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Infant respiratory distress syndrome

Infant respiratory distress syndrome ("RDS", also called "Respiratory distress syndrome of newborn", previously called hyaline membrane disease), is a syndrome caused by developmental lack of surfactant and structural immaturity in the lungs of premature infants. RDS affects about 1% of newborn infants. The incidence decreases with advancing gestational age (length of pregnancy), from about 50% in babies born at 26-28 weeks, to about 25% at 30-31 weeks. The syndrome is more frequent in infants of diabetic mothers and in the second born of premature twins. more...

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Clinical course

Respiratory distress begins shortly after birth, and is manifest by a whining noise, flaring of the nostrils and "sucking in" of the chest wall during breathing efforts. The baby may become cyanotic ("blue") from lack of oxygen in the blood. As the disease progresses, the baby may have respiratory failure, and prolonged cessations of breathing ("apnea"). If untreated, the baby's condition may worsen, and death may ensue. Complications include metabolic exhaustion (acidosis, low blood sugar), patent ductus arteriosus, low blood pressure, chronic lung changes, and intracranial hemorrhage.


The characteristic pathology seen in babies who die from RDS was the source of the name "hyaline membrane disease". These waxy-appearing layers line the collapsed tiny air sacs ("alveoli") of the lung. In addition, the lungs show bleeding, over-distention of airways and damage to the lining cells.


The lungs are developmentally deficient in a material called surfactant, which allows the alveoli to remain open throughout the normal cycle of inhalation and exhalation. Surfactant is a complex system of lipids, proteins and glycoproteins which are produced in specialized lung cells called Type II cells. The surfactant is packaged by the cell in structures called lamellar bodies, and extruded into the alveoli. The lamellar bodies then unfold into a complex lining of the alveoli. This layer serves the purpose of reducing the surface tension which would tend to cause the alveoli to collapse in the presence of gas. Without adequate amounts of surfactant, the alveoli collapse and are very difficult to expand. Microscopically, it is characterized by collapsed alveoli alternating with hyperaerated alveoli, vascular congestion and hyaline membranes (resulted from fibrin, cellular debris, red blood cells, rare neutrophils and macrophages). Hyaline membranes appear like an eosinophilic (pink), amorphous material, lining or filling the alveolar spaces and blocking the gases exchange . The blood (which normally receives oxygen from the alveolar gas and unloads carbon dioxide into the alveoli) passes through the lungs without this vital exchange. Blood oxygen levels fall, and carbon dioxide rises, resulting in rising blood acid levels. Structural immaturity, as manifest by low numbers of alveoli, also contributes to the disease process. It is also clear that the oxygen and breathing treatments used, while life-saving, can also damage the lung. The diagnosis is made by the clinical picture and the chest xray, which has a "ground-glass" appearance.


Most cases of hyaline membrane disease can be prevented if mothers who are about to deliver prematurely can be given a hormone-like substance called glucocorticoid. This speeds the maturation of the lungs and surfactant system. For very premature deliveries, glucocorticoid is given without testing the fetal lung maturity. In pregnancies of greater than 30 weeks, the fetal lung maturity may be tested by sampling the amount of lipid in the amniotic fluid, obtained by inserting a needle through the mother's abdomen and uterus. The maturity level is expressed as the lecithin-sphingomyelin (or "L/S") ratio. If this ratio is less than 2, the fetal lungs are probably immature, and glucocorticoid is given.


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Relapsing fever associated with ARDS in a parturient woman: a case report and review of the literature - adult respiratory distress syndrome
From CHEST, 8/1/92 by R. Dale Davis

We report a patient who survived acute respiratory failure associated with tick-borne relapsing fever in the third trimester of pregnancy. The fetus was delivered by cesarian section and did not have spirochetemia. The severity of the patient's illness may be related to the immunosuppressive effects of pregnancy.

Relapsing fever is an acute infectious disease caused by spirochetal bacteria belonging to the genus Borrelia. The infection is transmitted by two vectors: the body louse Pediculus humanus, and soft ticks of the genus Ornithodoros. Louse-borne relapsing fever is still a public health problem in developing nations, particularly in Africa and South America. In the United States, relapsing fever is a sporadic illness confined to the Western states and thought to be transmitted exclusively by soft ticks. The extent of infection in this country is unknown. A few outbreaks have been investigated,[1-3] but sporadic cases are generally diagnosed by the discovery of spirochetal bacteria on the Wright-stained blood smear.

The spectrum of illnesses from relapsing fever ranges from a mild self-limited illness to severe cases with death resulting from myocarditis[4] or hepatic failure.[5] Transplacental transmission of Borrelia infection has been reported and may result in abortion.[6,7] While relapsing fever may be associated with bronchitis and pneumonia, it has not been reported as a cause of respiratory failure due to adult respiratory distress syndrome (ARDS). We recently cared for a woman who was pregnant and had relapsing fever that was complicated by ARDS.


A 35-year-old woman in the 30th week of a previously uncomplicated pregnancy was admitted to the hospital September 11, 1988, with fever, thrombocytopenia, and shortness of breath. Two weeks earlier, she had been camping in the Wasatch Mountains of Utah. She had not noted any insect bites during this outing. Two days before hospital admission, she developed mild dyspnea and nausea. Bed rest and fluids were prescribed but her symptoms worsened. Vital signs included blood pressure of 100/80 mm Hg, pulse rate of 120/min, respiratory rate of 36 breaths/min, and temperature of 38.4 [degrees] C. Examination of the chest revealed bibasilar inspiratory and expiratory crackles. Results of cardiac examination were normal. Findings from the abdominal examination were compatible with an intrauterine pregnancy of 30 weeks' gestation. Pelvic examination revealed the cervical mucous plug to be intact with no effacement or dilation of the cervix. Noninvasive fetal monitoring disclosed no sign of fetal distress. She had no rash, ecchymosis, or petechiae, and results of neurologic examination were normal. Initial laboratory studies included WBC count of 8,300/cu mm with 45 percent band forms, 48 percent polymorphonuclear cells, 6 percent lymphocytes, and 1 percent mononuclear cells; hemoglobin level was 10.3 g/dl; and platelet count was 24,000/cu mm. Serum fibrinogen level was 780 mg/dl and fibrin split products were not detected. Specimens of blood and urine were obtained for culture; they were later reported as negative. Results from electrolyte and liver function studies were normal.

Chest roentgenogram at the time of hospital admission (Fig 1) showed diffuse bilateral fluffy infiltrates and no pleural effusion or cardiomegaly. Room air blood gas analysis showed profound hypoxemia with a pH of 7.48, PCO[2] of 25 mm Hg, and PO[2] of 45 mm Hg. The hematology technologist noted fine filamentous bacteria on the Wright-stained blood smear (Fig 2). On review, these were noted to have a corkscrew appearance characteristic of Borrelia and a diagnosis of relapsing fever was made.

Because of the combined risks to the fetus of maternal ARDS and of the Jarisch-Herxheimer reaction that may occur after treatment of relapsing fever, the fetus was delivered by cesarean section. There was no evidence of spirochetemia or sepsis in the infant. Following an uncomplicated cesarean section, the mother was transferred to an intensive care unit where she was treated with tetracycline hydrochloride 500 mg intravenously every 6 h. The patient did not experience any period of hemodynamic instability resembling a Jarish-Herxheimer reaction, but her oxygenation worsened and she was intubated. When the patient's respiratory status was at its worst, she required a positive end-expiratory pressure of 11 and FIO[2] of 0.50 to maintain a PO[2] of at least 50 mm Hg. Thrombocytopenia resolved over 48 h and all blood smears obtained after the first day were negative for any evidence of Borrelia. At no time did the patient produce copious amounts of sputum. She was febrile with a temperature to 38.5 [degrees] C through the fourth hospital day and her WBC count rose to 20,300/cu mm. There was no evidence of wound infection or pelvic thrombophlebitis. A lumbar puncture was performed on the fifth hospital day that yielded clear CSF with 1 WBC per cubic millimeter, protein level of 16 mg/dl, and CSF glucose level 77 mg/dl.

On the sixth hospital day, a computed tomographic (CT) scan of her abdomen showed evidence of a large splenic infarction and infarction of the right kidney. An echocardiogram showed no evidence of valvular abnormalities or pericardial effusion. The patient was continued on a regimen of antibiotic therapy. Her oxygenation improved rapidly and, on the day of discharge from the hospital, her arterial blood gas determination while breathing room air showed a pH of 7.43, PCO[2] of 40 mm Hg, and PO[2] of 57 mm. A subsequent chest roentgenogram was normal (Fig 3).


The list of causes of ARDS includes a wide variety of infections. Cases of ARDS due to leptospirosis and Lyme disease have been reported,[8,9] but other spirochete infections have not been associated with this complication. This patient had unequivocal evidence of Borrelia infection based on her blood smear. While one cannot precisely state the reasons for this patient's pulmonary problems, there was no evidence of suppurative pneumonia or cardiogenic pulmonary edema. She did not have a productive cough, and throughout her ventilator course, she had relatively small amounts of bronchial secretions. She had no evidence of congestive heart failure or myocarditis.

The extent and duration of this patient's pulmonary dysfunction may be related either to particular virulence of the organism, to overwhelming infection, or to the immunologic response to the spirochetal illness. The fact that the organism can be observed readily in thin smears of the blood indicates that a massive number of infecting organisms must be present. The occasional occurrence of Jarisch-Herxheimer reactions suggests the organisms may contain substantial amounts of endotoxin or some other mediator of sepsis. Pregnancy may also be a factor in the severity of our patient's illness. For example, in some infections such as influenza A and falciparum malaria, a higher mortality rate in pregnant women than in age-matched controls[10,11] has been attributed to the immunosuppressive effects of pregnancy. Nonspecific antibody rises may also occur in pregnancy and are additional evidence of altered immunologic responses in pregnant women.

Relapsing fever has been reported in Arizona, California, Idaho, Kansas, Montana, Nevada, New Mexico, Oklahoma, Oregon, Texas Utah, and Washington.[12] Victims of the illness generally have a history of outdoor activity but seldom recall a tick bite. Ornithodoros ticks have a painless bite and feed for short periods of time (5 to 20 min), often while the victim sleeps. The diagnosis should be considered in recent visitors to these areas in the setting of significant outdoor exposure, recurrent fevers, and no diagnosis after evaluation for other causes of fever. Relapsing fever has been successfully treated with [beta]-lactam antibiotics as well as erythromycin, chloramphenicol, and tetracyclines.

Tick-borne relapsing fever is generally mild, but both the disease and its treatment can result in serious morbidity and even death. We now add ARDS as another potentially fatal complication of this disease.


[1] Thompson RS, Burgdorfer W, Russell R, Francis BJ. Outbreak of tick-borne relapsing fever in Spokane County, Washington. JAMA 1969; 210:1045-50

[2] Boyer KM, Munford RS, Maupin GO, Pattison CP, Marshall DF, Barnes AM, et al. Tick-borne relapsing fever: an interstate outbreak originating at Grand Canyon National Park. Am J Epidemiol 1977; 5:459-79

[3] Edell TA, Emerson JK, Maupin GO, Barnes AM, Vernon TM. Tick-borne relapsing fever in Colorado: historical review and report of cases. JAMA 1979; 241:2279-82

[4] Parry EHO, Warrell DA, Perine PL, Vukotich D, Bryceson ADM. Some effects of louse-borne relapsing fever on the function of the heart. Am J Med 1970; 49:472-99

[5] Judge DM, Irwin S, Perine PL, Vukotic D. Louse-borne relapsing fever in man. Arch Pathol Lab Med 1974; 97:136-40

[6] Shirts SR, Brown MS, Bobitt JR. Listeriosis and borreliosis as causes of antepartum fever. Obstet Gynecol 1983; 62:256-61

[7] Fuchs PC, Oyama AA. Neonatal relapsing fever due to transplacental transmission of Borrelia. JAMA 1969; 208:690-92

[8] Berendson HH, Rommes JH, Hylkema BS, Meinesz AF, Sluiter HJ. Adult respiratory failure with leptospirosis. Ann Intern Med 1984; 101:402

[9] Kirsch M, Ruben FL, Steere AC, Duray PH, Norden CW, Winkelsein A. Fatal adult respiratory distress syndrome in a patient with Lyme disease. JAMA 1988; 259:2737-39

[10] Gibbs R, Sweet R. Maternal and fetal infections. In: Creasy R, Resnik R, eds. Maternal-fetal medicine. Philadelphia: WB Saunders Co, 1984:646-734

[11] Looareesuwan S, White NJ, Karbwang J, Turner RC, Phillips RE, Kietinun S, et al. Quinine and severe falciparum malaria in late pregnancy. Lancet 1985; 2:4-7

[12] Johnson WD Jr. Borrelia species (relapsing fever). In: Mandell GL, Douglas RG Jr, Bennett JE, eds. Principles and practice of infectious diseases, 3rd ed. New York: Churchill Livingstone Inc, 1990:1816-19

COPYRIGHT 1992 American College of Chest Physicians
COPYRIGHT 2004 Gale Group

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