History of Present Illness
An 81-year-old woman arrived in the emergency room (ER) because of progressive fatigue for 1 week, with worsening dyspnea and decreased urine output. Before that ER visit, the general practitioner had placed the patient on oral furosemide, with no improvement of symptoms. Two weeks earlier, the patient had also received a course of amoxicillin/clavulanic acid for urinary tract infection.
Past Medical History
The patient, who was a never-smoker, had a history of arterial hypertension, hypothyroidism, and ischemic heart disease. Eight years earlier, she had undergone coronary angiography with angioplasty and stent placement for myocardial infarction. The procedure was complicated by subacute occlusion of the superficial femoral artery. Two years before her current presentation, she had also undergone gastrectomy with esophagojejunostomy for gastric adenocarcinoma. Her home medication list included amlodipine, levothyroxine, acetylsalicylic acid, and furosemide.
Physical Examination and Early Clinical Findings
On presentation, the patient was pale, dyspneic, and tachycardic. She was anuric for the past 24 hours, did not have any vomiting or diarrhea, and did not take nonsteroidal anti-inflammatory drugs recently. Blood pressure was 115/80 mm Hg. Upon auscultation, the breath sounds were found to be slightly reduced, mainly at the bases. Physical examination findings of the abdomen were unremarkable. Blood tests showed severe renal failure (serum creatinine 11.99 mg/dL, urea 305 mg/dL); hyperkalemia (potassium 6.4 mEq/L), mild leukocytosis (white blood cell [WBC] count 10,820/mm 3 ); severe microcytic anemia (hemoglobin [Hb] 5.8 g/dL, mean corpuscular volume 74 fL; normal range 80–95 fL), and high brain-type natriuretic peptide (proBNP 32,500 pg/mL; values > 400 pg/mL strongly suggestive of ventricular dysfunction). The platelet count was 125,000 cells/μL, and the international normalized ratio (INR) was 1.09.
Although oxygen saturation on pulse oximetry (SpO2) was 93% while the patient was breathing room air, arterial blood gas analyses (ABG) analyses showed hypoxemic respiratory failure with a partial pressure of oxygen (Pa O 2 ) of 53 mm Hg.
Abdominal ultrasonography demonstrated a minimal amount of perihepatic intraperitoneal fluid. The sizes of both kidneys were slightly reduced (pole-to-pole length 10 and 9 cm for the left and right kidneys, respectively). Hydronephrosis and kidney stones were not observed. Chest ultrasonography revealed mild bilateral pleural effusion, pulmonary vertical artifacts, and large lower vena cava with inspiratory collapse less than 50%.
Chest radiography confirmed small left pleural effusion, with no evident lung parenchymal lesions ( Fig. 10.1 ).
Clinical Course
A central venous catheter was placed in the right deep femoral vein under ultrasound guidance. The patient immediately underwent red blood cell transfusion and diuretic therapy; then she was admitted to the nephrology department, where hemodialysis was initiated.
Further investigation showed anti–glomerular basement membrane (GBM) antibodies in serum and high-titer perinuclear antineutrophil cytoplasmic antibodies (p-ANCA). Therefore immunosuppression was initiated with high-dose systemic corticosteroids (intravenous methylprednisolone 500 mg/day for 3 days, followed by oral prednisone 1 mg/kg/day) and oral cyclophosphamide 2 mg/kg/day. After correction of anemia and electrolyte balance, the patient underwent ultrasound-guided percutaneous kidney biopsy. Histological examination showed crescentic glomerulonephritis with extensive signs of chronic vasculitis. Serum iron was 32 μg/dL (normal range 60–170 μg/dL), whereas transferrin was 330 mg/dL (normal range 250–350 μg/dL), with transferrin saturation 7% (normal range for women 15%–50%). Administration of intravenous iron and subcutaneous erythropoietin was initiated. The test for fecal occult blood showed a positive result. Esophagogastroduodenoscopy did not show any source of bleeding. The patient declined colonoscopy.
Five days after admission, renal function and urine output had not improved, and the patient was placed on three-times–weekly hemodialysis.
During hospitalization, a fever with and chills occurred, and systemic inflammation markers increased. The highest values of C-reactive protein (CRP) and procalcitonin (PCT) were 298 mg/L and 4.97 ng/mL, respectively. The patient also complained of shortness of breath, and high-flow oxygen (Fi O 2 ; 40% via a Venturi mask) supplement was necessary to obtain sufficient oxygen saturation (SpO 2 ).
Empirical antibiotic therapy was undertaken on the basis of the assumption that the patient could have a hospital-acquired lower respiratory tract infection with sepsis. Antibiotics active against methicillin-resistant Staphylococcus aureus (MRSA), gram-negative bacteria, and Pseudomonas aeruginosa were included: piperacillin/tazobactam 2.25 g intravenous (IV) every 8 hours and vancomycin, at a loading dose of 20 mg/kg IV and maintenance doses of 10 mg/kg IV after each dialysis. After 24 hours, the attending physicians were notified that blood culture results were positive for gram-positive cocci.
The central catheter was removed, and a tunneled hemodialysis catheter was placed in the left internal jugular vein (because of stenosis of the right internal jugular vein, usually preferred site). Definitive blood culture results revealed the growth of methicillin-sensitive Staphylococcus aureus (MSSA); thus vancomycin administration was stopped.
Despite optimization of fluid management, low-grade fever and respiratory failure persisted, and chest radiography revealed an increase in the left pleural effusion ( Fig. 10.2 ). A pulmonologist was consulted, and he ordered thoracic ultrasonography, which showed that the pleural effusion had an initial tendency to fibrinous organization ( Fig. 10.3 ).
High-resolution computed tomography (CT) of the chest with contrast medium was promptly performed. This confirmed a large area of left pleural effusion that compressed the adjacent pulmonary parenchyma. No frank pneumonia was present, and a small area of contralateral pleural effusion was also found ( Fig. 10.4 ).
