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Posterior urethral valves
Published in Mark Davenport, James D. Geiger, Nigel J. Hall, Steven S. Rothenberg, Operative Pediatric Surgery, 2020
Fardod O'Kelly, Martin A. Koyle
When the urine appears to be infected (urinalysis) following a catheter-specimen sample, both a blood sample and a urine sample should be sent for culture, following which ampicillin and an aminoglycoside or a third-generation cephalosporin should be started intravenously. When septicemia is suspected, blood coagulation studies should also be carried out.
Paediatrics
Published in Roy Palmer, Diana Wetherill, Medicine for Lawyers, 2020
In its early stages, septicaemia provokes little more than fever and nonspecific signs of infection such as lassitude, irritability, anorexia and vomiting. Every year, many thousands of infants and children are infected in this way. Often the condition is self-limiting, the organisms being killed by the body’s defences, or by prescribed antibiotics, before the cytokine system is irreversibly activated. Such children may be ill for only a day or two, and then only mildly. Treatment of early septicaemia (sometimes termed bacteraemia) using antibiotics alone is usually successful. As a result there are various protocols advising ‘care pathways’ for febrile infants. For example, one that is commonly used mandates intravenous broad-spectrum antibiotics for any ill-looking child under two years of age with a fever >39°C and a white blood count >15,000 (another quotes 20,000). The problem is that ‘ill-looking’ is a somewhat subjective criterion. It means something quite different to a parent than to a paediatrician. Claims may depend upon a court’s decision on whether or not an infant was ‘ill-looking’. Lawyers need to be aware that doctors often use the term ‘ill’ to mean what a lay person would call ‘seriously ill’ and ‘well’ to mean what a lay person might reasonably describe as ‘mildly ill’.
Galactosemia
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Patients with galactosemia may present first with sepsis neonatorum. The organism is most commonly Escherichia coli. In fact, prior to the advent of neonatal screening programs, the recommendation for the routine testing for galactosemia in all infants with sepsis led to most of the early diagnoses we encountered. A fulminant course of septicemia with early demise has been reported [18]. Complications of sepsis, such as osteomyelitis and meningitis, have also been observed. One patient developed gangrene of the toes bilaterally and of the dorsum of one foot [19]. Granulocyte function may be impaired [20, 21].
Why Does Sepsis Kill So Many Children?
Published in Comprehensive Child and Adolescent Nursing, 2023
So, what precisely is sepsis? In times past, sepsis was referred to as septicemia or blood poisoning. It is caused by a catastrophic immune response to infection which triggers “cytokine release syndrome” commonly referred to as a cytokine storm. Cytokines are a variety of different types of specific proteins which are part of the body’s immune defense strategy and whose functions are to signal and attract other immune cells. In simple terms, cytokines are chemical messengers that act on specific bodily cells to get them to enact the appropriate immune response to infection. For example, white cells can be instructed to proliferate the creation of more white cells to defend against an invading pathogen. Cytokines are also responsible for the cessation of the inflammatory response to infection when the onslaught by the pathogen has been successfully repelled. It is not fully clear why some individuals in reacting to infection then go on to develop sepsis, but certain groups are prone to develop the condition during an infective episode. This includes babies under one year of age, especially if born prematurely, and children who might have a weakened immune system following for example chemotherapy treatment (NHS, 2022).
A case report of a fulminant Aeromonas hydrophila soft tissue infection in a patient with acute lymphoblastic leukemia harboring a rare translocation
Published in Current Medical Research and Opinion, 2022
Emmanouil Charakopoulos, Panagiotis T. Diamantopoulos, Konstantinos Zervakis, Nefeli Giannakopoulou, Mina Psichogiou, Nora-Athina Viniou
Funada et al. showed that elderly male patients suffering from acute leukemia are the highest risk group among hematologic patients while most infections take place in the second half of the year. The most prominent underlying predisposing factors are neutropenia and recent chemotherapy whereas a history of exposure to water is uncommon. Regarding the infection site, 71% of patients develop gastrointestinal symptomatology ranging from mild diarrhea to severe enterocolitis; liver and biliary system involvement, anorectal infections, as well as pneumonia, occur in a minority of patients. The vast majority of patients survive more than one week after the onset of septicemia9. Interestingly, A. hydrophila colonizes the digestive tract in 8% of neutropenic and bone marrow transplant recipients, which is much more frequent than in the general population. This indicates that in febrile neutropenic patients Aeromonas might spread into the circulation through gut translocation, especially if there is also chemotherapy-induced disturbance of the gastrointestinal epithelial barrier9,10.
Excellent outcome following emergency deceased donor ABO-incompatible liver transplantation using rituximab and antigen specific immunoadsorption
Published in Scandinavian Journal of Gastroenterology, 2022
Ulrika Skogsberg Dahlgren, Gustaf Herlenius, Bengt Gustafsson, Johan Mölne, Lennart Rydberg, Andreas Socratous, William Bennet
In total, four ABOi recipients had biopsy proven T-cell mediated rejection (Table 4). Two adult patients had steroid resistant T-cell mediated rejection and both responded to anti-thymocyte globuline treatment. One patient developed AMR (Pat#12, Table 4). This patient was retransplanted with an ABOi graft due to acute-on-chronic liver failure, in turn due to therapy resistant chronic rejection. In addition to anti-AB antibody rebound, high MFI DSA (Class II DSA, MFI 12201) was detected post-transplantation. Multiple IA-, and PP-sessions were performed but were unsuccessful in controlling the Ab rebound (Figure 2(A,B)). A liver biopsy at POD 12 showed histological features of AMR (AMR-score 2, Figure 3(B)) with a strong C4d-deposition (C4d-score 3, Figure 3(C)). Several surgical complications also complicated the clinical course. During the first post-operative weeks the patient was re-operated three times, twice for bleeding with circulatory shock and once due to bile leakage. After the second bleeding episode a partial thrombosis in the hepatic artery proper was diagnosed. Thereafter intrahepatic necrosis developed followed by multiple intrahepatic biliary strictures. Septicemia contraindicated intensified immunosuppression and re-transplantation and the patient died four months post-transplantation.