelectrophoresis showed no immunoglobin defi-ciency. Intracerebral hemorrhage, abscess, and subdural hema-toma were ruled out because computerized tomography of the brain revealed no abnormality on day 1. An echocardiogram was normal. The patient's respiratory status stabilized, and he was switched to continuous positive a'\rway pressure (CPAP) on day 6. Progress was slow, and CPAP was required until day 18. Finally on day 30 the patient was discharged with an expressive aphasia, complete paralysis of the right arm, and minimal weakness of the right leg. 60 Mycoplasma pneumoniae Complications Fig.1 chest radiograph on admission revealed diffuse infiltrates. Discussion Frequent symptoms in the usual benign case of My-coplasma pneumoniae infection include fever, cough, headache, chills, and malaise. Nasal symptoms and sore throat are seen in approximately halfthe cases (1). When the lung becomes involved, the radiograph typically re-veals unilateral broncho-pneumonia ofthe lower lobes (3). Patients who are adequately treated improve rapidly with defervescence in one to three days. Our patient presented in this typical fashion, with upper respiratory tract symp-toms and a recent family history of a similar illness. How-ever, the onset of the pneumonia was extremely rapid and fulminant, and he developed the adult respiratory distress syndrome (ARDS), which is a rarely reported complication of M. pneumoniae infection. Fishman et al (2) described two cases of ARDS caused by M. pneumoniae, but the diagnosis was made retrospec-tively, and no specific therapy was given. Jastremski (7) reported three cases of ARDS in M. pneumoniae infection. One patient died within 24 hours, and the other two needed seven to ten days of PEEP before they recovered. The prolonged requirement for PEEP/CPAP (18 days) in our patient suggests that early administration of erythromycin (started on day 1) does not alter the clinical course of this complication. M. pneumoniae has been reported to cause unusually severe infections in both sickle cell (4) and sickle cell-hemoglobin C (5, 6) disease. The reason for this relation-ship is unclear, although complicating pulmonary infarc-tion has been suggested. In situ pulmonary thrombosis has been diagnosed in a patient with sickle cell trait (9), but whether in situ pulmonary thrombosis occurred in our patient and perpetuated the ARDS cannot be proven. The second feature of interest is the development of cere-bral infarction in a patient with sickle cell trait Sears (8) states that sickle cell trait is a benign disese in which only rare kidney and splenic abnormalities are proven com-plications. Although he cited case reports of large vessel occlusions involving cerebral and pulmonary arteries, he did not believe an association had been clearly established. Also, there have been no documented cases of hemiplegia in M. pneumoniae infection (3). Therefore, the etiology of the cerebral thrombosis in our patient is speculative; how-ever, two explanations seem feasible. Sickle cell trait erythrocytes have been shown to sickle in vitro when conditions of acidosis and hypoxia exist (14, 15). It is possible that the profound hypoxemia and acidosis secondary to the ARDS induced sickling, with resulting thrombosis in the cerebral circulation. A second possible mechanism involves cold agglutinins which cause a dis-ease of skin capillaries of exposed extremities, resulting in acrocyanosis and Raynaud's phenomenon (13). These alone, however, would not cause large vessel thrombosis. Burchmore (16) documented a case of tibial artery occlu-sion in a patient with sickle cell-hemoglobin C disease and high levels of cold agglutinins. Thus, some interaction between sickling and cold agglutinins is possible. Finally, it is doubtful that Down's syndrome had anything to do with the severity of our case, since Down's patients have only mild immunologic deficiencies (10, 11). In fact, there is some indication that immunodeficient states actu-ally lessen the degree of pneumonia in patients with M. pneumoniae infection (6, 12). We speculate that the un-usually prolonged and severe course of M. pneumoniae infection in this patient, with complications of ARDS and cerebral thrombosis, are due to the synergistic effects of hypoxemia, acidosis, high cold agglutinins, and sickle cell trait. 61 Pensler and Radke References 1. Purcell RH, Chanock RM. Role of Mycoplasma in human respiratory disease. Med Clin NA 1967;51:791. 2. Fishman RA, Marschall KE, Kislak JW, et al. Adult respiratory distress syndrome caused by Mycoplasma pneumoniae. CHEST 1978;74:471. 3. Murray HW, Masur H, Senterfit LB, et al. The protean manifestations of Mycop lasma pneumoniae in fect ion in adults. Am J Med 1975:58:229. 4. Schulman ST, Bartlett J, Clyde WA, et al. The unusual severity of Mycoplasma pneumonia in children with sickle-cell disease. N Engl J Med 1972;287:164. 5. Chusid MJ, Lachman BS, Lazerson J. Severe mycoplasma pneumonia and vesicular erupt ion in SC hemoglob inopathy . J Pediatr 1978:93:449. 6. Solanki DL, Bordoff RL. Severe Mycoplasma pneumonia with pleural effusions in a patient wi th sickle cell-hemoglobin C (SC) disease. Am J Med 1979:66:707. 7. Jastremski MS. Adul t respiratory distress syndrome due to My -coplasma pneumoniae. CHEST 1979;75:529. 8. Sears DA. The morbidity of sickle cell trait. Am J Med 1978:64:21. 9. Israel RH, Saliponte JS. Pulmonary infarction in sickle cell trait. Am J Med 1979:66:867. 10. Steihm ER, Fulginiti VA. Immunologic disorders in infants and chi l -dren. Philadelphia: WB Saunders, 1973:556. 11. Mil ler DG. Immunological disturbances in lymphoma and leukemia. In: Somter M, ed. Immunological diseases. Boston: Little, Brown, 1971. 12. Foy HM, Ochs H, Dans SD, et al. Mycoplasma pneumoniae infection in patients with immunodeficiency syndromes: Report of four cases. J Infect Dis 1973;127:388. 13. Schuboth H. The co ld hemagglu t in in disease. Semin Hemato l 1966:3:27. 14. Lange RD, Minnich V, Moore CV. Effect of oxygen tension and of pH on the sickling and mechanical fragility of erythrocytes wi th sickle cell anemia and the sickle cell trait. J Lab Clin Med 1951:37:789. 15. Barreras L, Diggs LW. Bicarbonate, pH and percentage of sickle cells in venous blood of patients in sickle cell crisis. Am J Med Sci 1964:274:710. 16. Burchmore |W, Buckle RM, Lehmann H, et al. Agglutinating-sickling arterial thrombosis. Lancet 1962:2:1008. 62 

ARDS and Cerebral Infarction Complicating Mycoplasma Pneumonia in Sickle Cell Trait

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ARDS and Cerebral Infarction Complicating Mycoplasma Pneumonia in Sickle Cell Trait

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