Neurological involvement in children with E. coli O104:H4-induced hemolytic uremic syndrome

Bauer, Angela; Loos, Sebastian; Wehrmann, Carola; Horstmann, Dirk; Donnerstag, Frank; Lemke, Johanna; Hillebrand, Georg; Löbel, Ulrike; Pape, Lars; Haffner, Dieter; Bindt, Carola; Ahlenstiel, Thurid; Melk, Anette; Lehnhardt, Anja; Kemper, Markus J.; Oh, Jun; Hartmann, Hans

doi:10.1007/s00467-014-2803-x

Cited by 34 publications

(23 citation statements)

References 26 publications

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“…The pathophysiology of neurological involvement in HUS is multifactorial 15. Cerebral thrombotic microangiopathy is only found in a minority of patients with HUS on autopsy, thereby emphasising that it may not be the major process leading to neurological symptoms and partially explaining why central nervous system dysfunction is often reversible.…”

Section: Discussionmentioning

confidence: 99%

A diagnosis of haemolytic-uraemic syndrome blurred by alcohol abuse

et al. 2014

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A 60-year-old man with a history of alcohol abuse was admitted to the intensive care unit (ICU) for status epilepticus. At first, laboratory and imagery findings were almost normal, and the symptoms were attributed to severe alcohol withdrawal due to a history of gastroenteritis reported by his family. But, during the following days, haemolytic anaemia, thrombocytopenia, acute renal failure, and ischaemic and haemorrhagic lesions seen on a cerebral CT scan led to the diagnosis of haemolytic-uraemic syndrome (HUS). Despite these severe complications, the patient made a good recovery following ICU and plasma exchange with fresh frozen plasma (FFP), but cognitive deficit still existed after 1 month. It is important to know that neurological manifestations can precede typical biological and radiological signs in HUS, and to not be misled in the diagnosis process, especially when a more common differential diagnosis is possible.

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Section: Discussionmentioning

confidence: 99%

A diagnosis of haemolytic-uraemic syndrome blurred by alcohol abuse

et al. 2014

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“…In our cohort, only 1 patient had persistent neurological symptoms at follow-up. However, additional detailed neuropsychological and neuromotor performance tests might reveal further impairment after HUS [13,31,32]. A neuropsychological analysis of adults affected during the 2011 outbreak did not show significant deficits 1 year after STEC infection [33].…”

Section: Discussionmentioning

confidence: 99%

“…The antiepileptic therapy was subsequently withdrawn, and the patient had no further seizures. (In previous publications, this patient was described with fine-motor disturbances during short-term follow-up and mild, still-improving hemiparesis during a specific neurological 6-month follow-up [12,13].) A third patient was treated prophylactically with an antiepileptic drug due to a pathological electroencephalogram.…”

Section: Neurological Outcomementioning

confidence: 99%

“…We previously reported clinical data on the acute phase of 90 children with HUS affected during the 2011 outbreak and a more specific neurological outcome report after 6 months of follow-up in 50 of the patients [12,13]. At initial short-term follow-up after a median of 4 months, 4 of 90 patients (4.4%) had CKD (n = 3 CKD stage 3-4, and n = 1 CKD stage 5), and neurological symptoms were present in 4 of 90 patients in total (n = 4/23 with major neurological symptoms during HUS) [12].…”

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confidence: 99%

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Intermediate Follow-up of Pediatric Patients With Hemolytic Uremic Syndrome During the 2011 Outbreak Caused by E. coli O104:H4

Loos

Aulbert

Höppe

et al. 2017

Clinical Infectious Diseases

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Background. In 2011 Escherichia coli O104:H4 caused an outbreak with >800 cases of hemolytic uremic syndrome (HUS) in Germany, including 90 children. Data on the intermediate outcome in children after HUS due to E. coli O104:H4 have been lacking.Methods. Follow-up data were gathered retrospectively from the medical records of patients who had been included in the German Pediatric HUS Registry during the 2011 outbreak.Results. Seventy-two of the 89 (81%) patients were included after a median follow-up of 3.0 (0.9-4.7) years. Hypertension and proteinuria were present in 19% and 28% of these patients, respectively. Of 4 patients with chronic kidney disease (CKD) > stage 2 at short-term follow-up, 1 had a normalized estimated glomerular filtration rate, and 3 (4%) had persistent CKD > stage 2. In 1 of these patients, CKD improved from stage 4 to 3; 1 who had CKD stage 5 at presentation received kidney transplantation; and 1 patient required further hemodialysis during follow-up. One patient (1.4%) still had major neurological symptoms at the latest follow-up. Dialysis during the acute phase (P = .01), dialysis duration (P = .01), and the duration of oligo-/anuria (P = .005) were associated with the development of renal sequelae. Patients treated with eculizumab (n = 11) and/or plasmapheresis (n = 13) during the acute phase of HUS had comparable outcomes.Conclusions. The overall outcome of pediatric patients after HUS due to E. coli O104:H4 was equivalent to previous reports on HUS due to other types of Shiga toxin-producing E. coli (STEC). Regular follow-up visits in patients are recommended after STEC-HUS.

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“…Injury to the central nervous system Central nervous system (CNS) affection carries a worse prognosis for full recovery and is observed in 30-60% of patients [18,133]. The pathogenetic mechanisms involved are similar to those described in the kidney with toxin binding to neurons and endothelial cells in the CNS [134], damage to the blood-brain barrier and the induction of multiple inflammatory mediators (for review, see [78]).…”

Section: Renal Failurementioning

confidence: 99%

Haemolytic uraemic syndrome

et al. 2016

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Abstract. Karpman D, Loos S, Tati R, Arvidsson I (Clinical Sciences Lund, Lund University, Lund, Sweden). Haemolytic uraemic syndrome (Review). J Intern Med 2017; 281: 123-148.Haemolytic uraemic syndrome (HUS) is defined by the simultaneous occurrence of nonimmune haemolytic anaemia, thrombocytopenia and acute renal failure. This leads to the pathological lesion termed thrombotic microangiopathy, which mainly affects the kidney, as well as other organs. HUS is associated with endothelial cell injury and platelet activation, although the underlying cause may differ. Most cases of HUS are associated with gastrointestinal infection with Shiga toxin-producing enterohaemorrhagic Escherichia coli (EHEC) strains. Atypical HUS (aHUS) is associated with complement dysregulation due to mutations or autoantibodies. In this review, we will describe the causes of HUS. In addition, we will review the clinical, pathological, haematological and biochemical features, epidemiology and pathogenetic mechanisms as well as the biochemical, microbiological, immunological and genetic investigations leading to diagnosis. Understanding the underlying mechanisms of the different subtypes of HUS enables tailoring of appropriate treatment and management. To date, there is no specific treatment for EHEC-associated HUS but patients benefit from supportive care, whereas patients with aHUS are effectively treated with anti-C5 antibody to prevent recurrences, both before and after renal transplantation.

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Neurological involvement in children with E. coli O104:H4-induced hemolytic uremic syndrome

Cited by 34 publications

References 26 publications

A diagnosis of haemolytic-uraemic syndrome blurred by alcohol abuse

A diagnosis of haemolytic-uraemic syndrome blurred by alcohol abuse

Intermediate Follow-up of Pediatric Patients With Hemolytic Uremic Syndrome During the 2011 Outbreak Caused by E. coli O104:H4

Haemolytic uraemic syndrome

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