BackgroundCases of acute pancreatitis (AP) have increased among pediatric populations worldwide; however, the natural course of this condition in Saudi Arabia was unknown.AimTo report the characteristics as well as outcomes of pediatric AP.Patients and methodsA retrospective chart review study was conducted to include acute pancreatitis in patients ≤ 19 years. The period was from 1994 until 2015. Demographic, clinical, laboratory, imaging and outcome data were collected and analyzed.Results50 patients (n = 26; 52% males vs. n = 24; 48% females) were included. The mean age at diagnosis was 11.6 years. The mean length of hospital stay was 10.5 days. 9 (18%) patients had a recurrence of AP and 4 (8%) had complications. Idiopathic AP was the most frequent etiology (n = 21; 42%), followed by cholelithiasis (n = 11; 22%). 2 patients (4%) had drug-induced AP, where one was taking isoniazid and the other had taken a large amount of erythromycin, amoxicillin and ibuprofen. 2 choledochal cysts complicated by AP (4%). Pancreaticobiliary diseases, as a complete entity, accounted for 34% (n = 17). Clinically, abdominal pain (n = 47; 94%) and vomiting (n = 38; 76%) were most commonly encountered. KUB was non-diagnostic in all patients. No patient died during their admission.ConclusionAlthough still relatively uncommon in Saudi Arabia, there are on average 2–3 cases of pediatric AP diagnosed annually in our institution. Idiopathic AP was the most common cause. Isoniazid and choledochal cysts are rare causes of AP and were reported in the study.

Patient: Female, 32Final Diagnosis: Progressive multifocal leukoencephalopathySymptoms: Progressive behavioral changes • seizuresMedication: —Clinical Procedure: ManagementSpecialty: NeurologyObjective:Rare diseaseBackground:Progressive multifocal leukoencephalopathy (PML) is a serious opportunistic infectious disease with high morbidity and mortality. Its incidence in multiple sclerosis (MS) patients has risen since the introduction of disease modifying drugs. In the absence of a specific treatment, the outcome depends heavily on early diagnosis, which illustrates the importance of the role of characteristic brain magnetic resonance imaging (MRI). However, when relying mainly on MRI, the diagnosis of cases with atypical radiological changes may be missed or delayed.Case Report:A 32-year-old female diagnosed with elapsing remitting MS in 2009 was started on interferon-beta-1b that was escalated to natalizumab due to progression of the disease. Later, she was shifted to fingolimod as testing for John Cunningham polyoma virus (JCV) antibodies was positive. Three years later, she presented with a 3-week history of progressive walking impairment associated with twitching of her facial muscles and abnormal sensation all over her body that was associated with left hemi-paresis and sensory changes, in addition to truncal ataxia, which was treated with steroids as a relapse of MS. However, the patient continued to deteriorate and developed significant cognitive and behavioral changes. In view of this clinical picture, the diagnosis of PML was raised in spite of her atypical brain MRI features. Treatment with fingolimod was stopped and a sample of her cerebrospinal fluid was sent for JCV DNA analysis, which came back positive at 11 copies/mL. Treatment with mirtazepine and mefloquine was started, but the patient deteriorated further, and MRI showed severe changes consistent with immune reconstitution inflammatory syndrome. Intravenous steroids and intravenous immunoglobulin were given, and within a few weeks, the patient was stabilized and started to gradually improve.Conclusions:In patients at risk for developing PML who present with typical clinical features, testing for JCV DNA is recommended even in the absence of typical radiological findings in order to prevent any delay in the diagnosis.

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Patient: Female, 42Final Diagnosis: Cauda Equina syndrome due to extensive DVTSymptoms: Back pain • incontinence • swelling legs • weakness of the lower limbsMedication: —Clinical Procedure: —Specialty: NeurologyObjective:Rare diseaseBackground:Epidural venous plexus (EVP) engorgement occurs due to many conditions, so it can be easily misdiagnosed. This becomes problematic when the diagnosis requires prompt treatment for a good outcome, especially when it results in cauda equina syndrome (CES). We report a case of extensive iliocaval thrombosis leading to epidural venous plexus and ascending lumbar vein engorgement as an outcome of deep venous thrombosis (DVT) due to probable adverse effects of oral combined contraceptive pills (OCCP).Case Report:A 42-year-old woman presented to a rural medical facility with bilateral lower-limb swelling and skin darkening for 2 days. She was transferred to a tertiary medical facility where her condition deteriorated to severe CES. A lower-limbs ultrasonography confirmed the presence of extensive DVT extending to the lower segment of the inferior vena cava. Spine magnetic resonance imaging showed abnormal enhancement of the conus medullaris with thick enhanced cauda equina nerve roots, consistent with a possible case of Guillain-Barré syndrome. However, there was engorgement of the EVP extending to the ascending lumbar, azygos, and hemiazygos veins, which was misdiagnosed. The patient was managed immediately with low-molecular-weight heparin and steroids. She died 4 weeks after admission due to hospital-acquired pneumonia and acute respiratory distress syndrome, probably due to the high dose of steroids.Conclusions:Acute CES has a wide differential diagnosis. This report describes an unusual cause of CES and emphasizes the importance of early recognition to avoid misdiagnosis and management delay. Early identification of this clinical entity markedly decreases morbidity and mortality and thus improves the prognosis. Likewise, underlying causing factors such as venous congestion due to OCCP-related DVT should be considered in the diagnosis.

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Submit Manuscript | http://medcraveonline.com with mobility. Otherwise she did not have any systemic complaints. Had no history of a recent infectious illness and did not use any medication. Her past and family history was unremarkable. On examination, she was alert, fully oriented with intact cognitive functions. The movements were noted as involuntary, rapid and purposeless generalized movements. She could not control it and had difficulty stabilizing her head. Auscultation revealed pansystolic murmur over the apex. She had no skin lesion, joint tenderness or swelling. Blood investigations showed normochromic normocytic anemia with thrombocytopenia (Hb: 8g/dl, MCV: 80 fl, WBCs: 4.5×10 9 Platelets: 84×10 9 ). Had normal renal and liver functions. Coombs test was positive, ANA and anti-dsDNA Abs were positive. Furthermore her cardiolipin IgG was positive (36.9 U/ml) and urine analysis shows hematuria (20-30/HPF) and proteinuria (100 mg/dl). Brain MRI demonstrated multiple bilateral old and recent ischemic lesions (Figure 1). Echocardiography show mildly thickened mitral valve with prolapsed of anterior segments of mitral leaflet & moderate mitral regurgitation.

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