613 cases of splenic rupture without risk factors or previously diagnosed disease: a systematic review

Background Rupture of the spleen in the absence of trauma or previously diagnosed disease is largely ignored in the emergency literature and is often not documented as such in journals from other fields. We have conducted a systematic review of the literature to highlight the surprisingly frequent occurrence of this phenomenon and to document the diversity of diseases that can present in this fashion. Methods Systematic review of English and French language publications catalogued in Pubmed, Embase and CINAHL between 1950 and 2011. Results We found 613 cases of splenic rupture meeting the criteria above, 327 of which occurred as the presenting complaint of an underlying disease and 112 of which occurred following a medical procedure. Rupture appeared to occur spontaneously in histologically normal (but not necessarily normal size) spleens in 35 cases and after minor trauma in 23 cases. Medications were implicated in 47 cases, a splenic or adjacent anatomical abnormality in 31 cases and pregnancy or its complications in 38 cases. The most common associated diseases were infectious (n = 143), haematologic (n = 84) and non-haematologic neoplasms (n = 48). Amyloidosis (n = 24), internal trauma such as cough or vomiting (n = 17) and rheumatologic diseases (n = 10) are less frequently reported. Colonoscopy (n = 87) was the procedure reported most frequently as a cause of rupture. The anatomic abnormalities associated with rupture include splenic cysts (n = 6), infarction (n = 6) and hamartomata (n = 5). Medications associated with rupture include anticoagulants (n = 21), thrombolytics (n = 13) and recombinant G-CSF (n = 10). Other causes or associations reported very infrequently include other endoscopy, pulmonary, cardiac or abdominal surgery, hysterectomy, peliosis, empyema, remote pancreato-renal transplant, thrombosed splenic vein, hemangiomata, pancreatic pseudocysts, splenic artery aneurysm, cholesterol embolism, splenic granuloma, congenital diaphragmatic hernia, rib exostosis, pancreatitis, Gaucher's disease, Wilson's disease, pheochromocytoma, afibrinogenemia and ruptured ectopic pregnancy. Conclusions Emergency physicians should be attuned to the fact that rupture of the spleen can occur in the absence of major trauma or previously diagnosed splenic disease. The occurrence of such a rupture is likely to be the manifesting complaint of an underlying disease. Furthermore, colonoscopy should be more widely documented as a cause of splenic rupture

Coeliac sprue-associated membranoproliferative glomerulonephritis (MPGN).

Coeliac sprue (CS) may occur in association with immune complex-mediated diseases, including IgA nephropathy, dermatitis herpetiformis and thyroiditis. An association of CS with membranoproliferative glomerulonephritis (MPGN) type 1 is rare, with only two prior cases reported. Here we describe a 45-year-old man with no prior medical history who presented initially with microhaematuria, subnephrotic proteinuria and hypocomplementaemia. A renal biopsy revealed MPGN type 1 with negative serologic workup for secondary causes. The patient was treated conservatively with angiotensin-converting enzyme inhibitors. Several months later, he developed daily non-bloody diarrhoea and was found to have worsening hypoalbuminaemia, hypophosphataemia and severe iron deficiency anaemia. A diagnosis of CS was established based on elevated tTGA (IgA anti-tissue transglutaminase) antibody and positive IgA antiendomysial antibody titres. Proteinuria resolved completely following the initiation of a gluten-free diet, without the use of immunosuppressive therapy and despite tapering of angiotensin-converting enzyme inhibitor. This case illustrates that CS-associated MPGN may precede overt clinical evidence of coeliac disease and may respond to gluten-free diet, without resort to immunosuppressive therapy

Fluorescence of experimental atheromatous plaques with hematoporphyrin derivative.

Fluorescence of hematoporphyrin derivative (HPD) has been used clinically to localize malignant neoplasms because of its selective accumulation in these tissues. We tested the hypothesis that HPD may also be selectively concentrated within atheromatous plaques. 48 h after HPD injection in a variety of species, selective fluorescence of atheromatous plaques of the aorta was seen in each animal (rabbits and Patas monkey) exhibiting such lesions. No fluorescence could be demonstrated in aortic segments free of atheromatous involvement. Since the efficacy of photodynamic destruction of malignant tumors with HPD has been demonstrated in clinical studies, the observations of the present study may have therapeutic implications in atheromatosis

Experimental myocardial ischemia. IV. Shape and volume changes during "isolvolumetric relaxation" in normal and ischemic ventricles.

Shape and volume changes were studied in mongrel dogs between end-systole and mitral valve opening (MVO). Biplane left ventricular cineangiograms were performed at 200 frames/sec. The dogs were studied during the control state and during regional myocardial ischemia produced by balloon occlusion of the left anterior descending coronary artery. Outward wall motion, called pre-inflow relaxation (PIR), occurred in all 10 dogs in the control state, most frequently in the apical (seven of 10) and equatorial planes (seven of 10). PIR was seen less frequently during ischemia (13 of 40 measurements vs 19 of 40 measurements during control state), usually in the basal plane (five of 10). The ventricular volume between end-systole and MVO increased in all 10 dogs during the control state (mean increment 4.4 +/- 0.7 ml). Volume increased in eight of 10 dogs during ischemia (mean increment 3.0 +/+ 1.1 ml). The characteristic patterns of wall motion occurring between end-systole and MVO are altered by regional myocardial ischemia. During ischemia PIR occurs in segments of the myocardium with normal perfusion, but usually not in ischemic segments. Biplane ventricular volume between end-systole and MVO increased in 18 of 20 measurements (mean increment 3.6 +/- 0.9 ml).</jats:p