History of Present Illness
An 83-year-old man was taken to the emergency room (ER) because of fever, shortness of breath, swelling of the legs, weakness, confusion, and nausea.
Past Medical History
The patient suffered from arterial hypertension, hyperuricemia, type 2 diabetes mellitus, diabetic nephropathy with proteinuria, and stage 4 chronic kidney disease. An indwelling peritoneal catheter had recently been implanted because peritoneal dialysis was considered a therapeutic option (not yet started). Many years earlier, the patient had been diagnosed with left fibrothorax with fluid collection resulting from previous tuberculous pleurisy.
Physical Examination and Early Clinical Findings
Upon arrival at the ER, the patient had a fever (38.7° C [101.7° F]) and low oxygen saturation (oxygen saturation [Sp O 2 ] 87% at rest while breathing in ambient air). Arterial blood gas (ABG) analyses showed metabolic acidosis and acute partial respiratory failure (pH 7.28; partial pressure of carbon dioxide [Pa CO 2 ] 39.3 mm Hg; partial pressure of oxygen [Pa O 2 ] 54.8 mm Hg; bicarbonate [HCO 3 −] 14 mmol/L). Respiratory rate was 21 breaths/min, heart rate was 114 beats/min, and arterial blood pressure was 130/85 mm Hg. Auscultation revealed a reduction in vesicular murmur in the left lower field, crackles in the right middle and basal fields, and widespread rales. Chest x-ray showed large opacity in the left middle and lower areas and opacity in the right middle zone ( Fig. 12.1 ). Chest ultrasonography confirmed the presence of fluid collection and calcified pleura on the left side. Moreover, lung hepatization with air bronchogram in the left lower lobe was seen ( Fig. 12.2 ).
Blood tests showed leukocytosis (white blood cells [WBC] count: 18,200/mm 3 ) and a marked increase in the indices of inflammation (C-reactive protein [CRP]: 330 mg/L; procalcitonin [PCT]: 1.56 mcg/L) and volume overload (N-terminal–pro–brain natriuretic peptide [NT-proBNP]: 13,650 pg/mL). Renal failure, hyperglycemia, and electrolyte imbalance were also evident: serum creatinine was 5.3 mg/dL, glucose 215 mg/dL, and potassium 5.8 mEq/L. Urinalysis revealed the presence of leukocytes, hemoglobin, proteins, glucose, and bacteria in urine.
Supplemental 40% oxygen via a Venturi mask was delivered to obtain oxygen saturation of 96%. A loop diuretic (intravenous furosemide, bolus dose of 40 mg, followed by continuous infusion of 0.1 mg/kg/h) and a broad-spectrum antibiotic with dose adjustment for renal impairment (intravenous meropenem 500 mg every 24 hours) were promptly initiated. The patient was admitted to the nephrology unit.
The day after admission, serum creatinine increased to 6.8 mg/dL. Urine output was low (about 100 mL/24 hr). The physicians proposed hemodialysis, but the patient refused it; thus peritoneal dialysis was started. Kayexalate, oral sodium bicarbonate, and insulin, in addition to antibiotics and a diuretic, were administrated. Glycated hemoglobin (HbA1c), measured to determine the 3-month average blood glucose level, was high (8.1%) and confirmed uncontrolled diabetes. Sputum smear microscopy was negative for acid-fast bacilli (AFB), as well as the search for Mycobacterium tuberculosis DNA by means of polymerase chain reaction (PCR) on three consecutive sputum samples. The urine culture was positive for Proteus mirabilis, but no aerobic or anaerobic microorganism growth was detected on blood cultures. In 3 days, the fever disappeared, and the patient experienced progressive clinical improvement.
Chest computed tomography (CT) was not feasible for a few days because of technical problems. The patient underwent bronchoscopy, which showed a diffusely atrophic and inflamed bronchial mucosa. Some mucous secretions from both bronchial hemisystems were aspirated, and bronchoalveolar lavage (BAL) was performed in the lower left lobe. The recovered BAL fluid was analyzed, and no mycobacteria or malignant tumor cells were found.
In a week, edema in the lower limbs decreased, and oxygen saturation became sufficient without administration of oxygen. The WBC count normalized, and the CRP value decreased to 28 mg/L.
Chest radiography and CT showed that the pulmonary opacities in the middle right and lower left areas had disappeared. The pulmonary opacity caused by the known left calcific fibrothorax was still very evident ( Figs. 12.3 and 12.4 ).