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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dapsone (4,4'-diaminodiphenylsulfone) is recommended as an alternative agent for prophylaxis against Pneumocystis carinii in children with human immunodeficiency virus infection. We reviewed our experience over the past 100 months with 20 children (age range, 2 months to 13 years) who received dapsone and examined the safety and efficacy of this regimen. Dapsone was taken for an average of 7.33 months/patient or a total of 4410 days by those children in whom safety could be assessed. Three of the 20 patients had an adverse reaction to dapsone. One had mild elevation of blood methemoglobin values (5.6%) and transient elevation of serum transaminases that resolved without discontinuing drug. The other two developed allergic skin rashes which necessitated discontinuation. Efficacy of dapsone in preventing P. carinii pneumonia (PCP) was assessed in 16 children at high risk for developing PCP (defined by CD4 counts or prior PCP infection). These 16 children took dapsone for an average of 6.88 months and a total of 3300 days. Two of the 16 high risk children, one who had had a previous P. carinii pneumonia, developed PCP while taking dapsone. Both had CD4 counts < or = 200 cells/mm3 and were taking dapsone for > or = 12 months before developing PCP. Dapsone is well-tolerated in children and appears to be as effective in preventing PCP in children with human immunodeficiency virus infection as it is in adults.
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PMID:Efficacy and safety of dapsone prophylaxis against Pneumocystis carinii pneumonia in human immunodeficiency virus-infected children. 817 Jul 43

Sickle cell anemia (SCA) is a disease caused by production of abnormal hemoglobin, which binds with other abnormal hemoglobin molecules within the red blood cell to cause rigid deformation of the cell. This deformation impairs the ability of the cell to pass through small vascular channels; sludging and congestion of vascular beds may result, followed by tissue ischemia and infarction. Infarction is common throughout the body in the patient with SCA, and it is responsible for the earliest clinical manifestation, the acute pain crisis, which is thought to result from marrow infarction. Over time, such insults result in medullary bone infarcts and epiphyseal osteonecrosis. In the brain, white matter and gray matter infarcts are seen, causing cognitive impairment and functional neurologic deficits. The lungs are also commonly affected, with infarcts, emboli (from marrow infarcts and fat necrosis), and a markedly increased propensity for pneumonia. The liver, spleen, and kidney may experience infarction as well. An unusual but life-threatening complication of SCA is sequestration syndrome, wherein a considerable amount of the intravascular volume is sequestered in an organ (usually the spleen), causing vascular collapse; its pathogenesis is unknown. Finally, because the red blood cells are abnormal, they are removed from the circulation, resulting in a hemolytic anemia. For the patient with SCA, however, the ischemic complications of the disease far outweigh the anemia in clinical importance.
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PMID:Sickle cell anemia. 1145 73

This report describes a case of methemoglobinemia in association with dapsone therapy. The patient, an immunocompromised child with chronic immune thrombocytopenic purpura, presented with fever, cough, perioral cyanosis, bilateral lower lobe rales, and low O2 saturation by pulse oximetry (89%). His medications included prednisone and rituximab for chronic immune thrombocytopenic purpura, and dapsone for Pneumocystis carinii pneumonia prophylaxis. Because of his lack of dyspnea and tachypnea, and the temporal association of his perioral cyanosis with the initiation of dapsone therapy, a methemoglobin (MetHb) level was obtained and found to be elevated at 9.6%. The authors discuss the mechanism and treatment of methemoglobinemia secondary to dapsone. They also stress the importance of monitoring for signs and symptoms of methemoglobinemia in immunocompromised patients on dapsone therapy for P. carinii pneumonia prophylaxis.
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PMID:Methemoglobinemia associated with dapsone therapy in a child with pneumonia and chronic immune thrombocytopenic purpura. 1679 11

Posttransplant lymphoproliferative disorder (PTLD) is a serious complication after solid organ transplantation. An elevated serum lactate dehydrogenase (LDH) is a marker of PTLD activity. We report the case of a 58-year-old female renal transplant patient with a prior history of extranodal PTLD, which developed 19 years after a second transplant. She was successfully treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) and maintained subsequently on sirolimus and prednisone. She presented 3 years later with fever, dyspnea, cough, lung infiltrates and elevated serum LDH concerning for recurrence of PTLD. Bronchoscopy revealed Pneumocystis carinii (jiroveci) pneumonia. The patient was treated with trimethoprim-sulfamethoxazole, but developed nausea and was converted to dapsone. The patient was readmitted 4 weeks later with increasing dyspnea and hypoxemia and found to have a methemoglobin level of 16%. Dapsone was discontinued with resolution of all symptoms. We discuss the diagnostic and clinical challenges in this complex case.
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PMID:Didactic lessons from the serum lactate dehydrogenase posttransplant: a clinical vignette. 1829 52

Previously, we have shown that gaseous Nitric oxide (gNO) has great potential as an effective topical anti-infective agent for non-healing wounds due to its non-specific antimicrobial properties. These same antimicrobial attributes may be useful for pulmonary infections. However, gNO would have limited usefulness as an inhaled antimicrobial agent as continuous exposure to the concentration required for a bactericidal effect (160-200 ppm) leads to methemoglobinemia. To overcome this problem, we investigated whether a thirty minute exposure of 160 ppm every four hours would retain the same antimicrobial effect as continuous delivery. In vitro, exposure of clinical multi-drug resistant Staphylococcus aureus and Escherichia coli strains isolated from the lungs of nosocomial pneumonia patients and a lethal antibiotic-resistant strain of Pseudomonas aeruginosa, isolated from a deceased cystic fibrosis patient resulted in over a 5 log(10) reduction in bacterial load after multiple thirty minute treatments (4 cycles) every four hours to 160 ppm gNO. The intermittent regimen required 320 (SD=0)ppm h for 100% lethality whereas the continuous exposure required 800 (SD=160)ppm h. We have also shown that selection for a gNO resistant phenotype did not lead to decrease sensitivity to gNO therapy (p>0.05). In addition, no host cellular toxicity was observed in human THP-1 monocytes and macrophages following intermittent delivery of a high concentration of gNO, and the proliferation and migration of pulmonary epithelial cells was not adversely affected by the administration of intermittent high-dose gNO. These results justify further studies that should focus on whether intermittent delivery of 160 ppm of gNO every four hours can technically be administered while keeping inhaled NO(2) levels less than 2 ppm and methemoglobin saturation less than 2.5 percent.
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PMID:Gaseous nitric oxide bactericidal activity retained during intermittent high-dose short duration exposure. 1878 93

In most cases of uncomplicated lobar pneumonia the decrease of respiratory surface is completely compensated for, and the oxygen content of the blood is within normal limits. Occasional cases of uncomplicated pneumonia have an oxygen content of the venous blood which is below normal. In the two cases reported here, this was associated with a carbon dioxide content of the blood which was higher than normally, and the condition was apparently due to an interference with the respiratory exchange of gases. In the terminal stage of the fatal cases of pneumonia in which death does not occur with great suddenness, there is often a progressive diminution in the oxygen content of the blood. Synchronous with this is a progressive decrease in the oxygen-combining capacity of the blood. These changes are usually seen in patients in whom an intense bacteremia has developed and are analogous to those found in the arterial blood of infected rabbits, and to those resulting from the growth of the pneumococcus in blood in vitro. In all three conditions there is probably a change of oxyhemoglobin to methemoglobin. This change of the hemoglobin molecule, so that it no longer takes up and gives off oxygen readily, is probably a factor in the immediate cause of death in many cases of pneumonia.
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PMID:THE OXYGEN CONTENT OF THE BLOOD IN LOBAR PNEUMONIA. 1986 86

1. A simple method for arterial puncture is given which does no permanent injury to the artery. Arterial and venous punctures have been done on 33 cases of pneumonia and five normal subjects, and the blood thus obtained has been studied with reference to the oxygen capacity and arterial and venous unsaturation. 2. In five normal subjects the mean arterial unsaturation was 5 per cent of the total oxygen capacity; the mean venous unsaturation was 26.8 per cent. 3. In the pneumonia cases the arterial oxygen unsaturation varied over a wide range. The arterial unsaturation varied from 0.0 to 68.2 per cent, the venous from 14.4 to 85.5 per cent. In the fatal cases as opposed to the non-fatal cases of pneumonia, the mean arterial oxygen unsaturation was 32 per cent as against 13.9 per cent. As a rule, an arterial unsaturation of over 20 per cent was associated with a fatal outcome. Similarly, the mean venous oxygen unsaturation was 57 per cent in the fatal cases and 36.3 per cent in the non-fatal cases. 4. In five cases in which no cyanosis was observed at any time the mean arterial oxygen unsaturation was 5.4 per cent, the mean venous oxygen unsaturation 31.5 per cent. In cases which showed cyanosis of varying degree during the course of the illness, the mean arterial unsaturation was 24.7 per cent, and the mean venous unsaturation 44.5 per cent. Cases without cyanosis have an arterial unsaturation close to the normal. 5. There is a definite relation between the degree of cyanosis and the per cent of arterial unsaturation. With increasing cyanosis the arterial unsaturation becomes greater. The venous unsaturation varies similarly. 6. In individual cases with marked cyanosis associated with high arterial unsaturation, the clinical improvement of the patient and the diminution of the cyanosis are accompanied by a similar diminution in the arterial and venous unsaturation. Conversely, an increase of cyanosis is accompanied by an increase in arterial unsaturation. It is evident that the cyanosis of pneumonia patients is due to the incomplete saturation of venous blood with oxygen in the lungs, and that the various shades of blue observed in the distal parts are caused by an admixture of reduced hemoglobin and oxyhemoglobin in the superficial capillaries. 7. No unusually low total oxygen capacities were observed, even in fatal cases with intense cyanosis. On the contrary, in these cases the total oxygen capacity was unusually high, pointing toward a concentration of the blood. Again in only one case was there any marked fall in the oxygen capacity during the illness. Therefore, methemoglobin formation, in these cases, can hardly have occurred to such an extent as to be an important factor in the production of cyanosis. Of the 33 cases studied, however, only seven were lobar pneumonia, the rest being of types ordinarily unusual, which have accompanied the recent influenza epidemic; and of the seven, not all were in all respects typically lobar. The possibility still remains, therefore, that in typical lobar pneumonia caused by the pneumococcus methemoglobin may play a part in the cyanosis. 8. The oxygen consumption, i.e. difference between arterial and venous contents, was within normal limits, indicating that the cardiac output was not diminished in the cases (chiefly post influenza) of pneumonia studied.
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PMID:THE OXYGEN OF THE ARTERIAL AND VENOUS BLOOD IN PNEUMONIA AND ITS RELATION TO CYANOSIS. 1986 55

In the occasional cases of pneumonia which show a decrease in the oxygen capacity of the blood, the decrease is probably due to a formation of methemoglobin. The latter is removed from the circulation, however, as rapidly as it is formed, so that it can seldom be detected even qualitatively, and is probably never a cause of cyanosis.
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PMID:STUDIES ON BLOOD CHANGES IN PNEUMOCOCCUS INFECTIONS : AN EXPERMENTAL STUDY OF THE FORMATION AND FATE OF METHEMOGLOBIN IN THE BLOOD. 1986 22

The introduction of pulse oximetry in clinical practice has allowed for simple, noninvasive, and reasonably accurate estimation of arterial oxygen saturation. Pulse oximetry is routinely used in the emergency department, the pediatric ward, and in pediatric intensive and perioperative care. However, clinically relevant principles and inherent limitations of the method are not always well understood by health care professionals caring for children. The calculation of the percentage of arterial oxyhemoglobin is based on the distinct characteristics of light absorption in the red and infrared spectra by oxygenated versus deoxygenated hemoglobin and takes advantage of the variation in light absorption caused by the pulsatility of arterial blood. Computation of oxygen saturation is achieved with the use of calibration algorithms. Safe use of pulse oximetry requires knowledge of its limitations, which include motion artifacts, poor perfusion at the site of measurement, irregular rhythms, ambient light or electromagnetic interference, skin pigmentation, nail polish, calibration assumptions, probe positioning, time lag in detecting hypoxic events, venous pulsation, intravenous dyes, and presence of abnormal hemoglobin molecules. In this review we describe the physiologic principles and limitations of pulse oximetry, discuss normal values, and highlight its importance in common pediatric diseases, in which the principle mechanism of hypoxemia is ventilation/perfusion mismatch (eg, asthma exacerbation, acute bronchiolitis, pneumonia) versus hypoventilation (eg, laryngotracheitis, vocal cord dysfunction, foreign-body aspiration in the larynx or trachea). Additional technologic advancements in pulse oximetry and its incorporation into evidence-based clinical algorithms will improve the efficiency of the method in daily pediatric practice.
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PMID:Pulse oximetry in pediatric practice. 2193 May 54

Gaseous nitric oxide (NO) is bactericidal in vitro. However whether and how it can be used for the treatment of bacterial lung infections in patients with cystic fibrosis is unclear. Here we assessed the bactericidal effect of intermittently inhaled 160 ppm NO for 30 min every 4 h in a Pseudomonas aeruginosa pneumonia model in rats. NO significantly reduced P. aeruginosa colony count in rat lungs but did not affect neutrophil myeloperoxidase function methemoglobin percentage nor plasma nitrite/nitrate levels. This regimen warrants exploration in infected patients with cystic fibrosis.
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PMID:Inhaled nitric oxide decreases the bacterial load in a rat model of Pseudomonas aeruginosa pneumonia. 2348 Oct 89


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