Treatment of Hypertensive Cardiogenic Edema with Intravenous High-Dose Nitroglycerin in a Patient Presenting with Signs of Respiratory Failure: A Case Report and Review of the Literature.

BACKGROUND Pulmonary edema is the accumulation of fluid in the lung secondary to increased hydrostatic pressure. Hypertensive cardiogenic pulmonary edema presents with a sudden onset of severe dyspnea, tachycardia, and tachypnea, and can occur when the systolic blood pressure exceeds 160 mmHg in association with acute decompensated congestive cardiac failure (CCF). A case is presented of hypertensive cardiogenic pulmonary edema treated with high-dose nitroglycerin and includes a review of the literature. CASE REPORT A 63-year-old Hispanic male with a medical history of hypertension, coronary artery disease, heart failure with a reduced ejection fraction of 35%, chronic kidney disease (CKD) and diabetes mellitus, presented as an emergency with acute, severe dyspnea. The patient was initially managed with 100% oxygen supplementation and intravenous (IV) high-dose nitroglycerin (30 mcg/min), which was titrated every 3 minutes, increasing by 15 mcg/min until a dose of 120 mcg/min was reached. After 18 minutes of aggressive therapy, the patient's condition improved and he no longer required mechanical ventilation. CONCLUSIONS Hypertensive cardiogenic pulmonary edema is a challenging clinical condition that should be diagnosed and managed as early as possible, and distinguished from respiratory failure due to other causes. Although hypertensive cardiogenic pulmonary edema is usually managed acutely with high-dose diuretics, this case has highlighted the benefit of high-dose IV nitroglycerin, and review of the literature supports this treatment approach.

Pneumomediastinum and Pneumothorax Associated with Herpes Simplex Virus (HSV) Pneumonia.

BACKGROUND Pneumonia is one of the most common causes of death from infectious disease in the United States (US). Although most cases of community-acquired pneumonia (CAP) are secondary to bacterial infection, up to one-third of cases are secondary to viral infection, most commonly due to rhinovirus and influenza virus. Pneumonia due to herpes simplex virus (HSV) is rare, and there is limited knowledge of the pathogenesis and clinical complications. This report is of a fatal case of HSV pneumonia associated with bilateral pneumothorax and pneumomediastinum. CASE REPORT A 36-year-old homeless male Hispanic patient, who was a chronic smoker, with a history of intravenous drug abuse and a medical history of chronic hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infection, not on highly active antiretroviral therapy (HAART), was admitted to hospital as an emergency with a seven-day history of productive purulent cough. The patient was admitted to the medical intensive care unit (MICU) with a diagnosis of CAP, with intubation and mechanical ventilation. Broncho-alveolar lavage (BAL) was performed and was positive for HSV. The patient developed bilateral pneumothorax with pneumomediastinum, which was fatal, despite aggressive clinical management. CONCLUSIONS Pneumonia due to HSV infection is uncommon but has a high mortality. Although HSV pneumonia has been described in immunocompromised patients, further studies are required to determine the pathogenesis, early detection, identification of patients who are at risk and to determine the most effective approaches to prophylaxis and treatment for HSV pneumonia.

Hartmannella vermiformis isolated from the cerebrospinal fluid of a Young male patient with meningoencephalitis and bronchopneumonia

Meningoencephalitis and bronchopneumonia were documented in a patient from Puebla, Mexico. The patient began with symptoms and signs of a common flu and 12 days after the onser of his disease he was admitted to the hospital presentin symptoms and signs of meningoencephalitis. The clinical course evolved into an endocraneal hypertension syndrome with bronchopneumonia, coma and death. Wide-spectrum antibiotics, immunosuppressive and anti-tuberculosis therapy were unsuccessfully administered. Important antecedents were degree I malnutrition and repeated contact with polluted water. Post-mortem autopzy was not performed. Gram-positive cocci were isolated from the spinal fluid 2 days after admission, and then active amebae were isolated from three different samples of the spinal fluid at days 16, 18 and 19 after admission. Such samples were concentrated and inoculated onto specific culture media. Identification of amebae was based on their morphology and biochemistry. All amebae were hartmannella veriformis. Amebae were apparently not the cause of the disease and might be considered as an opportunistic colonizer which may have caused the evolution of the disease to become worse