Evidence Of Pulmonary Hemorrhage Research Articles

Acute leptospirosis in horses: A retrospective study of 11 cases (2015-2023).

Reports of leptospirosis in horses are limited. To describe the clinical and diagnostic findings of acute systemic leptospirosis in horses. Eleven client-owned horses presented to an equine hospital because of acute onset of disease between 2015 and 2023. Retrospective case series. Horses diagnosed with leptospirosis by 1 or more of urine PCR, serologic microscopic agglutination test (MAT), and histopathology. Common clinical signs included lethargy (10), anorexia (10), fever (9), tachypnea (9), abnormal lung sounds (9), and epistaxis (6). Acute kidney injury was present in all cases. Evidence of pulmonary hemorrhage and liver disease was found in 8 (73%) and 6 (55%) horses, respectively. In 6 (55%) horses, kidneys, lungs, and liver were affected. Urine quantitative polymerase chain reaction for detection of pathogenic Leptospira spp. was positive in 6 (55%) cases. On serology Leptospira interrogans serovar Australis, Autumnalis, and Bratislava accounted for 86% of all titers ≥1 : 800. Overall case fatality rate was 4/11 (36%). Main findings on necropsy were tubular necrosis, interstitial nephritis, hemorrhage in the alveoli, pulmonary edema, periportal hepatitis and necrosis, cholestasis, and cholangitis. Leptospirosis should be considered as a differential diagnosis in horses with evidence of acute systemic inflammation and acute renal injury, epistaxis, or hepatic disease. For increased likelihood of identifying positive cases, both MAT serology and urine PCR should be performed.

Hemoptysis and Upper Gastrointestinal Bleeding In Two Patients Presenting With Aluminum Phosphate Intoxication (Oral and Inhaled): A Case Study

Introduction: The inhalation of aluminum phosphate and ingestion of aluminum phosphate tablets lead to clinical toxicity with different and nonspecific clinical symptoms. Two patients referred to Imam Reza Hospital Poisoning Emergency Center of Mashhad, Iran, one of whom was a 28-year-old male with oral consumption of four aluminum phosphide tablets, and the second case was a 29-year-old woman who was poisoned by inhalation. Both cases had symptoms of pulmonary and upper gastrointestinal bleeding during the brief hospitalization that resulted in their mortalities. Case Report: The first case is a 29-year-old man who consumed four oral tablets about 1.5 h before referral. He was intubated with the evidence of hemoptysis and upper gastrointestinal bleeding after about 4 h. The second patient is a young woman who had abdominal pain, nausea, and vomiting since the day before referral, and she told that she did not have any underlying diseases. During stabilization and patient evaluation, she suddenly became unresponsive with asystole. The CPR started with the evidence of hemorrhage within the intubation tube. Conclusion: There are currently no studies or reports of hemorrhagic complications in patients. In these two cases, there was no evidence of pulmonary hemorrhage and upper gastrointestinal bleeding which warrants further investigation and evaluation considering that these patients were young and with no underlying disease.

Management with High Frequency Ventilation of Acute Idiopathic Pulmonary Hemorrhage in Infants

Acute idiopathic pulmonary hemorrhage in infants (AIPHI) is characterized by a sudden onset of pulmonary hemorrhage in previous healthy infants. Evidence of pulmonary hemorrhage may present as hemoptysis or a finding of blood in the nose or airway with no evidence of upper respiratory or gastrointestinal bleeding. Patients presenting with acute, severe respiratory distress or failure, and those requiring mechanical ventilation and often demonstrate bilateral infiltrates by chest radiography. We report a case of AIPHI which developed during the induction of anesthesia. A 3-month-old male infant received right herniorraphy under general endotracheal anesthesia. After intubation, blood tinged fluid was aspirated using an endotracheal tube during operation. Chest radiography showed bilateral ground glass opacity. We transferred the patient to the ICU and applied conventional mechanical ventilation. However hypoxemia and respiratory acidosis were persisted. We then switched to a high frequency ventilator (HFV), the hypoxemia and respiratory acidosis were corrected. The patient was transferred to the general ward on the 7th postoperative day.

Sudden death among patients with acute promyelocytic leukemia treated with arsenic trioxide

Arsenic trioxide has been shown to be effective in treating acute promyelocytic leukemia (APL), with minimal overall toxicity reported to date. A phase I/II study was initiated in June 1998 using arsenic trioxide for relapsed APL to determine the maximum tolerated or minimal effective dose and to determine the efficacy of treatment at that dose. Ten patients received 1 to 4 monthly cycles of treatment with 0.1 mg/kg per day intravenous arsenic trioxide. Six of 7 patients evaluable for response achieved cytogenetic or molecular complete remission. However, 3 patients died suddenly during the first cycle of treatment. Autopsies obtained on 2 of these failed to identify a cause of sudden death, despite evidence of pulmonary hemorrhage in one. A third patient, for whom an autopsy was not performed, became asystolic and died while on continuous cardiac telemetry. These observations suggest that arsenic trioxide may be significantly or even fatally toxic at doses currently used and that caution is warranted in its use.

Exercise-induced pulmonary hemorrhage

Exercise-induced pulmonary hemorrhage (EIPH) is characterizedby the presence of blood in the tracheobronchial airways after exercise. Most breeds used for strenuous exercise are affected. The prevalence of EIPH, irrespective of geographical location, has been reported to vary from 30% in Standardbred racehorses to 70% in Thoroughbred horses used for racing, jumping, eventing, steeplechase and polo. In addition to endoscopic confirmation, pulmonary hemorrhage can be recognized by identification of hemosiderophages (macrophages containing intracytoplasmic hemosiderin) in aspirates of tracheobronchial secretions. Detailed examinations of lungs from horses with a confirmed history of EIPH have identified certain consistent morphologic features that provide strong circumstantial evidence for bronchial arterial bleeding. Evidence of pulmonary hemorrhage is characteristically seen in the dorsocaudal regions of the caudal lung lobes. Stained a light brown-bronze color these regions are symmetrically distributed and in the inflated lung have a fine reticular pattern. The subpleural bronchial arteries are more prominent and appear enlarged and more tortuous in stained regions of the lung. Subgross examination of transverse slices of the caudal lung suggest that the hemorrhage occurs primarily in the dorsal bronchopulmonary segments with the dorsobasal bronchopulmonary segment being most severely involved. Affected regions have gross evidence of small airway disease with increased bronchial arterial supply around these airways and within the parenchyma. On microscopy, affected parenchymal regions have extensive interstitial fibrosis. Large accumulations of hemosiderophages are located within airspaces, terminal airways and within the increased connective tissue around airspaces and airways. Microangiographs of lung sections perfused with latex and barium sulfate revealed marked proliferation of the bronchial arterial circulation in lung regions with evidence of pulmonary hemorrhage. The expanded vascular network appeared to be focused on diseased small airways.

Amphotericin-B promotes leukocyte aggregation of nylon-wool-fiber- treated polymorphonuclear leukocytes

Severe pulmonary reactions have been reported in patients receiving leukocyte transfusion and amphotericin-B. To study the interaction of amphotericin-B with polymorphonuclear leukocytes (PMN), purified human PMN were incubated with 200 mg of nylon wool fiber for 60 min either in the absence or presence of 2 mM EDTA. PMN were recovered in acid citrate dextrose solution and were suspended in balanced salt solution for determination of their aggregation properties. The cells exposed to nylon wool fibers without EDTA aggregated in response to concentration as low as 1.25 micrograms/ml of amphotericin-B. Cells initially treated with EDTA, however, failed to aggregate. Serum from a patient treated with amphotericin-B aggregated PMN exposed to nylon wool fiber but not control cells, whereas serum taken before amphotericin was given without effect on the PMN treated with nylon wool fiber. Amphotericin-B at 5 micrograms/ml failed to potentiate the release of beta- glucocuronidase or lactic dehydrogenase by PMN treated by nylon wool beyond that seen with exposure to the fibers alone. Rabbit peripheral blood was similarly incubated with nylon wool fibers and the recovered PMN were infused into recipient rabbits that had received 1 mg/kg of amphotericin-B intravenously 1 hr prior to the infusion of the leukocytes. Rabbits were sacrificed 30 min after transfusion of PMN, and their lungs were excised for histologic sectioning. Those rabbits receiving a combination of amphotericin-B and 4 x 10(7) nylon-wool- fiber-treated PMN had evidence of pulmonary hemorrhage and accumulation of leukocytes in the pulmonary vasculature whereas those animals who received such cells alone had normal appearing lung tissue. In summary, amphotericin-B at concentrations achievable in vivo enhanced the aggregation of PMN damaged by incubation with nylon fiber with subsequent accumulation of the phagocytes in pulmonary tissue.

Amphotericin-B Promotes Leukocyte Aggregation of Nylon-Wool-Fiber-Treated Polymorphonuclear Leukocytes

AbstractSevere pulmonary reactions have been reported in patients receiving leukocyte transfusion and amphotericin-B. To study the interaction of amphotericin-B with polymorphonuclear leukocytes (PMN), purified human PMN were incubated with 200 mg of nylon wool fiber for 60 min either in the absence or presence of 2 mM EDTA. PMN were recovered in acid citrate dextrose solution and were suspended in balanced salt solution for determination of their aggregation properties. The cells exposed to nylon wool fibers without EDTA aggregated in response to concentrations as low as 1.25 µg/ml of amphotericin-B. Cells initially treated with EDTA, however, failed to aggregate. Serum from a patient treated with amphotericin-B aggregated PMN exposed to nylon wool fiber but not control cells, whereas serum taken before amphotericin was given was without effect on the PMN treated with nylon wool fiber. Amphotericin-B at 5 µg/ml failed to potentiate the release of beta-glucocuronidase or lactic dehydrogenase by PMN treated by nylon wool beyond that seen with exposure to the fibers alone. Rabbit peripheral blood was similarly incubated with nylon wool fibers and the recovered PMN were infused into recipient rabbits that had received 1 mg/kg of amphotericin-B intravenously 1 hr prior to the infusion of the leukocytes. Rabbits were sacrificed 30 min after transfusion of PMN, and their lungs were excised for histologic sectioning. Those rabbits receiving a combination of amphotericin-B and 4 × 107 nylon-wool-fiber-treated PMN had evidence of pulmonary hemorrhage and accumulation of leukocytes in the pulmonary vasculature whereas those animals who received such cells alone had normal appearing lung tissue. In summary, amphotericin-B at concentrations achievable in vivo enhanced the aggregation of PMN damaged by incubation with nylon fiber with subsequent accumulation of the phagocytes in pulmonary tissue.