Purpura fulminans is an acute illness characterized by rapidly progressive dermal vascular thrombosis, leading to hemorrhagic necrosis of the skin. Here, we describe the case of a healthy woman who developed acute disseminated intravascular coagulation (DIC) with purpura fulminans after intramuscular administration of a single dose of ketorolac. Review of literature showed only one case description of non-steroidal anti-inflammatory drug (diclofenac)-related purpura fulminans with DIC.
Myostatin recovered to baseline in both groups. Finally, we demonstrated that GDF-15 caused atrophy of myotubes in vitro (average control myotube diameter was 26.3±9.0 µm versus 22.3±7.5 µm for GDF-15 treated myotubes, equating to 15% myotube atrophy, p= 0.011). Conclusion This data supports the hypothesis that acute muscle loss occurs as a result of an imbalance between drivers of muscle atrophy and hypertrophy. GDF-15 is a potential novel mediator of muscle atrophy in ICUAP, which may become a therapeutic target in patients with ICUAP and other forms of acute muscle wasting.
Introduction Hp causes peptic ulcer disease (PUD) and is potentially carcinogenic. Hp eradication is done in conditions like PUD, uncomplicated dyspepsia and persistent iron deficiency anaemia. 'Test and treat' implies testing specifi cally with intent to treat, if positive. CLO test is read in real time and acted on promptly. Hp serology is used in acute upper GI (UGI) bleed or endoscopy on PPI as CLO test is less sensitive. Results take 5-7 days by when in-patients have been discharged and positive Hp serology (Hp+ve) results overlooked. This audit was prompted by two such missed cases of Hp+ve PUD with rebleed in one. Aim To review action taken on Hp+ve results in our hospital, assess factors contributing to inaction, impact on patient care and remedial steps needed. Methods Retrospective study of all patients with Hp+ve requested by hospital clinicians in 12 months (1 April 2009 to 31 March 2010). Serology data from our microbiology department was matched with subsequent urea breath tests (UBT), our standard test to confi rm eradication. Patients with sequential serology and UBT were deemed to have received eradication. Case notes of the others were reviewed for test indication, point of fi rst contact, gastroscopy fi ndings (if
Thumbprinting'i mj_2320 666A 68-year-old man presented with fever, non-bloody diarrhoea and diffuse abdominal pain of 7 days' duration. Two weeks earlier, he had received moxifloxacin for a week for acute sinusitis. He had a history of diabetes and rheumatoid arthritis and was taking methotrexate. On examination, the patient was dehydrated, tachycardic, tachypnoeic and hypotensive. The abdomen was diffusely tender with hyperactive bowel sounds; guarding and rebound tenderness were noted in the left lower quadrant. Laboratory evaluation showed leucocytosis (17.3 ¥ 10 9 /L) and renal failure.An upright abdominal radiograph ( Fig. 1) revealed dilated large and small bowel loops with air-fluid levels. The transverse colon and descending colon showed 'thumbprinting' (arrows). Computed tomography of the abdomen (not shown) showed diffuse wall thickening of the large bowel with pericolonic soft tissue stranding. He was treated for presumed Clostridium difficile colitis with IV metronidazole. Despite supportive measures, including aggressive fluid resuscitation, he developed worsening renal failure and acidosis. He underwent subtotal colectomy and end ileostomy 4 days after hospitalization. Intraoperatively, the bowel mucosa was inflamed and oedematous with pseudomembranes. Toxin assay and pathology confirmed pseudomembranous colitis (PMC) because of C. difficile. His recovery was complicated by partial small bowel obstruction which was managed conservatively. The patient is doing well more than a year after surgery.'Thumbprinting' describes the unusually wide transverse bands of thickened bowel which replace normal haustral folds, secondary to submucosal oedema and hemorrhage from capillary leakage. 'Thumbprinting' is seen in ischaemic colitis, inflammatory diseases of the colon, infectious causes of colitis including PMC and in patients with coagulation disorders. 1,2
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