Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the correlation between postmortem magnetic resonance imaging (MRI) of the head and autopsy findings in suspected child abuse. Postmortem MRI was performed within 24 h of death and before autopsy in 11 children 2 years old or younger whose deaths were unexplained or suspected to be due to child abuse. MRI findings were available to the pathologist at the time of autopsy. In eight cases of death from non-accidental trauma, cerebral edema, contusion, shearing injury, ischemia, and infarction were well demonstrated on MRI. In the three deaths determined not to be due to trauma, there were no false-positive MRI findings. Autopsy was superior in detection of subarachnoid hemorrhage, suture separation, extracranial injuries, and very small subdural hematomas. MRI findings were useful in directing the autopsy and brain-cutting to focal areas of abnormality. Postmortem MRI and autopsy are complementary, and each may disclose abnormalities missed by the other. In half of the eight cases of child abuse examined, the combination of MRI and autopsy added valuable information compared with the results of autopsy alone. Postmortem MRI can be a valuable addition to autopsy findings in the investigation of fatalities potentially due to child abuse.
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PMID:Postmortem cranial MRI and autopsy correlation in suspected child abuse. 887 Aug 72

The neuropathology of trauma is reviewed based on the mechanism of injury. Pathology is divided into primary and secondary injury, based on the relationship to the time of injury. It is further divided by mechanism, with primary impact injury including skull fracture, epidural hematoma, brain contusion and laceration, and intracerebral hemorrhage; primary inertial injury including subdural hematoma, diffuse axonal injury, and diffuse vascular injury; and secondary injury including hypoxia/ischemia, brain swelling, infection, and increased intracranial pressure. The neuropathology of child abuse is also reviewed.
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PMID:Traumatic neuropathology. 952 63

This review illustrates the changing paradigms in the understanding of the pathogenesis of pneumatosis intestinalis. Although many theories have been evoked, pragmatically there appear to be four major clinical and diagnostic imaging considerations. The most common and most emergent life-threatening cause of intramural bowel gas is the result of bowel necrosis due to bowel ischemia, infarction, necrotizing enterocolitis, neutropenic colitis, volvulus, and sepsis. In the stomach, intramural gas can be caused by emphysematous gastritis or ingestion of caustic agents. These situations represent surgical emergencies. Pneumatosis is found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma, including the trauma of child abuse. Disruption can also be iatrogenic from intracatheter jejunal feeding tubes, stent perforation, sclerotherapy, or surgical or endoscopic trauma. In these cases, the gas may be focal or linear. Treatment depends on the extent of the disruption and the underlying cause. A more subtle form of mucosal disruption may occur due to mucosal erosions and also to defects in intestinal crypts secondary to acute and subclinical enteritides that allow intraluminal bacterial gas under pressure to percolate into the bowel wall layers, particularly the submucosa (29). Pneumatosis, often linear or cystic in appearance, is seen with increased frequency in patients who are immunocompromised because of steroids, chemotherapy, radiation therapy, or AIDS. In these cases, the pneumatosis may result from intraluminal bacterial gas entering the bowel wall due to increased mucosal permeability caused by defects in bowel wall lymphoid tissue. Clinical and imaging findings are important in the differentiation of this transient pneumatosis from fulminant life-threatening causes in this subset of patients. A pulmonary cause must still be considered in cases of chronic obstructive pulmonary disease, asthma, and cystic fibrosis. It can occur with barotrauma and after chest tube placement. It may relate to increased intrathoracic pressure associated with retching and vomiting. The possibility remains that occasionally the origin of pneumatosis intestinalis will remain cryptogenic--caused but unexplained.
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PMID:Pneumatosis intestinalis: a review. 953 Feb 94

Leukocyte-endothelial adhesion molecules, critical to the development of acute inflammation, are expressed in brain as part of the acute inflammatory response to traumatic brain injury (TBI). We measured the concentrations of the adhesion molecules P-selectin, ICAM-1, E-selectin, L-selectin, and VCAM-1 in ventricular cerebrospinal fluid (CSF) from children with severe TBI (Glasgow coma score < 8) and compared these findings with those from children with bacterial meningitis. P-selectin, an adhesion molecule associated with ischemia/reperfusion, was increased in children with TBI versus meningitis and control. Univariate and multivariate regression analyses demonstrated associations between CSF P-selectin and child abuse and age of < 4 years, and a significant, independent association between CSF intercellular adhesion molecule-1 (ICAM-1) and child abuse. These results are consistent with a specific acute inflammatory component to TBI in children. Future studies of secondary injury mechanisms and therapy after TBI should assess on the roles of P-selectin and ICAM-1 in injury and repair processes in brain after TBI.
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PMID:Soluble adhesion molecules in CSF are increased in children with severe head injury. 981 34

Rapid induction of 72-kD heat shock protein (Hsp70) is a key component of the stress response and is seen after a variety of insults to the brain including experimental hyperthermia, ischemia, seizures, and traumatic brain injury (TBI). Little is known about the endogenous stress response in pediatric patients after brain injury. Accordingly, the concentration of Hsp70 was determined in 61 cerebrospinal fluid (CSF) samples from 20 infants and children after TBI. Peak Hsp70 level were increased in TBI patients vs. controls (4.60 [1.49-78.99] vs. 2.18 [1.38-4.25] ng/mL, respectively, median (range), p = 0.01) and occurred most often on day 1 after injury. Strikingly, CSF levels of Hsp70 were positively and independently associated with inflicted vs. non-inflicted TBI (7.03 [2.30-27.22] vs. 2.06 [1.06-78.99] ng/mL, respectively, p = 0.05). Endogenous Hsp70 expression was confirmed by Western blot and immunocytochemistry using brain tissue samples removed from patients who underwent decompressive craniotomy for refractory intracranial hypertension or at autopsy. These data suggest that the endogenous stress response, as measured and quantified by the Hsp70 concentration in CSF, occurs in infants and children after TBI. The endogenous stress response is more robust in victims of child abuse, compared with patients with accidental TBI, supporting age-dependence or a difference in either injury frequency, duration, severity, or mechanism in this subgroup of TBI patients. Further studies are needed to determine the role of Hsp70 in both non-inflicted and inflicted TBI in infants and children.
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PMID:Induction of the stress response after inflicted and non-inflicted traumatic brain injury in infants and children. 1511 98

Cerebral blood flow, and its control, vary as a function of age. This review focuses on the perinatal period and compares/contrasts this age period to that of the juvenile/adult. Additionally, this review describes mechanisms important in the control of the cerebral circulation as a function of age during physiologic and pathologic conditions. Two topics of pathophysiology are considered: cerebral hypoxia ischemia, often seen in perinates due to problems with delivery or respiratory management post delivery, and traumatic brain injury, described as the shaken impact syndrome, an example of child abuse. Clinically, it is important to understand the pathophysiology of the cerebral circulation in order to optimize mechanistically appropriate therapeutic modalities.
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PMID:Age and cerebral circulation. 1592 20

Abusive head trauma (AHT) is the most common cause of severe traumatic brain injury (TBI) in infants and the leading cause of child abuse-related deaths. For reasons that remain unclear, mortality rates after moderate AHT rival those of severe nonintentional TBI. The vulnerability of the developing brain to injury may be partially responsible for the poor outcomes observed after AHT. AHT is mechanistically more complex than nonintentional TBI. The acute-on-chronic nature of the trauma along with synergistic injury mechanisms that include rapid rotation of the brain, diffuse axonal injury, blunt force trauma, and hypoxia-ischemia make AHT challenging to treat. The anesthesiologist must understand the complex injury mechanisms inherent to AHT, as well as the pediatric TBI treatment guidelines, to decrease the risk of persistent neurologic disability and death. In this review, we discuss the epidemiology of AHT, differences between AHT and nonintentional TBI, the severe pediatric TBI treatment guidelines in the context of AHT, anesthetic considerations, and ethical and legal reporting requirements.
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PMID:The Anesthesiologist's Role in Treating Abusive Head Trauma. 2719 39