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At least 19 recordsLinked to original sources
PubMed1992

Smoking is a factor in causing acute chest syndrome in sickle cell anemia.

A link between cigarette smoking and "acute chest syndrome" in sickle cell anemia is suggested. Acute chest syndrome in the patient with sickle cell anemia is characterized by fever, leukocytosis, cough, chest pain, and pulmonary infiltrates in the chest radiograph. This article describes the results of a study of 69 adolescent and young adult sickle cell anemia patients. Twenty-nine of these patients were smokers, three were former smokers, and 37 were nonsmokers. Patients completed respiratory questionnaires that focused on smoking habits and included a history of chest syndrome. Information obtained was confirmed by review of clinical records. The chi-square test demonstrated a strong relationship between cigarette smoking and chest syndrome in sickle cell anemia. All 29 smokers had a history of chest syndrome, but only 24 of 37 nonsmokers had such a history. Although the exact mechanism of the relationship between smoking and the development of acute chest syndrome remains speculative, cigarette smoking joins infection, hypoxia, acidosis, infarction, dehydration, and analgesics as a causative factor in adolescent and adult patients with sickle cell anemia. Behavioral modification of the smoking habit in patients with sickle cell anemia may decrease the frequency of acute chest syndrome and sequelae of sickle cell lung disease.

Acute Disease↗
PubMed1991

Role of Chlamydia pneumoniae in acute chest syndrome of sickle cell disease.

Children with sickle cell disease and acute chest syndrome were investigated for infection with Chlamydia pneumoniae and Mycoplasma pneumoniae. Of 30 patients who had 32 episodes of acute chest syndrome, four (13%) had C. pneumoniae isolated from the nasopharynx; two of these also had serologic evidence of acute infection, and one had positive nasopharyngeal isolates on two subsequent occasions during the course of 1 year with stable, elevated titers of anti-C. pneumoniae IgG, suggesting chronic infection. Two patients with negative cultures had serologic evidence of infection with C. pneumoniae. None of 32 cultures for M. pneumoniae were positive, and although anti-M. pneumoniae IgM developed in two patients, one of these patients had evidence of C. pneumoniae infection (positive culture and seroconversion). We conclude that C. pneumoniae infection is prevalent in our sickle cell population with acute chest syndrome. Until further studies clarify the pathophysiologic significance of C. pneumoniae infection, we believe that early inclusion of erythromycin as antimicrobial therapy for acute chest syndrome seems reasonable.

Adolescent↗
PubMed1991

Results of bronchoscopically obtained lower airway cultures from adult sickle cell disease patients with the acute chest syndrome.

PURPOSE: The purpose of this study was to determine the frequency of bacterial pneumonia as a cause of the acute chest syndrome in adult patients with sickle cell disease based on bronchoscopically obtained lower airway cultures and to describe the clinical, laboratory, and roentgenographic features of the acute chest syndrome in a series composed entirely of adult patients with sickle cell disease. PATIENTS AND METHODS: We reviewed the hospital records from 19 episodes (18 patients) of acute chest syndrome in adult patients with sickle cell disease (greater than or equal to 19 years of age) who had undergone flexible bronchoscopy to obtain lower airway cultures between January 1979 and July 1987. We also recorded patients' clinical, laboratory, and roentgenographic characteristics. RESULTS: Pneumonia was diagnosed in four of 19 episodes (21%) of acute chest syndrome based on quantitative cultures obtained at bronchoscopy. The pneumonia was caused by Streptococcus pneumoniae in two patients and mixed aerobic and anaerobic organisms in the other two patients. Forty-four of 45 blood cultures were negative, and one grew Staphylococcus epidermidis, which was considered a contaminant. Chest roentgenograms revealed lower lobe involvement in 17 episodes (90%) and bilateral infiltrates in six (32%). Pleural effusions occurred in seven episodes (37%), and pleural fluid samples obtained from five of these revealed sterile exudates. CONCLUSION: The results of this retrospective study suggest that bacterial pneumonia is an uncommon cause of acute chest syndrome in adult patients with sickle cell disease. These results are consistent with previous retrospective studies using noninvasive techniques to diagnose pneumonia. Nevertheless, there appeared to be no reliable noninvasive variables that could accurately differentiate between patients with and without pneumonia and, consequently, we recommend empiric antibiotic therapy in addition to usual supportive care of these patients.

Adult↗
PubMed1985

Acute chest syndrome in sickle cell disease: etiology and clinical correlates.

Acute chest syndrome (ACS) is a new pulmonic process in a clinically ill patient with sickle cell disease. We prospectively analyzed 102 episodes of ACS in patients in our hospital during a 2-year period to study cause and clinical correlates. In 12% of the episodes, ACS was judged to be secondary to bacterial pneumonia (including only 3% secondary to Streptococcus pneumoniae), 8% was associated with uncomplicated viral pneumonias, and 16% with mycoplasmal pneumonias. The clinical course and seasonal variations in these groups were compared with those in the remaining 64% of episodes. In comparison with episodes of ACS of undetermined origin (presumably secondary to pulmonary infarct, atelectasis, or missed infections), patients with bacterial pneumonia were sicker, as shown by fever and hospitalization of longer duration, the percent of those requiring red blood cell transfusion, and the presence of pleural effusions. The lower incidence of bacterial pneumonias among our patients compared with that previously reported may reflect our use of penicillin prophylaxis and pneumococcal immunization to prevent S. pneumoniae infections.

Acute Disease↗
PubMed1991

Peak expiratory flow rate and the acute chest syndrome in homozygous sickle cell disease.

The peak expiratory flow rate (PEFR) was studied in 20 matched pairs of children with homozygous sickle cell disease with either no episodes or six or more episodes of acute chest syndrome. The pairs were carefully matched for height and a highly significant reduction in PEFR was observed in children with multiple episodes of acute chest syndrome. Lateral and anteroposterior chest diameters and chest circumference correlated with PEFR but did not differ between index and control cases. The most likely cause of the reduced PEFR in children with multiple episodes of acute chest syndrome is an accumulating pulmonary fibrosis that decreases lung compliance.

Acute Disease↗
PubMed1985

Acute reversible pulmonary ischemia. A cause of the acute chest syndrome in sickle cell disease.

A 6-year-old girl with sickle cell disease was admitted to the hospital with the diagnosis of the acute chest syndrome. The laboratory findings and the radionuclear lung scan supported a diagnosis of pulmonary infarction rather than pneumonia. She improved with intravenous fluids, oxygen, penicillin, and theophylline. The most likely explanation for the rapid resolution of the clinical syndrome, the chest x-ray, and lung scan abnormalities is that masses of sickled cells caused transient pulmonary vascular occlusion leading to perfusion defects and ischemia, and that the sickled cell thrombi were dislodged before the infarction occurred. To our knowledge, this phenomenon has not been described as a cause of the acute chest syndrome in sickle cell disease in children.

Acute Disease↗
PubMed1979

"Acute chest syndrome" in adults with sickle cell anemia. Microbiology, treatment, and prevention.

Fifty-two episodes of fever, chest pain, increased leukocytosis, and pulmonary infiltrate ("acute chest syndrome") were studied in 28 adults with sickle cell anemia. Possible bacterial pathogens were identified in sputum cultures from less than half of the episodes; no pneumococci were found, and Staphylocococcus aureus was the only bacterium associated with a longer illness than that seen when only normal flora were recovered. Much disease diagnosed as "pneumonia" in adults with sickle cell anemia is probably pulmonary infarction. Many of these patients will recover with no more than modest supportive care; if antibiotics are used they should be directed against S aureus (and possibly Hemophilus species). Pneumococcal polysaccharide vaccine has great potential for preventing life-threatening infection in children with sickle cell anemia, but may not change the incidence or severity of the acute chest syndrome in adults.

Acute Disease↗
PubMed1990

Acute chest syndrome in children with sickle cell anemia.

Vaso-occlusive crisis is the most common cause of morbidity in patients with sickle cell anemia (SCA). Those patients are frequently admitted with chest signs and symptoms suggesting an infective process. The term acute chest syndrome (ACS) is used to describe those chest episodes in SCA patients, and it is postulated that a primary bone vaso-occlusive crisis may be the cause of the acute chest syndrome in SCA patients. In this study we report 52 episodes of ACS in a group of 22 children with SCA. Chest pain, fever, and leukocytosis were a constant clinical finding. The hematological, radiological, and bacteriological studies are reported. There is a constant and significant fall in hemoglobin levels from 88 +/- 10 g/L (8.8 +/- 1.0 g/dl) to 68 +/- 15 g/L (6.8 +/- 5 g/dl). Unilateral or bilateral pulmonary basal infiltrations were found in 50 episodes. Pleural effusion was noticed in 60 episodes, and it was bilateral in three. No significant bacteriological findings were present.

Adolescent↗
PubMed1986

Acute chest syndrome in children with sickle cell disease. A retrospective analysis of 100 hospitalized cases.

We reviewed the clinical features of 100 cases of the sickle cell chest syndrome in 57 pediatric patients hospitalized with radiographic findings of pulmonary or pleural disease. Pulmonary infiltration was more common in the lower lobes (86%) than in the upper (25%) or middle lobes (22%). Pleural effusions were present in 38% of cases. Chest syndrome was recognized on presentation in 79% of cases, but was recognized only later in 21% of patients admitted for other indications. Patients recognized initially were more often febrile on admission (68%) than were subsequently recognized patients (33%) (p less than 0.01), but fever eventually occurred in 99 of 100 cases. Pain was an antecedent or coincident problem in 67% of cases. Median hospital stay was 7 days in those 58 cases in which narcotics were given, but only 4 days in those 42 cases in which narcotics were not administered (p less than 0.001). Polyvalent pneumococcal vaccine had been administered to 44 of our 57 patients at some time before their hospitalizations, and 18 patients had been on oral penicillin prophylaxis. Blood was cultured in 93 cases and in only two instances grew Streptococcus pneumoniae. Serologic evidence of Hemophilus influenzae type b infection was found in two additional patients. We conclude that the sickle cell chest syndrome is an acute febrile pulmonary disease frequently associated with pain and/or narcotic analgesic therapy but infrequently associated with proven bacterial infection.

Adolescent↗
PubMed1991

Rib infarcts and acute chest syndrome in sickle cell diseases.

In the absence of evidence for pneumonia or pulmonary embolus, primary pulmonary infarction has been assumed to be the cause of the syndrome of chest pain, fever, and pulmonary infiltrate on chest X-ray that commonly complicates sickle cell anaemia. To find out whether the syndrome might be due to rib infarction, 99mTc-diphosphonate bone scans were done. In the eleven episodes thus investigated (10 patients) the scans showed segmental areas of increased radionuclide uptake in ribs, indicative of bone infarction. A possible sequence of events is that the rib infarcts are primary and cause bone pain, followed by soft tissue reaction, pleuritis, and splinting. The resultant hypoventilation leads to atelectasis and subsequent development of the radiographic changes of the acute chest syndrome. Prevention of hypoventilation and treatment of bone pain are important therapeutic goals.

Acute Disease↗
PubMed1989

Evolution of acute chest syndrome in sickle cell trait: an ultrastructural and light microscopic study.

Light and electron microscopic studies of a patient with sickle cell trait who had an episode of sickling during coronary artery surgery, from which he died, showed fibrin thrombi, focal alveolar wall necrosis, and epithelial cell damage. It is suggested that in cases of sickle trait full precautionary measures should be taken to prevent sickling in these circumstances.

Acute Disease↗
PubMed1991

The red cell distribution width in sickle cell disease--is it of clinical value?

The red cell distribution width (RDW) has been studied during the clinical steady state in 1121 patients with homozygous sickle cell (SS) disease, 344 with sickle cell-haemoglobin C (SC) disease, 68 with sickle cell-beta+ thalassaemia, 49 with sickle cell beta 0 thalassaemia and in 130 control subjects with a normal (AA) genotype. The mean RDW was moderately increased in S beta + thalassaemia and SC disease and markedly increased in S beta 0 thalassaemia and SS disease. In SS, SC and S beta 0 thalassaemia genotypes, lower RDW values occurred in females and with alpha thalassaemia. The RDW correlated negatively with total haemoglobin, mean cell haemoglobin concentration, mean cell volume, and fetal haemoglobin (HbF) and positively with reticulocyte count in SS disease. A low RDW was associated with higher weight and less frequent dactylitis, painful crisis, acute chest syndrome, acute splenic sequestration, and hospital admissions. A low RDW in SS disease is consistent with a high total haemoglobin, high HbF, low reticulocyte count, alpha thalassaemia, and a more mild clinical course.

Adolescent↗
PubMed1986

Plasma exchange for acute cholestasis in homozygous sickle cell disease.

A child with sickle cell disease presented acute chest syndrome, acute cholestasis and a neurological syndrome. Bilirubin, LDH, alkaline phosphatase, urea and creatinines were markedly increased. Circulating immune complexes were slightly elevated. The patient improved dramatically after a plasma exchange.

Acute Disease↗
PubMed1989

Management of acute chest pain syndrome.

In differentiating the various etiologies of acute chest pain syndromes, the clinician is faced with identifying life-threatening situations. This article has presented a diagnostic approach for establishing the cardiovascular and noncardiovascular etiologies of acute chest pain syndromes. Cardiovascular etiologies must be identified early upon presentation in order to minimize morbidity and mortality. Myocardial ischemia and particularly necrosis is time dependent: early intervention preserves myocardium, particularly when initiating thrombolytic therapy. Aortic valvular disease, particularly critical aortic stenosis, if unrecognized, can precipitate rapid patient deterioration if inappropriately treated with nitrate therapy for presumed ischemic disease. Aortic dissection, if not properly diagnosed, can progress to stroke, MI, paralysis, and death. Noncardiovascular etiologies are similarly complex but often have less potential for life-threatening consequences. In identifying gastrointestinal bleeding, a careful rectal exam may be safely performed even in the setting of MI. A tension pneumothorax can suddenly compromise vascular return and progress to sudden death if unrecognized. Finally, chest wall symptoms, though seldom life-threatening, can be debilitating to the patient and often respond to anti-inflammatory therapy. In conclusion, the goals of this article were to present a step-wise approach to the diagnosis and management of an often complex presentation. By systematically approaching these patients with a thorough understanding of etiologies, diagnostic options, and therapeutic considerations, both physician anxiety as well as patient complications will be greatly diminished.

Angina Pectoris↗