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Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
This patient suffered a motorcycle accident, with brain tissue visible through the wound.
Traumatic brain injury (TBI) is a widespread global public health problem with potentially catastrophic consequences.[1] In 2013, approximately 2.5 million TBI-related emergency department (ED) visits occurred in the United States, along with about 56,000 TBI-associated deaths.[2,3] Therefore, it is critical that emergency physicians, trauma surgeons, and other clinicians be able to identify TBI, initiate focused and appropriate workup, and administer efficient and effective care.
Adapted image from the United States Navy / Photographers Mate 2nd Class Jayme Pastoric.
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
In the image above, a college football player receives a direct blow to the head and neck.
Etiology of TBI
Leading causes of TBI in the general population are falls, direct blows (shown), and motor vehicle collisions.[3] Blast injuries are the most common cause of TBI in war zones.
TBI involvement in sports and recreational activities is common, especially in children as they grow older.[4] However, although there are a reported 1.6-3.8 million sports-related head injuries each year, these figures are an underestimate due to the lack of reporting.[4,5]
Adapted image from the medical gallery of Blausen Medical 2014 via Wikimedia Commons.
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
Anatomy of the Brain
The brain consists of three main structures: the cerebrum, the cerebellum, and the brainstem. It is engulfed in and bathed by cerebrospinal fluid (CSF), which is constantly resorbed and produced in the ventricles.[6,7] At the level of the cerebral hemispheres, the lateral ventricles are connected to each other, as well as to the third ventricle, by the interventricular foramen of Monroe. The third ventricle communicates with the fourth ventricle via the cerebral aqueduct of Sylvius. The fourth ventricle allows CSF to flow into the subarachnoid space around the brain and spinal cord; it is then absorbed within the subarachnoid space into the venous system via arachnoid villi.[7]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
The brain is protected by osseous and tissue components.
The meninges are the three tissue layers that cover the brain. The innermost layer, the pia mater, conforms to the gyri of the brain and is rich with blood vessels. The next layer, the arachnoid mater, is thin and weblike. The subarachnoid space between these two layers holds CSF around the brain and also houses the major arterial blood supply for the brain. The dura makes up the outermost layer, which is divided into the meningeal dura and the periosteal dura. For the most part, the two dura are fused, except where they are separated at the venous sinuses.[7,8]
The space under the dura is known as the subdural space, and the space above the dura is the epidural space. The separations of the dura are important to recognize as they are critical points of vascular compromise in TBI.[7,8]
Adapted image from Sobotta J, McMurrich J. Atlas and Textbook of Human Anatomy. Philadelphia, Pa / London, UK: WB Saunders Co; 1908 [public domain]. Via Wikimedia Commons.
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
Two dural structures—the falx cerebri and tentorium cerebelli—divide the brain into three compartments. The tentorium cerebelli separates the brain into the supratentorium, or the cerebrum, and the infratentorium, which consists of the brainstem and cerebellum. The falx cerebri divides the supratentorium into right and left hemispheres. These anatomic distinctions are crucial in the development and identification of herniation.[6,7]
Finally, all of the brain structures are enclosed in a dense fusion of osseous portions that ultimately form the skull. The many structures enveloping the brain for protection stand as challenges during TBI. Because the brain essentially floats in the CSF, it moves with high velocity during acceleration/deceleration motions and with direct blows, causing direct damage to the brain, disruption of the meninges, and vascular insult.[8] The most pertinent areas of skull anatomy to keep in mind with regard to TBI are the frontal and temporal bones—their irregular surfaces can lead to direct brain contusions.[7,8]
Adapted image from Meguins LC, Sampaio GB, Abib EC, et al. J Med Case Rep. 2014;8:153. [Open access.] PMID: 24886310, PMCID: PMC4066315.
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
These computed tomography (CT) scans depict a right acute subdural hematoma, hemispheric edema, and midline shift with compression of the right lateral ventricle. The scans were part of a series of admission images obtained in a male victim of a motorcycle accident. Although he was hemodynamically stable on presentation, his Glasgow Coma Scale (GCS) score was 6 points and he had right eye mydriasis. Despite undergoing a right decompressive craniectomy and evacuation of a later contralateral extradural hematoma, the patient's condition worsened within 48 hours and he died on postoperative day 9.
Intracranial pressure
Normal intracranial pressure (ICP) is about 5-15 mmHg (10 mmHg in the resting state[9]). Bleeding, edema, and necrosis occurring in an enclosed space within the skull leads to a rise in ICP.[8] As the body tries to autoregulate for the elevated ICP, a constellation of clinical signs known as the "Cushing reflex" occurs (eg, hypertension, bradycardia, irregular respirations).[10] It is paramount to identify these indications of worsening injury and respond promptly; poor outcomes are associated with an ICP of over 20 mmHg.[9] If the increased ICP is not relieved, clinical deterioration can quickly ensue—with potentially catastrophic results.[10]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
This lateral scout brain CT scan was taken in a patient who presented with a lodged metal ice pick. The tip of the ice pick is in the suprasellar cistern, and the entire tool overlies the anterior cranial fossa.
Initial Evaluation
The initial evaluation of TBI is integrated into the primary trauma survey. Barring any circumstances that make such an assessment not possible, clinicians should examine the patient's pupillary and vocal responses, as well as their extremity movement.[9]
The GCS is a well-established tool that has been incorporated into the Advanced Trauma Life Support (ATLS) protocol for rapid and comprehensive evaluation of neurologic status.[11] The ATLS program and American College of Surgeons (ACS) use the following GCS scores to classify a patient's level of TBI and to help guide initial management of the injury[9]:
GCS score above 12: Mild/minor TBI
GCS score of 9-12: Moderate TBI
GCS score below 9: Severe TBI
The 10th edition of the ATLS updated the GCS scoring system to include a "non-testable" designation, with the aim of expressing patients' mental status.[12]
Adapted image from Iannella G, Manno A, Pasqualitto E, et al. Case Rep Otolaryngol. 2016;2016:7521798. [Open access.] PMID: 27597915, PMCID: PMC4997066.
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
The above images are coronal T2-weighted magnetic resonance imaging (MRI) scans. Left: A hyperintense CSF leak to the posterior skull base (red arrows) and CSF leakage in the mastoid cells (yellow arrow) are seen. Right: A very large, hyperintense CSF leak extends between the lateral skull base and the first cervical vertebra (red arrows). Note the cerebellar compression.
A combination of the GCS score, clinical history, and examination helps to direct healthcare providers toward additional patient evaluation and management. Further assessment in TBI should include investigation for the presence of open or basilar skull fracture(s), CSF leak(s), and penetrating head injury. CT scanning has become the standard initial radiologic study for TBI owing to its speed and accuracy.[9,13]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
An acute, left-sided epidural hematoma (EDH) with midline shift of the ventricular system is visible in this CT scan. Immediate surgical evacuation of the hemorrhage is required.
Epidural Hematoma
EDH is a hemorrhage between the skull and dura mater, usually caused by an inciting focused blow to the head, such as from a baseball bat. Approximately 80% of these injuries occur in the temporoparietal region of the skull.[14] Blood quickly accumulates as the skull fractures, with the majority of cases involving injury to the middle meningeal artery. Occasionally, EDH can be caused by a venous bleed, typically in the posterior fossa or parietal-occipital region.[14]
Patients suffering an EDH classically lose and then regain consciousness, an episode known as a "lucid interval." These individuals then undergo a rapid deterioration in their level of consciousness, neurologic function, and hemodynamic stability.[15]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
The above CT scans show (left) a right-sided EDH in association with a small intracerebral hemorrhage and (right) a right skull fracture revealed on the bone window with edge accentuation.
EDH can be managed surgically or conservatively. Craniotomy is the treatment of choice for this injury. Bedside burr holes can be created by a trauma surgeon or an emergency medicine physician in select patients, such as those awaiting transfer to a high-level trauma center or hemodynamically unstable individuals.[16] This procedure can be a rapid, safe, and accurate method for finding and partially decompressing most extracerebral intracranial hematomas.[16]
Although clinical judgment is crucial in determining how best to treat EDH, the criteria for conservative management includes an EDH that is smaller than 30 mL, is less than 15-mm thick, has a less than 5-mm midline shift, does not involve focal neurologic deficit, and is associated with a GCS score above 8.[14] Interventional radiologic middle meningeal artery embolization is indicated in particular patients with active extravasation on CT scans.[17,18]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
The above noncontrast CT scan depicts an acute, right-sided subdural hematoma (SDH) with midline shift.
Subdural Hematoma
SDH is caused by a shearing of bridging veins that leads to blood collecting between the dura and arachnoid mater.[19] Because this is a venous bleed under low pressure, the blood accumulation is slow; consequently, the patient's symptomatic presentation can be varied and may be delayed for up to weeks—and thus easily missed. The wide clinical spectrum of SDH presentation includes complaints of headache, a decreased level of consciousness, gait difficulty, confusion, and other cognitive dysfunction.[20]
Those at risk for SDH include individuals with more prominent subdural spaces, such as infants, as well as alcoholics and elderly patients, in whom brain shrinkage increases the subdural space.[21]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
This coronal T1-weighted MRI scan without contrast shows an SDH.
If an SDH occurs, prompt diagnosis and treatment are essential, as there can be extensive blood accumulation and brain damage. Emergent surgical intervention is recommended if there has been a 2-point or greater decrease in the GCS score between the injury's occurrence and the hospital evaluation, fixed and dilated pupils are present, and/or the ICP exceeds 20 mmHg.[20,22] Clues obtained in the patient's history, including comorbidities, also aid emergency clinicians in determining the presence of SDH.
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
A 47-year-old woman presented to the ED with headache and vomiting. Her CT scan (above) revealed subarachnoid hemorrhage (SAH).
Subarachnoid Hemorrhage
Trauma is the most common cause of SAH.[23] Traumatic SAH (tSAH) can be difficult to diagnosis, as only 39% of such occurrences are seen on CT scan.[24] However, early recognition is essential owing to this lesion not only correlating with a two-fold increase in mortality but also having a high association with arterial spasm. Multiple studies have shown poor outcomes with tSAH, including those from the Head Injury Trials (HIT I-IV).[25,26]
The clinical presentation of tSAH includes headache and neurologic deficit. Complications such as hydrocephalus, herniation, and dyselectrolytemia may ensue.[25,27] Conflicting and incomplete data exist regarding whether nimodipine (typically given in doses of 60 mg every 4 hours for 21 days to control vasospasms) improves outcomes in tSAH.[25,28,29]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
In the above noncontrast CT scan, the presence of multiple petechial hemorrhages (arrows) located at the gray-white matter interface is consistent with diffuse axonal injury (DAI).
Diffuse Axonal Injury
DAI is caused primarily by shearing of the axons in the brain as a result of sustained acceleration-deceleration forces.[30,31] Subsequent edema and degeneration lead to further damage. DAI is one of the most common pathologic features in TBI. Although it is most often caused by motor vehicle accidents, this condition is also seen in athletes involved in high-speed collisions.[30,31]
DAI is believed to be present in every patient with TBI who loses consciousness, including victims of motor vehicle accidents.[30,32,33] Other symptoms/signs include memory loss and cognitive derangements. However, although DAI typically induces prolonged loss of consciousness, it rarely causes brainstem-associated hemodynamic changes.[34]
Adapted image from Mehan WA Jr, Gonzalez RG, Buchbinder BR, et al. PLoS One. 2014;9(10):e110803. [Open access.] PMID: 25343371, PMCID: PMC4208779.
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
Left: Axial diffusion-weighted trace MRI scan. Compatible with nonhemorrhagic DAI, a focus of restricted diffusion occurs within the left dorsolateral midbrain (arrow). Right: Axial gradient recalled echo MRI. Compatible with hemorrhagic DAI, a punctate foci of susceptibility effect exists within the right temporal lobe (arrows).
CT scanning is the preferred imaging evaluation in the acute setting of TBI. Findings such as multiple small (<2 cm) intraparenchymal hemorrhages, hemorrhagic contusions, and foci with altered signaling that signifies white matter shearing are included in the diagnostic criteria for DAI.[32,33] However, despite the preference for CT imaging, up to 20% of lesions are not recognized on the initial CT-scan evaluation.[34] Thus, MRI is the favored imaging modality for the diagnosis of DAI, with findings described as diffuse, hyperintense foci. Emerging therapies for DAI include therapeutic hypothermia, steroids, and oxygen radical scavengers.[35]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
Basilar Skull Fracture
Basilar skull fractures are linear breaks in the base of the skull (arrow), with the most frequently involved region being the petrous portion of the temporal bone.[36] The presence of these types of fractures are usually identified by signs such as periorbital ecchymosis ("raccoon eyes"), posterior auricular bruising ("battle sign"), hemotympanum, and CSF rhinorrhea.[36]
Thorough evaluation and close management is required for patients with basilar skull fractures, as these wounds are typically associated with other injuries, including middle meningeal artery injury, which can lead to EDH.[37] An estimated 50% of basilar skull fractures are associated with delayed vascular injury secondary to carotid disruption;[38,39] about 8.5% of cases of blunt basilar skull fractures have related vascular injuries.[40]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
This lateral 24-hour cranial scintigraphic image in a patient with clinically evident right-sided CSF rhinorrhea demonstrates increased tracer accumulation in the nasal region (arrow).
In general, conservative management is administered for basilar skull fractures in patients who are neurologically intact.[36] Prophylactic antibiotics are not recommended, as they have not been shown to be of benefit in reducing the frequency of meningitis in those with skull base fractures or CSF leakage,[41,42] nor in preventing postcraniotomy meningitis or meningitis following CSF shunt placement.[41] Surgical intervention is typically reserved for severe and coexisting injuries, such as persistent CSF leak.[43,44]
In patients with a basilar skull fracture and a CSF leak, the Infectious Diseases Society of America (IDSA) recommends (1) leak repair attempts if the CSF leakage persists longer than 7 days and (2) pneumococcal vaccination (due to a high risk of Streptococcus pneumoniae infection in the setting of head trauma and CSF leak).[41]
Basilar skull fractures, which result from high-velocity trauma, are associated with a 400-fold increase in the incidence of EDH.[12]
Adapted image from Chung P, Khan F. J Med Case Rep. 2015;9:173. [Open access.] PMID: 26282266, PMCID: PMC4539919.
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
This CT scan, taken 24 hours after the patient sustained a mild TBI (GCS score = 14-15), shows a right posteromedial parietal intraparenchymal hemorrhage with vasogenic edema, subarachnoid and subdural extension, and right anterolateral subdural hematoma.
Posttraumatic Intraparenchymal Hemorrhage
Traumatic intraparenchymal hemorrhage (tIPH) is a catastrophic complication of TBI that can occur in the acute setting with direct injury. However, tIPH more often has a delayed presentation in the form of hemorrhagic progression of contusion, with inflammatory responses inducing hemorrhage.[45] tIPH typically occurs within the first 12 hours of the injury, but it may appear as late as 3-4 days later.
It is imperative to reverse any abnormal coagulation that will permit hemorrhagic conversion.[46] Hemorrhagic progression of contusion is one of the most important secondary injuries that can occur following tIPH; the associated delayed presentation may lead to challenges in diagnosis and management.[47]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
A nonenhanced head CT scan at the level of the suprasellar cistern is shown above. A large right frontotemporal subdural hematoma is exerting mass effect on the right frontal and temporal lobes, effacing the suprasellar cistern and the ipsilateral temporal horn and resulting in right-sided uncal herniation, as well as dilatation of the contralateral temporal horn. Subfalcine herniation and narrowing of the contralateral ambient and quadrigeminal plate cisterns are also present.
Cerebral Herniation
Brain herniation is also a potential catastrophic consequence of TBI; primarily resulting from increased ICP, it can be fatal if not immediately addressed.[48] Six main types of cerebral herniation are recognized: cingulate (subfalcine, transfalcine), uncal (transtentorial), central, transcalvarial, upward (upward cerebellar/reverse coning), and tonsillar (downward cerebellar/coning).[49] Cingulate herniation is the most common type, followed by uncal herniation.[50] Management includes ICP reduction and, potentially, surgical decompression.[48]
Adapted image from Bigler ED. Front Hum Neurosci. 2013;7:395. [Open access.] PMID: 23964217, PMCID: PMC3734373.
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
The above images, from an adult male who sustained a severe TBI (GCS score = 3), demonstrate differences in the brain before (A: MRI) and after (B-F: CT scans) the head injury. As seen in the CT scans, the ventricle-to-brain ratio (VBR), a global measure of brain integrity, progressively increases over time, reflecting parenchymal degeneration.
Management of TBI
In addition to standard medical care with a multidisciplinary team (eg, cardiopulmonary/hemodynamic stabilization), elevate the patient's head to decrease dependent blood flow and pressure. Minimize metabolic and hemodynamic cerebral insults, including through maintenance of appropriate blood pressure, euglycemia, and normocapnia.[51]
Management of TBI includes strategies such as decompressive craniectomy or craniotomy; hyperosmolar therapy; CSF drainage; ventilation therapies; use of anesthetics, analgesics, and sedatives; nutritional support; and/or deep vein thrombosis and seizure prophylaxis.[51,52] (For example, guidelines support antiepileptic drug administration for prevention of early, but not late, posttraumatic seizures [PTS]).[52,53]
In severe TBI, a large frontotemporoparietal decompressive craniectomy is recommended over a small one to reduce mortality and improve neurologic outcomes
Early, short-term, prophylactic hypothermia is not recommended to improve outcomes in patients with diffuse injury
Mannitol is effective in controlling raised ICP; avoid arterial hypertension; limit mannitol use before ICP monitoring to those with signs of transtentorial herniation or progressive neurologic deterioration not due to extracranial causes
An external ventricular drainage device system zeroed at the midbrain with continuous, rather than intermittent, CSF drainage may be considered to more effectively reduce ICP; CSF drainage may be considered to lower ICP in those with an initial GCS score below 6 within the first 12 hours postinjury
Giving a high-dose barbiturate is recommended to control elevated ICP refractory to maximum standard medical/surgical therapy; hemodynamic stability is crucial before and during barbiturate therapy
Steroids are not recommended for improving outcome or reducing ICP; high-dose methylprednisolone is contraindicated in severe TBI
Feed patients to gain basal caloric replacement by at least postinjury day 5 and at most by day 7; transgastric jejunal feeding is recommended to reduce the incidence of ventilator-associated pneumonia (VAP)
Povidone-iodine oral care is not recommended to reduce VAP and may raise the risk of acute respiratory distress syndrome
Antimicrobial-impregnated catheters may be considered to prevent catheter-related infections during external ventricular drainage
Phenytoin or valproate is not recommended for prophylactic prevention of late PTS; not enough efficacy data exist to recommend levetiracetam versus phenytoin for prevention of early PTS and toxicity[54]
Sagar Dave, DO; Matthew B Tichauer, MD | March 11, 2019 | Contributor Information
Close view of the brain during a craniotomy.
Refractory TBI
In refractory cases of TBI with persistently elevated ICP, it can be difficult to optimize cerebral perfusion pressure (and, thus, cerebral blood flow). Unilateral and bilateral decompressive craniotomy or craniectomy helps to increase the intracranial compartment space and reduce ICP in severe TBI cases.[55-57] Continuous renal replacement therapy aids in stabilization of fluid balance and electrolyte disturbances, thus decreasing spikes in ICP elevation.[58-60]
The use of therapeutic hypothermia in TBI remains controversial; however, it may lower metabolic demand to the injured brain, potentially improving outcomes in severe cases and in patients with TBI-related coagulopathy.[61,62] Case reports indicate that decompressive laparotomy shows some benefit in relieving intracranial compartment pressure in refractory cases of elevated ICP in TBI, particularly in patients with polytrauma.[63-65]
8 Cases of Food Poisoning: Find the Pathogen Responsible
Approximately 1 in 6 Americans will contract food poisoning this year. Review our slideshow for the signs and symptoms that can lead you to the correct diagnosis and treatment of foodborne diseases.Slideshows, February 2019
The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes. SAH constitutes half of all spontaneous atraumatic intracranial hemorrhages; the other half consists of bleeding that occurs within the brain parenchyma.Diseases/Conditions, December 2018
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Authors
Sagar Dave, DO
Resident, PGY-3
Department of Emergency Medicine and Critical Care
Hartford Hospital–University of Connecticut School of Medicine
Hartford, CT
Disclosure: Sagar Dave, DO, has disclosed no relevant financial relationships.
Matthew B Tichauer, MD
Director of Emergency Critical Care
Assistant Professor of Traumatology
Department of Emergency Medicine and Critical Care
Hartford Hospital–University of Connecticut School of Medicine
Hartford, CT
Disclosure: Matthew B Tichauer, MD, has disclosed no relevant financial relationships.
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Olivia Wong, DO
Section Editor
Medscape Drugs & Diseases
New York, NY
Disclosure: Olivia Wong, DO, has disclosed no relevant financial relationships.
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