A 7-year-old male Shih Tzu was examined because of acute onset of abnormal gait in pelvic limbs. Physical examination revealed pain at the level of the lumbar spine, paraparesis, ataxia, and decreased postural reactions in pelvic limbs. Muscle tone was normal. Normal patellar and cranial tibial reflexes were normal but flexor reflex was mildly reduced in the left pelvic limb. The neuroanatomic diagnosis was a focal or diffuse lesion between T 3 -L 3 . Hematologic and serum biochemical analysis revealed severe anemia (RBC 3.9, HB, HCT 27.5,, and on the following day paraparesis and ataxia increased.Bone marrow biopsy performed under general anesthesia at the level of humerus head revealed a leishmaniasis infection, with a high presence of amastigotes. Bone marrow plasmacytosis was present and numerous histiocytes containing Leishmania spp. were evident. Leishmania spp. were detected extracellulary microscopically. IFA titre for Leishmania was 4320. PCR for Ehrlichia and Borrelia spp. were negative.An MRI study was performed with an open permanent magnet operating in 0.2 T (ESAOTE). The study included T1-weighted spin echo (SE) sequences [800/26/ 3; repetition time (TR) echo time (TE)], T2-weighted SE sequences (3000/100/1; TR/TE), gadoliniumdimeglumide (0.5 mmol/mL, GE Healthcare Omniscan, Paderno Dugnano, Milan, Italy) enhanced T1-weighted SE sequences (gadolinium chelate dose was 0.1 mmol/kg, IV), in the 3 orthogonal planes, and Gradient echo STIR sequences (1490/25/1; TR/TE/IR).The MRI revealed the presence of an extradural mass ventral to the spinal cord and lateralized to the left localized on the L 4 -L 5 intervertebral disk to the midbody of L 5 , displacing the spinal cord. The lesion was hyperintense on T1-weighted, T2-weighted, and STIR images, and had heterogeneous postconstrast enhancement (Fig 1).As neurological signs were rapidly progressing, surgery was performed to decompress the spinal cord by means of a left L 4 -L 5 hemilaminectomy, an ill-defined extradural mass, located ventrolaterally, was identified. The mass was yellow and hardly distinguishable from the epidural fat, neither encapsulated nor adhesive and with friable appearance. The diseased tissue was then removed and fixed in 10% buffered formalin.After surgery, cephalosporine (20 mg/kg PO q12h for 10 days) and prednisolone (0.5 mg/kg PO q12h for 5 days) were administered.The surgically removed tissue consisted of epidural fat tissue heavily infiltrated by macrophages, lymphocytes, plasma cells, and neutrophils. Proliferation of capillaries and scattered hemorrhages were also seen. The cytoplasm of many foamy macrophages contained multiple Leishmania amastigotes (Fig 2). The parasites were also identified free within the interstitium. The organisms were strongly labeled by immunohistochemical staining by the streptavidin-biotin immunohistochemical method with canine hyperimmune serum as the primary antibody.

IntroductionCardiac transplantation remains the gold standard for end-stage cardiomyopathies and congenital heart defects in pediatric patients.ObjectiveThis study aims to report on 20 years of experience since the first case and evaluate our results.MethodsWe conducted a retrospective analysis of the database and outpatient follow-up. Between October 1992 and April 2012, 109 patients underwent 114 transplants. 51.8% of them being female. The age of patients ranged from 12 days to 21 years with a mean of 8.8±5.7 years and a median of 5.2 years. The underlying diagnosis was dilated cardiomyopathy in 61.5%, congenital heart disease in 26.6% and restrictive cardiomyopathy in 11.9%. All patients above 17 years old had congenital heart disease.ResultsSurvival rate at 30 days, 1, 5, 10, 15, and 20 years were 90.4%, 81.3%, 70.9%, 60.5%, 44.4% and 26.7%, respectively. Mean cold ischemic time was 187.9 minutes and it did not correlate with mortality (P>0.05). Infectious complications and rejection episodes were the most common complications (P<0.0001), occurring, respectively, in 66% and 57.4% of the survivors after 10 years. There was no incidence of graft vascular disease and lymphoproliferative disease at year one, but they affected, respectively, 7.4% and 11% of patients within 10 years.ConclusionTwenty-year pediatric heart transplant results at our institution were quite satisfactory and complication rates were acceptable.

Congenital cardiopathies; ventricular septal defect, aortic coarctation, pulmonary artery /abnormalities. trunk and the pulmonary arteries demonstrates the presence of pulmonary flow directly from the left ventricle to the right ventricular outflow tract, as in the subpulmonary location of the ventricular septal defect. Differential diagnosisAll other acyanotic congenital cardiopathies with left-toright shunt must be recalled, such as interatrial communication and patent ductus arteriosus, as long as they present a marked hemodynamic effect, which occurs, however, at more advanced ages. This alteration of marked dilatation of the pulmonary trunk is also seen in cyanotic cardiopathies with pulmonary hyperflow, such as total anomalous pulmonary venous connection. Diagnostic confirmationThe clinical elements were decisive for the diagnosis of the ventricular septal defect and aortic coarctation. The echocardiogram confirmed the presence of a ventricular defect with a direct connection with the pulmonary valve in a subpulmonary location, measuring 10 mm in diameter, in addition to the aortic coarctation in the isthmus region, measuring 3 mm in diameter, in relation to 7 mm of the ascending aorta and 5 mm of the aortic arch. The right ventricle was not dilated, considering the preferential flow from the left ventricle to the pulmonary artery tree. The left ventricle was enlarged and the left ventricular function was preserved (LVEF: 68%, Ao: 14, LA: 18, LV: 27) (Fig.2). ManagementAt surgery, the resection of the aortic coarctation in terminoterminal anastomosis with the aortic arch resulted in an adequate diameter of the region. The 10-mm subpulmonary or committed ventricular septal defect was closed through an incision in the pulmonary trunk, using a bovine pericardial patch. The heart failure condition was resolved. CommentsThe marked dilatation of the pulmonary trunk is seldom detected in infants, even in those with cardiopathies with marked pulmonary hyperflow. This anatomical confirmation, in this case, was due to the direct flow from the left ventricle to the pulmonary artery tree, through the ventricular septal defect. Moreover, this defect, when doubly committed to the great vessels, pathogenically explains the concomitant existence of aortic coarctation, considering the increased Clinical dataThe patient remained asymptomatic up to three months before, when he started to present fatigue even at rest, which grew progressively worse.Physical examination: the patient was tachydyspneic, had normal skin color, ample pulses in both upper extremities and decreased in the lower extremities. Weight was 5,130g. The blood pressures in the right upper limb and right lower limb were 150/80 and 100/80 mmHg, respectively. HR: 130 bpm. The aorta was not palpated at the suprasternal notch. The patient presented slight precordial impulses at the left sternal border and the ictus cordis was diffuse and palpated at the 5th intercostal space on the hemiclavicular line. Heart sounds were hyperphonetic and there was a holosystolic...

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All other acyanotic congenital cardiopathies must be recalled, both with left-right shunt and obstructive ones, as long as they have a mild hemodynamic impact. Diagnostic confirmationThe clinical elements were decisive for the diagnosis of myocardial ischemic damage, which led to the heart failure condition, represented by the anomalous origin of the left coronary artery. The echocardiogram confirmed the diagnosis, considering the connection between the anterior interventricular artery and the pulmonary trunk. The left cavities were enlarged ( Figure 2). ManagementAt surgery, a fistula with an external diameter of 1 mm was identified between the anterior interventricular artery and the pulmonary trunk, with a shunt toward the pulmonary artery tree. The fistula was disconnected with suture. The anomalous origin of the coronary artery was not detected. As a result, the systolic murmur disappeared and the electrocardiogram showed a normal ventricular repolarization. The postoperative arterial hypertension was treated with sodium nitroprusside and subsequently, with captopril. CommentsIn spite of the arteriovenous fistula with a left-to-right shunt (increased pulmonary vascularity and left cavities), the patient's main condition was the myocardial ischemia due to the escape of blood from the coronary circulation (altered electrical repolarization and myocardial dysfunction). Thus, the patient's condition mimicked an anomalous origin of the left coronary artery.The surgical anatomical finding (fistula between the anterior interventricular artery and the pulmonary trunk) is in fact characterized as an unusual congenital heart defect in the absence of other abnormalities, such as pulmonary atresia with ventricular septal defect and other situations that accompany pulmonary flow obstruction.The early surgical correction prevents the unfavorable evolution related to the left ventricular enlargement and dysfunction, in addition to the progressive worsening of the ischemic process. Clinical dataThe patient presented tiredness since birth, which was carried out by Caesarean section at 38 weeks of gestation. The infant had improved slightly after receiving specific medication (digoxin and captopril) about a month before. The assessment was requested after the diagnosis of anomalous origin of the left coronary artery (LCA), with preserved ventricular function (ejection fraction = 53%).At physical examination, the patient was dyspneic, had normal skin color and normal pulses. The aorta was not palpable at the suprasternal notch.There were slight precordial impulses at the left sternal border and the ictus cordis was not palpable. The heart sounds were normal and there was a protomesosystolic murmur of +/2 intensity, in the two hemithoraces. The lungs and abdomen were normal.The electrocardiogram (ECG) showed sinus rhythm and signs of electrical ischemia in the anterior wall, with a negative T wave in V1 to V6, accompanied by ST-segment depression and low-voltage QRS complexes (Figure 1). Radiographic imageSlightly enlarged car...