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Cardiopulmonary Resuscitation
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Refer all the following patients to the neurosurgery team: Coma continues after resuscitation (GCS <9).Deterioration in neurological status, e.g. worsening in conscious state (2 points or more decrease in GCS), seizures, increasing headache, focal neurological signs.Skull fracture: compound depressed fracturebasal skull fracture (see p. 31)any skull fracture with confusion, decreased level of consciousness or focal neurological signs.Penetrating head injury.Confusion or other neurological disturbance (GCS 9–13) for more than 2 h with no defined skull fracture.Radiological abnormality on CT head scan.
Questions and Answers
Published in David Browne, Brenda Wright, Guy Molyneux, Mohamed Ahmed, Ijaz Hussain, Bangaru Raju, Michael Reilly, MRCPsych Paper I One-Best-Item MCQs, 2017
David Browne, Brenda Wright, Guy Molyneux, Mohamed Ahmed, Ijaz Hussain, Bangaru Raju, Michael Reilly
Answer: D. A penetrating head injury has a poorer prognosis than a closed head injury. Anterograde amnesia of 12 hours or less usually has a good prognosis with no long-term sequelae. Retrograde amnesia is not a good prognostic indicator of clinical course. [H. p. 193]
A Rare Fungal Orbital Infection in an Immunocompetent Young Male Caused by Lichtheimia corymbifera (Absidia corymbifera)
Published in Ocular Immunology and Inflammation, 2022
Vazhipokkil Anju Chandran, Kirthi Koka, Lily Therese, Bipasha Mukherjee
Moon et al. reported a case of an immunocompetent individual developing absidial infection in the scalp following an electrical burn.4 Similar cases of Lichtheimial invasion were seen in healthy individuals with an antecedent crush foot injury and penetrating head injury.6 However, our patient gave no such history of trauma, making this the first case report of orbital cellulitis caused by L. corymbifera and the first case to occur in an immunocompetent patient with no history of trauma. Fungi are notorious for angioinvasion causing thrombosis and infarction.1,2 Sudden loss of vision in these cases is attributed to central artery occlusion, direct invasion into the optic nerve, or thrombosis of the vessels supplying the optic nerve.1,2 Our patient also received a course of steroids before presenting to us, which may have accelerated the course of the disease, leading to loss of vision.
Longitudinal changes in blood-based biomarkers in chronic moderate to severe traumatic brain injury: preliminary findings
Published in Brain Injury, 2021
Caroline Schnakers, James Divine, Micah A. Johnson, Evan Lutkenhoff, Martin M. Monti, Katrina M. Keil, John Guthrie, Nader Pouratian, David Patterson, Gary Jensen, Vanessa C. Morales, Kathleen F. Weaver, Emily R. Rosario
The Centers for Disease Control and Prevention has defined a traumatic brain injury (TBI) as a “disruption in the normal function of the brain that can be caused by a bump, blow, or jolt to the head, or penetrating head injury” (1). In 2014, the number of TBI-related emergency department visits, hospitalizations, and deaths was approximately 2.88 million in the United States. The prevalence increased by 53% from 2006 (i.e., 1.88 million) and is often referred to as a “silent epidemic.” Moderate to severe TBI represents 15% of the total population with a TBI but accounts for 90% of total medical costs related to such injury (around 4 USD billion in direct medical cost per year) (1). In contrast, no effective treatment has been validated for patients with TBI, leading patients to deal with the aftermath of the injury for months or years. Recently, the importance of considering TBI as a chronic disease rather than an acute event has been highlighted by the TBI Model system (TBIMS; a program, sponsored by the National Institute on Disability, Independent Living, and Rehabilitation Research). Indeed, research has shown that, within 5 years post-injury, 52% of the patients with moderate to severe TBI have either declined functional outcome or die (2). These patients also have a poorer quality of life, face various chronic health issues (e.g., seizures, neuroendocrine dysregulation, psychiatric diseases, or neurodegenerative diseases), and have a shorter life expectancy as compared to individuals without TBI (2).
The consequences of traumatic brain injury from the classroom to the courtroom: understanding pathways through structural equation modelling
Published in Disability and Rehabilitation, 2020
Betony Clasby, Matthew Bennett, Nathan Hughes, Emma Hodges, Hannah Meadham, Darren Hinder, Huw Williams, Avril Mewse
Traumatic brain injury (TBI) is one of the leading causes of paediatric death and disability worldwide and comes with enormous economic, social, and personal costs [1–3]. Any damage or injury to the brain caused by a bump, blow, or jolt to the head or a penetrating head injury (HI) is considered a TBI [4], and severity is usually defined as mild, mild-complicated, moderate, or severe. Severity may be determined by multiple routes in the acute stages of injury: including loss of consciousness (often measured by the Glasgow Coma Scale) [5], structural brain imaging techniques, or measures of post-traumatic amnesia. In community settings, these determinants may be problematic, and studies typically rely on self-reported measures of time spent unconscious post-injury. However, this measure can be problematic as it often relies on participants’ to accurately self-report length of time spent unconscious.