Atypical presentation of varicella-zoster virus reactivation in a lung transplant patient: a case report.

Background. Varicella-zoster virus (VZV) is a human neurotropic virus which commonly causes infection during childhood, presenting as chickenpox. Later in life it may reactivate as herpes zoster. We report a rare manifestation of reactivation of VZV infection presenting as cutaneous vasculitis and varicella pneumonia in a lung transplant recipient. Case presentation. A 65-year-old man was lung transplanted bilaterally for emphysema and had repeated posttransplant chest infections and colonization with Pseudomonas aeruginosa. Nine months post-transplant he presented with dyspnoea and a cutaneous vasculitis-like eruption with a predilection over face, thorax and distal extremities. Initially, VZV reactivation was not suspected due to absence of the typical vesicular eruptions. The diagnosis was confirmed by VZV PCR from the swabs of the ulcer after skin punch biopsy of a lesion and from bronchoalveolar lavage (BAL). The histology of skin biopsy demonstrated epithelial damage and vascular damage but no typical epithelial virus associated changes. The patient responded to antiviral therapy with total remission of rash and VZV DNA was finally not detectable from repeated BAL after 29 days of therapy. However, the pulmonary radiological features and dyspnoea persisted due to reasons possibly unrelated to the VZV infection. Conclusion. Had it not been for the patient to mention the resemblance of the vasculitic rash with his primary VZV infection, the diagnosis would easily have been overlooked. In this case, the biopsy did not show typical histopathologic findings of VZV-vasculitis. What led the diagnosis was a PCR from the wound swab taken after the punch biopsy. This case serves as a reminder for atypical presentation of common conditions in immunosuppressed patients and that extensive diagnostic sampling may be warranted in this group.

Correlation between the Wells score and the Quanadli index in patients with pulmonary embolism.

BACKGROUND AND AIMS: Determining clinical probability of pulmonary embolism (PE) with Wells scoring system is the first step towards diagnosis of PE. Definitive diagnosis of PE is confirmed by computed tomography pulmonary angiography (CTPA). METHODS: This was a prospective study on 80 patients referred to the Institute for Pulmonary Diseases of Vojvodina with suspected PE between April 2010 and August 2012. Clinical probability of PE was determined according to the Wells and modified Wells scoring system. CTPA was performed in 60 patients. The degree of pulmonary vascular obstruction was quantified by the Qanadli index. RESULTS: Low clinical probability of PE was present in one patient (1.6%), moderate in 43 (71.6%) and high in 16 (26.6%) patients. PE was confirmed in 50 (83.3%) patients. There were 21 patients (42%) whose Quanadli index was <25%, 18 (36%) between 25%-50%, while Quanadli index was ≥50 in 11 patients (22%). When compared to CTPA findings, modified Wells scoring system showed 90% sensitivity [95% confidence interval (CI) 78.2%-96.6%], and 20% specificity (95% CI 3.11%-55.6%), positive predictive value (PPV) 84.9% (95% CI 72.4%-93.2%) and negative predictive value (NPV) 28.6% (95% CI 4.5%-70.7%). There was weak positive correlation between Wells score and Quanadli index (r = 0.14; P = 0.29), without statistical significance. Wells score was significantly higher in haemodynamically unstable than in haemodynamically stable patients (6.8 vs 5.6, P = 0.014). There was no statistically significant difference between the values of Quanadli index in these two groups (31.33% vs 26.64%, P = 0.062). CONCLUSION: Modified Wells criteria have high sensitivity but low specificity in PE diagnostics. The Wells score does not correlate well with the Quanadli index.

Pneumothorax after transbronchial needle biopsy.

Currently there several diagnostic techniques that re used by radiologists and pulmonary physicians for lung cancer diagnostics. In several cases pneumothorax (PNTX) is induced and immediate action is needed. Both radiologists and pulmonary physicians can insert a chest tube for symptom relief. However; only pulmonary physicians and thoracic surgeons can provide a permanent solution for the patient. The final solution would be for a patient to undergo surgery for a final solution. In our current work we will provide all those diagnostic cases where PNTX is induced and treatment from the point of view of expert radiologists and pulmonary physicians.

Pneumothorax after transthoracic needle biopsy of lung lesions under CT guidance.

Transthoracic needle biopsy (TTNB) is done with imaging guidance and most frequently by a radiologist, for the aim is to diagnose a defined mass. It is integral in the diagnosis and treatment of many thoracic diseases, and is an important alternative to more invasive surgical procedures. FNAC is a method of aspiration cytopathology, which with transthoracic biopsy ("core biopsy") is a group of percutaneous minimally invasive diagnostic procedures for exploration of lung lesions. Needle choice depends mostly upon lesion characteristics and location. A recent innovation in biopsy needles has been the introduction of automatic core biopsy needle devices that yield large specimens and improve the diagnostic accuracy of needle biopsy. Both computed tomography and ultrasound may be used as imaging guidance for TTNB, with CT being more commonly utilized. Common complications of TTNB include pneumothorax and hemoptysis. The incidence of pneumothorax in patients undergoing TTNB has been reported to be from 9-54%, according to reports published in the past ten years, with an average of around 20%. Which factors statistically correlate with the frequency of pneumothorax remain controversial, but most reports have suggested that lesion size, depth and the presence of emphysema are the main factors influencing the incidence of pneumothorax after CT-guided needle biopsy. On the contrary, gender, age, and the number of pleural passes have not been shown to correlate with the incidence of pneumothorax. The problem most responsible for complicating outpatient management, after needle biopsy was performed, is not the presence of the pneumothorax per se, but an increase in the size of the pneumothorax that requires chest tube placement and patient hospitalization. Although it is a widely accepted procedure with relatively few complications, precise planning and detailed knowledge of various aspects of the biopsy procedure is mandatory to avert complications.

Aortic dissection or renal infarction--multislice computed tomographic angiography can tell.

INTRODUCTION: Acute renal infarction as a consequence of renal artery occlusion often goes unrecognized, mostly due to the non-specific clinical features. A quick diagnosis, ideally within three hours of presentation, is a key to renal function recovery. CASE OUTLINE: A 62-year-old male patient was admitted with a sudden abdominal pain, right flank pain and nausea. He had a diastolic hypertension at admission and his previous medical history showed atrial fibrillation. Initial clinical diagnosis was aortic dissection. Laboratory findings included elevated lactate dehydrogenase (LDH) and serum creatinine levels. There were no signs of aortic dissection or aneurismatic lesions registered during a multislice computed tomographic (MSCT) angiography. However, MSCT angiography demonstrated left "upper" renal artery thrombosis and renal infarction--avascular area of the upper two thirds of the left kidney sharply demarcated from the surrounding parenchyma. Both kidneys excreted the contrast. Anticoagulant therapy was initiated, along with antiarrythmic and antihypertensive medications. The follow-up by computed tomography was performed after nine weeks, and it showed a partial revascularization of the previously affected area. CONCLUSION: Concomitant presence of flank/abdominal pain, an increased risk for thromboembolism and an elevated LDH suggested a possibility of renal infarction. MSCT angiography is a non-invasive and accurate method in the diagnosis of renal artery occlusion and the resulting renal infarction.