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Intracranial haematomas
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
The clinical presentation is classically a history of head injury followed immediately by a period of concussion – this may be brief. This is followed by recovery – a lucid interval. It is during this period that blood accumulates within the cranial cavity to give rise to the features of a space-occupying lesion, with features of raised intracranial pressure and eventual lapse into coma. The time course for the lucid interval is variable ranging from several minutes to hours to several hours but may rarely be of day's duration (see Chapter 2). The presence of other brain injury may also modify the clinical picture.
Trauma of the Brain and Spinal Cord
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Fernando D. Goldenberg, Ali Mansour
SDH and EDH are often the result of mechanical injury of nearby vascular structures. EDH (Figure 11.1) frequently constitutes a surgical emergency. Radiologically, it is described as a lens-shaped extra-axial hematoma limited by suture lines, commonly resulting from an arterial bleed from a meningeal artery (middle meningeal artery usually). A lucid interval after the trauma may be present; however, clinical deterioration can be rapid. The mortality of acute EDH continues to decrease in recent decades as outcome is largely related to triage and timely surgical management. Acute SDHs (Figures 11.2 and 11.3) are extra-axial blood collections that cross sutures lines and may lead to brain compression, and in some cases possible focal underlying cerebral ischemia. Because they are often the result of tearing of the bridging veins between the cerebral cortex and the dural sinuses, conditions associated with brain atrophy (old age, alcoholism, and dementia) render those individuals more susceptible to SDH.
Trauma
Published in Sam Mehta, Andrew Hindmarsh, Leila Rees, Handbook of General Surgical Emergencies, 2018
Sam Mehta, Andrew Hindmarsh, Leila Rees
Extradural haematoma: blood accumulates in the extradural space and therefore has a lentiform appearance on CT. A classic ‘lucid interval’ is described where the patient appears to improve shortly before death. Extradural haemorrhage often results from damage to the meningeal vessels (especially the middle meningeal artery) over the temporal fossa. If evacuated, the prognosis is better than with a subdural haematoma as there is usually less associated direct injury to the brain itself.
Serum neuron-specific enolase levels at presentation and long-term neurological sequelae after acute charcoal burning-induced carbon monoxide poisoning
Published in Clinical Toxicology, 2018
J. M. Moon, B. J. Chun, S. D. Lee, E. J. Jung
Long-term neurological outcomes were classified into three groups according to the GOS score after discharge: good neurological outcomes (scores of 4–5 on the GOS after discharge), acute persistent severe neurological sequelae, and delayed persistent severe neurological sequelae. Acute persistent severe neurological sequelae were defined as an altered mental status (GCS score <13) at presentation and progression to dependency on assistance with daily activities (scores of 1–3 on the GOS after discharge) without recovery. Dependency on assistance with daily activities (scores of 1–3 on the GOS) that developed after a lucid interval was designated delayed persistent severe neurological sequelae. Because the lucid interval reportedly ranged from 2 to 45 days [2], delayed persistent severe neurological sequelae must have developed within 3 months.
Serum N-terminal proBNP, not troponin I, at presentation predicts long-term neurologic outcome in acute charcoal-burning carbon monoxide intoxication
Published in Clinical Toxicology, 2018
Jeong Mi Moon, Byeong Jo Chun, Min Ho Shin, Seung Do Lee
Acute carbon monoxide (CO) poisoning accounts for more than 50,000 annual emergency department (ED) visits [1]. Two neurologic syndromes occur after acute CO poisoning: persistent neurologic sequelae, which are evident immediately following CO poisoning and might be persistent, and delayed neurologic sequelae [2]. The incidences of persistent neurologic sequelae in intentional and severe CO poisoning (defined in a previous study as a Glasgow Coma Scale score <9, COHb >25% and S100B protein >0.165 ug/L) were 10.1 and 13.3%, respectively [2,3]. Delayed neurologic sequelae develop after a lucid interval ranging from 2 to 45 days. Most delayed neurologic sequelae resolve over the first few months; however, some severe neurologic sequelae persist, resulting in patient dependence [2]. Weaver et al. [4] observed cognitive sequelae in 37% of patients at 6 weeks after CO poisoning, and this incidence of cognitive sequelae decreased to 17% at follow-up reassessment conducted at 12 months after acute CO poisoning.
Evaluation of relationship between coronary artery status evaluated by coronary computed tomography angiography and development of cardiomyopathy in carbon monoxide poisoned patients with myocardial injury: a prospective observational study
Published in Clinical Toxicology, 2018
Yong Sung Cha, Hyun Kim, Yoonsuk Lee, Woocheol Kwon, Jung-Woo Son, Hyun Youk, Hyung Il Kim, Oh Hyun Kim, Kyung Hye Park, Kyoung-Chul Cha, Kang Hyun Lee, Sung Oh Hwang
The clinical parameters were assessed as follows: age; gender; intention for self-harm; source of CO; duration of CO exposure; time elapsed from rescue to arrival at the ED; cardiovascular risk factors including diabetes mellitus, hypertension, hyperlipidaemia, and smoking; symptoms and signs including cognitive dysfunction according to the Korean version of the Mini-Mental State Examination, which was developed for use in the Korean population (cognitive dysfunction was defined as scores less than 24 points); vital signs (blood pressure, heart and respiratory rates) and Glasgow Coma Scale (GCS) upon ED arrival; and HBOT utilization. The duration of CO exposure was investigated from the patients or their guardians. The duration of exposure was recorded as the estimated maximum duration of CO exposure measured from the time of normal consciousness to the time of detected CO exposure. In the ED, a 12-lead electrocardiogram (ECG) was obtained and ischemic changes were classified as new ST-segment elevation (≥1 mm), depression (≥0.5 mm), or T-wave inversion (≥2 mm) in two consecutive leads [15]. Final neurologic outcomes including full recovery, delayed neuropsychiatric sequelae (DNS), and permanent neurologic sequelae (PNS) were investigated for at least two months based on Choi et al.’s [16] observation of a lucid interval generally lasting from 2 to 40 days of follow-up. DNS was defined as the delayed onset of neuropsychiatric symptoms after the apparent recovery of neurocognitive symptoms due to acute CO poisoning [16]. In-hospital mortality was also evaluated.