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Nephrology, including fluid and electrolytes
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
10.10. Which of the following statements is/are true of post-streptococcal glomerulonephritis?More than 10% of children develop chronic renal failure.Hypertensive encephalopathy is a recognized complication.ASO titre is the most useful marker of streptococcal infection.Life-long penicillin prophylaxis is recommended.Abnormalities of serum complement usually persist for more than 3 months.
Neurological Manifestations of Medical Disorders
Published in John W. Scadding, Nicholas A. Losseff, Clinical Neurology, 2011
David and John Scadding Werring, John Scadding
Specific treatment will depend on the underlying cause. Dialysis relieves the uraemia, and effects reversal of many of the neurological symptoms. Convulsions can usually be controlled with low doses of anticonvulsants. Hypertensive encephalopathy may also arise in patients with renal failure.
Hypertensive Emergencies
Published in Karim Ratib, Gurbir Bhatia, Neal Uren, James Nolan, Emergency Cardiology, 2010
Karim Ratib, Gurbir Bhatia, Neal Uren, James Nolan
Hypertensive encephalopathy is an acute medical emergency characterized by headache, irritability and an altered conscious level. Other potential complications of a hypertensive crisis are an intracerebral or subarachnoid haemorrhage and a thrombotic infarction in an individual with predisposing atherosclerotic cerebrovascular disease.
Scorpion envenomation: a deadly illness requiring an effective therapy
Published in Toxin Reviews, 2021
Faez Amokrane Nait Mohamed, Fatima Laraba-Djebari
Sweating is a clinical sign resulting from an uncontrollable catecholamine release and from sympathic and parasympathic nervous system activity (Sedziwy et al.1968). It is more marked in cases with pulmonary edema (Abroug et al.2020). Anxiety and agitation are important indicators of the severity of scorpion envenomation and can be associated with other neurological symptoms such as convulsions (Aboumaâd et al.2014, Yang et al.2014); it is well associated with an increase of sympathetic tone swelling left ventricular after-load and causing intense vasoconstriction, thus raising left ventricular filling pressures and inducing elevated pulmonary artery wedge pressures, leading to hydrostatic pulmonary edema and cardiac dysfunction (Bouaziz et al.2006, Bahloul et al.2013). Other neurological problems may appear, resulting from hypertensive encephalopathy (Rebahi et al.2015). Pulmonary edema is preceded by high blood pressure, which could lead to neurological damage, which could explain the observed neurological signs in these patients (Bahloul et al.2013).
PRES secondary to autonomic dysreflexia: A case series and review of the literature
Published in The Journal of Spinal Cord Medicine, 2021
Molly E. Hubbard, Aaron A. Phillips, Rebecca Charbonneau, Jordan W. Squair, Ann M. Parr, Andrei Krassioukov
One possible etiology of PRES is that an abrupt and severe rise in BP overcomes the brain’s ability for autoregulation, leading to edema as fluid leaks from capillaries. The resolution of symptoms with BP treatment and several animal studies support this theory.27 Hypertensive encephalopathy has been documented in many other pathologic states in which systemic BP surpasses the limits of autoregulation.28 Furthermore, abnormal autoregulation of cerebral vasculature seen in SCI may predispose the posterior circulation to hypoperfusion.29 Conversely, some evidence exists that there is hypoperfusion and vasoconstriction, notable in patients who develop PRES in the absence of hypertension6,30 Another theory suggests that systemic toxicity (from chemotherapeutics, infection etc) leads to endothelial cell dysfunction and hypoperfusion,27 and this is supported by the diversity of conditions associated with PRES.
Bilateral cortical visual impairment resulting in Anton's syndrome
Published in Clinical and Experimental Optometry, 2020
Kendra C Pollard, Grace A Brown bissonnette, Stephanie R Norberg
Anton's syndrome is characterised by unawareness and denial of vision loss despite evidence of cortical blindness.2009 The prognosis for visual recovery in Anton's syndrome can vary based on aetiology but is typically poor.2014 Better prognosis has been found in cases of treated hypertensive encephalopathy and cortical hypoperfusion.2009 Improvement in symptoms can occur within three to six-months post‐injury, with the greatest improvement occurring in the first three-months.2016 In this case there was no visual recovery due to extensive encephalomalacia of both occipital lobes (Figure 2). The patient was referred to visual impairment services. His case was complicated by myoclonus, which limited his ability to use low‐vision devices. The patient had limited tolerance for blind rehabilitation services and stated he did not need visual aids as he could see well. He accepted a talking watch and a subscription for talking books through the National Library Service but deferred all other services.