They are usually characterized on CT as hyperdense foci in the frontal lobes adjacent to the floor of the anterior cranial fossa and in the temporal poles. Contusions, by definition, result from head trauma and are thus seen more frequently in young males. Typical causes include motor vehicle accidents or situations in which the head strikes the ground. Most contusions represent the brain coming to a sudden stop against the inner surface of the skull contrecoup accentuated by the natural contours of the skull see below. Cerebral contusions can occur anywhere, but have a predilection for certain locations, as a result of the direction of the head strike and the intrinsic shape of the skull cavity. Typically cortical contusions become more apparent on follow-up imaging due to further bleed or surrounding edema.

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If the address matches an existing account you will receive an email with instructions to reset your password. If the address matches an existing account you will receive an email with instructions to retrieve your username. The magnitude of damage to cerebral tissues following head trauma is determined by the primary injury, caused by the kinetic energy delivered at the time of impact, plus numerous secondary injury responses that almost inevitably worsen the primary injury. When head trauma results in a cerebral contusion, the hemorrhagic lesion often progresses during the first several hours after impact, either expanding or developing new, non-contiguous hemorrhagic lesions, a phenomenon termed hemorrhagic progression of a contusion HPC.

Because a hemorrhagic contusion marks tissues with essentially total unrecoverable loss of function, and because blood is one of the most toxic substances to which the brain can be exposed, HPC is one of the most severe types of secondary injury encountered following traumatic brain injury TBI. Historically, HPC has been attributed to continued bleeding of microvessels fractured at the time of primary injury.

This concept has given rise to the notion that continued bleeding might be due to overt or latent coagulopathy, prompting attempts to normalize coagulation with agents such as recombinant factor VIIa. Recently, a novel mechanism was postulated to account for HPC that involves delayed, progressive microvascular failure initiated by the impact. Here we review the topic of HPC, we examine data relevant to the concept of a coagulopathy, and we detail emerging data elucidating the mechanism of progressive microvascular failure that predisposes to HPC after head trauma.

T raumatic brain injury TBI is the most disabling of traumatic injuries, often leading to lifelong physical, cognitive, behavioral, and emotional impairments Langlois et al. Nearly half of hospitalized survivors of TBI experience long-term disabilities Selassie et al. TBI encompasses numerous types of insults to the brain, with one of the most severe being a hemorrhagic cerebral contusion. TBI associated with cerebral contusion is a frequent cause of death and disability in trauma victims who reach the hospital alive Alahmadi et al.

Excellent reviews on the natural history of cerebral contusions have been published Alahmadi et al. Here we focus specifically on the phenomenon of hemorrhagic progression of a contusion HPC , a secondary injury process that designates the enlargement or new appearance of a parenchymal hemorrhagic contusion due to delayed bleeding. Not only does HPC greatly exacerbate an already grave situation, but most frustrating to healthcare providers and patients, it does so during the several hours or early days after trauma when patients are already hospitalized.

Ample opportunity would be available to intervene if proper intervention could be devised. In this review, we begin by documenting the characteristic features of HPC. Then we examine two mechanisms that have been implicated in its development. First, we consider the conventional explanation, that an explicit or latent coagulopathy leads to continued or delayed bleeding of microvessels fractured at the time of primary injury.

Next we consider a novel, recently discovered mechanism postulating that microvessels in the region of injury penumbra receive kinetic energy from the impact that is not sufficient to fracture them, but is sufficient to induce a series of maladaptive molecular events that eventually results in their structural failure, leading to delayed formation of petechial hemorrhages which then coalesce to produce hemorrhagic progression. Distinguishing between these two mechanisms is important, because the implications for treatment are quite different.

For the first mechanism, treatment must be aimed at normalizing coagulation, whereas for the second, treatment must block the maladaptive molecular events in microvascular endothelial cells. Tissue damage after head trauma is due to primary injury plus secondary injury. Primary injury refers to the physical destruction of tissues that occurs within moments of impact. Kinetic energy deposited by the impact causes shearing of the tissues. The primary injury ruptures neurons, astrocytes, and oligodendrocytes, causing their immediate necrotic death.

Necrotic cell death releases intracellular substances e. The primary injury also ruptures microvessels, causing extravasation of blood and the loss of function of those vessels, which leads to ischemia. Breakdown products of extravasated blood are extremely toxic to central nervous system CNS cells and also incite secondary injury responses.

Secondary injury responses are numerous Table 1. All lead, more or less, to further tissue injury that worsens the primary injury. Many secondary injury responses are simply the natural consequence of primary tissue damage, such as the release of excitotoxic substances, free radical damage from blood breakdown products, and ischemia due to loss of microvessels. Other secondary injury responses are evolutionarily favored to accomplish useful functions, such as clearing tissue debris.

The classic example is the inflammatory response, involving both endogenous microglia and exogenous neutrophils and macrophages cells. Neutrophils phagocytize cellular debris, serving to clear it, but in the process they release free radicals that harm otherwise normal cells nearby, inadvertently propagating tissue injury Blight, ; Hampton et al.

Table 1. Contusive injury to the brain invariably is complicated by secondary injury due to microvascular dysfunction Yokota, , which worsens with time and leads to growth or expansion of the primary lesion.

Microvascular dysfunction has numerous causes and correlates, including endothelial swelling, vasoconstriction, vasospasm, and occlusion due to platelet and leukocyte aggregation and adhesion.

Microvascular dysfunction leads to: 1 tissue ischemia due to impairment of blood flow; 2 the formation of vasogenic edema, which causes tissue swelling that further exacerbates ischemia; and 3 in the worst cases, loss of the structural integrity of surrounding microvessels, which results in expansion or progression of the hemorrhagic lesion, known as HPC. The extravasated blood from the primary contusion, the edema, and the additional extravasated blood resulting from HPC together produce mass effect, which compresses adjacent healthy tissues, and if unchecked, leads to further ischemia.

Together, these processes raise intracranial pressure ICP , may cause herniation syndromes, and may necessitate surgical decompression to prevent death. On a computed tomography CT scan, a contusion generally appears as a hemorrhagic lesion, although sometimes injured tissues or part of a contusive lesion can appear normal isodense or as a hypodensity.

A contusion is distinguished from a laceration by the fact that with a contusion, the pia mater remains intact. A contusion is distinguished from a hematoma by the fact that with a contusion, blood is intermixed with brain tissue. When head trauma results in a contusion, the hemorrhagic lesion often expands or a new hemorrhagic lesion may develop remotely non-contiguously from the original contusion during the first several hours after impact Fig. Hemorrhagic progression of a contusion HPC. Note the expansion of the right frontal contusion.

Note the appearance of a new hemorrhagic lesion at a remote location marked by a hypodensity on the initial scan arrows. Such broad usages are imprecise, and the molecular mechanisms responsible for progression in each case is likely to be different.

By using this term, we convey two things: 1 our focus is on the traumatic cerebral contusion and its hemorrhagic progression; and 2 our goal is not simply to characterize the phenomenology of more blood on the CT scan, but to illuminate the process, the molecular mechanisms responsible for hemorrhagic progression. In our subsequent analysis, we use the term HPC where appropriate, and we add clarification in instances when the authors being reviewed did not make such a distinction. In the earliest description, Gudeman and associates Gudeman et al.

In another early paper, Fukamachi and colleagues Fukamachi et al. Servadei and co-workers Servadei et al. Fifteen of these patients had initial diagnoses of diffuse injury that evolved, whereas the remaining seven patients had already undergone surgery and developed new, non-contiguous, hemorrhagic lesions.

This study reinforced the early observations of Gudeman and associates Gudeman et al. That HPC frequently continues after craniotomy also is noted in more recent literature Aarabi et al. Oertel and co-workers Oertel et al. Their study examined progression of all hemorrhagic lesions, including epidural, subdural, subarachnoid, and intraparenchymal contusion hemorrhages. They also observed that about half of the patients who underwent craniotomy after the first CT scan later showed evidence of hemorrhagic progression, in accord with the aforementioned study by Servadei and associates Servadei et al.

In a prospective study, Narayan and colleagues Narayan et al. They also found that while small hemorrhagic lesions may expand, lesions that were larger at baseline tended to have substantially greater increases, with an associated greater likelihood of clinical impact. Alahmadi and associates Alahmadi et al. They also determined that patients with large contusions and low initial Glasgow Coma Scale GCS scores were at greater risk for delayed deterioration. HPC may be detected on CT scan even in cases of mild head injury.

In two studies Sifri et al. From the foregoing, it is evident that a contusion on the admission CT scan should be a cause for vigilance regarding possible HPC. A traumatic subarachnoid hemorrhage tSAH may be similarly predictive Chieregato et al. Independent factors associated with significant CT progression were the amount of tSAH and the presence or volume of brain contusions at admission. HPC was associated with poor clinical outcomes. The aforementioned reports represent a sampling of the available articles on HPC.

Other studies have contributed to our understanding of this phenomenon Allard et al. Edema formation and HPC are both manifestations of microvascular dysfunction, but there is a critically important distinction: one is associated with potentially reversible injury, whereas the other is associated with almost certain irreversible harm. Disregarding the underlying cause that induces formation of edema e.

This is not the case with HPC. Contused tissues consist of blood intermixed with brain tissue. For over a century, neuropathologists have recognized that extravasated blood is exquisitely toxic to brain cells, and that the presence of blood generally is associated with necrosis of intermixed CNS tissues hemorrhagic necrosis; Ramon y Cajal, In addition, a hemorrhagic contusion inevitably results in the formation of edema, further contributing to the mass of extravasated blood Engel et al.

A hemorrhagic contusion on CT scan demarcates tissues with essentially total, unrecoverable loss of function. The volume and location of a hemorrhagic contusion observed during the acute phase after head trauma predicts the volume and location of dysfunctional tissue that will exist after recovery. The predictive power of the CT scan in contusive head trauma resembles the predictive power of diffusion weighted imaging DWI on magnetic resonance imaging MRI in stroke; although the two are not equivalent, both identify tissues that are essentially irretrievably lost.

This pessimistic assessment of pathology is corroborated by clinical experience. Although not universal Gudeman et al. In the study by Stein and associates Stein et al. Servadei and colleagues Servadei et al. In the study by Chieregato and co-workers Chieregato et al. Allard and associates Allard et al. Thus, HPC is detrimental because it results in irrevocable loss of brain tissue that was ostensibly intact immediately following the primary injury.

Even in patients in whom HPC is not fatal, there is significant likelihood of increased morbidity. HPC is a progressive, secondary injury that occurs relatively late after trauma, and almost invariably occurs while under medical care. As such, it may be preventable if underlying molecular mechanisms can be identified so that appropriate treatments can be applied. This concept has given rise to the notion that continued bleeding might be due to an overt or latent coagulopathy Van Beek et al.

In the TBI literature, coagulopathy is often broadly defined as any perturbation in a patient's coagulation parameters, and may include a prolongation of the prothrombin time PT , an elevation of the International Normalized Ratio INR , an elevation of the activated partial thromboplastin time aPTT , or a decrease in the platelet PLT count Engstrom et al.

Coagulopathy can develop up to 5 days after injury, and the incidence appears to be linearly correlated with increasing severity of injury Lustenberger et al. The exact mechanisms that account for coagulopathy in TBI have not been fully elucidated, and disagreements persist as to the cause Cohen et al.

Tissue factor tissue thromboplastin is abundant in the brain Astrup, , and may be released in large quantities following trauma. Diffuse activation of the extrinsic coagulation pathway may lead to disseminated intravascular coagulation DIC.

Subsequent consumption of clotting factors may underlie a bleeding diathesis.


Cerebral contusion

Introduction: Traumatic brain injury TBI is a global medical problem. After TBI patients may show motor, behavioral and cognitive disabilities. Objective: The intention of this paper is to develop the patho-physiology of the head injury, beginning with epidemiological, anatomical, and physiological bases. Discussion and conclusions: The knowledge of the pathophysiology of TBI will help us to have a context with in we will try to describe and conceptualize in general way the most important patho-physiological process related to the head injury.


Contusiones y laceraciones cerebrales

Cerebral contusion , Latin contusio cerebri , a form of traumatic brain injury , is a bruise of the brain tissue. Contusions are likely to heal on their own without medical intervention. The symptoms of a cerebral contusion depend on the severity of the injury, ranging from minor to severe. Individuals may experience a headache, confusion, sleepiness, dizziness, loss of consciousness, nausea and vomiting, seizures, difficulty with coordination and movement, lightheadedness, tinnitus, and spinning sensations. They may also have difficulty with memory, vision, speech, hearing, managing emotions, and thinking.

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Hemorrhagic Progression of a Contusion after Traumatic Brain Injury: A Review




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