The nurse is alerted to a possible acute subdural hematoma in the patient who
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Figure 1: Cranial CT scan of case 1 showing a left frontal chronic subdural hematoma with mass effect. Note the small hyperdensity (red arrow) near the edge of the collection. This case was managed with burr-hole irrigation and closed-system drainage with good results. Show
The patient underwent burr-hole irrigation followed by a closed system drainage for 48 hours. He made a good post-operative recovery with only a mild upper extremity weakness (4/5). He was fully awake and alert. At 6 month follow-up there is no evidence of recurrence.
 Figure 2: A (top pict): T1-weighted MR image (sagital view) showing the high-intensity subdural collection. B (bottom pict): T2-weighted MR image (axial view) also shows a high-intensity subdural collection with accompanying mass effect. Neurosurgery was consulted for an "acute" subdural hematoma. Indeed this represented a chronic subdural hematoma as also seen on the cranial CT scan obtained in the ER (Figure 3). Figure 3: Cranial CT scan of case 2 shows the chronic right-sided subdural hematoma with mass effect. This was seen as a high-intensity collection on aT1-weighted MR image (figure 2). This patient was successfully managed with burr-hole irrigation and closed-system drainage. The patient underwent burr-hole irrigation followed by a closed system drainage. She made a very good post-operative recovery and was sent back to the nursing home awake and alert as well as fully oriented. She had no focal neurological deficits. Follow-up cranial CT scan at 9 months shows just a small amount of subdural fluid- no mass effect and asymptomatic. Case 3 Figure 4: Cranial CT scan of case 3 at time of head injury showing an inconsequential right-sided acute subdural hematoma (note the asymmetry on the right). She was doing well until one week prior to admission from the clinic when the frontal headaches recurred and became constant. In addition, she had balance difficulty and increasing forgetfulness. A cranial CT scan one month after the injury revealed a chronic subdural hematoma on the right side (Figure 5). Figure 5: Cranial CT scan performed one month after head injury in case 3 shows a large right- sided chronic subdural hematoma with mass effect. She underwent burr-hole irrigation of the hematoma without any drainage system. Intraoperatively, the brain was seen to re-expand after irrigation of the CSDH. She did well postoperatively with improvement in the headaches and balance. At 8 month follow-up she continues to do well, no recurrence. Figure 6: Cranial CT scan (after the burr hole irrgation) in case 4 showing the recurrent subdural collection with mass effect. Andreas Adam CBE, MB, BS(Hons), PhD, PhD (hon caus), DSc (hon caus), FRCP, FRCR, FRCS, FFRRCSI(Hon), FRANZCR(Hon), FACR(Hon), FMedSci, in Grainger & Allison's Diagnostic Radiology, 2021Subdural HaemorrhageA subdural haematoma (SDH) typically occurs owing to injury to the cortical bridging veins that extend radially away from the cortical surface to drain into the dural venous sinuses. Even relatively minor trauma can result in damage to these veins with haemorrhage into this potential, rather than naturally occurring, space between the inner dural layer and arachnoid mater. An SDH has a typical crescentic configuration (Fig. 54.22) due to the absence of anatomical constraint because the haemorrhage is free to extend along the subdural space, coursing over the cerebral convexity. An SDH may extend medially to lie adjacent to the falx and inferiorly towards the floor of the anterior and middle cranial fossae. SDH may also be seen along the tentorium (Fig. 54.23) and evaluation of the multiplanar reconstruction images will assist in visualising these, particularly as a small volume of haemorrhage may be relatively inconspicuous on the axial images. Associated calvarial fractures may or may not be present with SDHs contrary to EDHs when they are usually always present. The density of SDH on unenhanced CT will depend upon the interval between the initial traumatic event and imaging. If imaging is performed within a few hours, a SDH will appear hyperdense relative to brain parenchyma (seeFig. 54.22). As is the case with EDH, areas of reduced density within a predominantly hyperdense SDH can indicate the presence of active bleeding and further haematoma expansion. A low threshold for repeat imaging in the event of clinical deterioration should be maintained. Acute SDH appearing of only mildly increased density or isodense to brain parenchyma can occasionally be seen in patients with low haematocrit or if there is coexistent arachnoid mater injury that results in CSF leakage into the subdural space. If the interval between the onset of SDH and imaging is prolonged, then the density of the SDH on initial imaging will be reduced as the clot is degraded. In the subacute period following the initial haemorrhage, from several days up until several weeks, subacute SDHs can vary from being slightly hyperdense to isodense to the brain parenchyma (Fig. 54.24A and B). The density decreases even further when imaging is performed in the chronic phase (from several weeks and longer) (seeFig. 54.24D and E). In addition to a reduction in density of the haematoma, subacute and chronic SDH can be differentiated from acute SDH by the formation of membranes of reactive granulation tissue, which form within the subdural space. These have a typical appearance on imaging, appearing as septations within an iso- to hypodense haematoma (seeFig. 54.24C–E). If there is acute haemorrhage into a chronic SDH, these membranes can limit the distribution of the acute blood products within the chronic haematoma (seeFig. 54.24D and E), giving a characteristic appearance. View chapter on ClinicalKey Chronic Subdural HematomaJoel A. Vilensky Phd, ... Stephen W. Carmichael PhD, Dsc, in Medical Imaging of Normal and Pathologic Anatomy, 2010 Axial CT image of the head of a patient with a chronic subdural hematoma on the left side. The subdural fluid collection can be identified as chronic because an acute hematoma would be much brighter (see p. 10). Subdural hematomas are usually of venous origin and progress slowly, as opposed to epidural hematomas that are of arterial origin and may reach maximum size within minutes. On the patient's right side, cortical atrophy results in diffusely thin gyri and widened sulci. Cortical atrophy increases the length of venous segments bridging the subdural space, making them susceptible to shear injury. In this patient, bilateral cortical atrophy predisposed the patient to developing a subdural hematoma. The mass effect of the chronic subdural hematoma has compressed underlying cortex and effaced the sulci on the patient's left. View chapterPurchase book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9781437706345000110 Structural Imaging Using Magnetic Resonance Imaging and Computed TomographyJoseph Jankovic MD, in Bradley and Daroff's Neurology in Clinical Practice, 2022 Subdural hemorrhageSubdural hematomas are common sequelae of head trauma and are thought to result from rupture of the bridging veins (veins that drain from the cerebral surface and pierce the dura to enter the adjacent venous sinus). Morphologically they follow the contour of the cerebral surface and can cross the cranial suture lines but not the midline at the falx cerebri and cerebelli. Depending on the size, there is a varying degree of mass effect on the adjacent brain; in the more severe cases, effacement of the adjacent ventricles, midline shift, and various herniation syndromes may occur. As subdural hematomas age, their imaging appearance changes both on CT and MRI. On CT, acute subdural hematomas appear hyperdense. If the patient remains in a recumbent position, the cellular elements settle to the lower part of the hematoma, which will appear more hyperdense, whereas the “supernatant” is less so. With time, hemoglobin degradation occurs, and the density of the hematoma will decrease, eventually becoming hypodense. During this process there is a transitional stage when the density of the hematoma will be very similar or the same as that of the brain, rendering its detection more difficult. Just as with intraparenchymal hematomas, the density depends on the hematocrit, and in severely anemic patients, even acute subdural hematomas may appear iso- or hypodense, leading to erroneous dating. On MRI, subdural hematomas exhibit a signal evolution similar to that seen with intraparenchymal hemorrhages, but the pace of evolution is different due to a slower decrease of the oxygen content within the hematoma. Acute subdural hematomas (Fig. 40.67) are initially isointense on T1 and hyperintense on T2, but as deoxyhemoglobin appears, the signal on T2-weighted images becomes hypointense. In the subacute phase, the signal is hyperintense on T1 and hypointense on T2, but in the late subacute stage, the signal will be hyperintense on both T1- and T2-weighted images because of extracellular methemoglobin (Fig. 40.68). It is important to remember that these stages are not separated sharply, and mixed patterns are often seen; this is due to the presence of oxy- and deoxyhemoglobin in the acute stage and intra- and extracellular methemoglobin in the chronic stage. Rebleeding into an existing subdural hematoma may also occur, resulting in the presence of clots of various ages. Chronic subdural hematomas (Fig. 40.69) are hypointense relative to the brain but, having higher protein content, are mildly hyperintense relative to the CSF on T1-weighted images and hyperintense on T2-weighted images. Hemosiderin deposition is not as prominent as in parenchymal hemorrhages because macrophages tend to be cleared by the meningeal circulation. Chronic subdural hematomas may look similar to hyperacute ones on noncontrast images, but because of their vascular membrane, with gadolinium they exhibit enhancement along their periphery. On CT, chronic subdural hematomas appear as hypodense subdural collections. Mass effect is variable depending on the size of the hematoma and degree of cerebral atrophy. If repeated hemorrhage occurs into the subdural collection, the hyperdense fresh blood is seen within the chronic hypodense collection (Fig. 40.70). View chapter on ClinicalKey HEAD TRAUMAH. Gordon Deen, in Neurology and Clinical Neuroscience, 2007 Subdural HematomaSubdural hematoma is the result of bleeding over the surface of the brain, beneath the dura. Subdural hematoma may be acute or chronic. Acute subdural hematoma usually occurs after severe, high-impact injuries and is often associated with contusions of the adjacent areas of the brain. If the subdural hematoma is small (<5 mm in thickness) and the patient is stable clinically, a period of observation may be reasonable. If conservative management is elected, careful clinical observation and follow-up imaging are needed, because there is potential for the subdural hematoma to enlarge. Craniotomy to remove the hematoma is necessary if there is significant mass effect with raised ICP. At surgery, the hematoma is found to have a solid, jelly-like consistency. Chronic subdural hematoma represents the gradual accumulation of liquefied hematoma in the subdural space, occurring over 2 or more weeks. Chronic subdural hematoma is usually present in elderly persons, who have more prominent subdural spaces as a result of cerebral atrophy. Chronic subdural hematoma, occurs most commonly after minor head injury. Sometimes the patient and family cannot even recall when the injury occurred. Over time, the hematoma gradually enlarges as a result of repeated episodes of minor bleeding and/or the drawing of fluid into the hematoma as a result of an osmotic effect. As in other forms of intracranial hemorrhage, risks of chronic subdural hematoma are elevated in individuals with coagulopathy caused by liver disease or anticoagulant medications. Surgery is often required and may involve either burr hole drainage or a craniotomy. At surgery, a chronic subdural hematoma is liquefied and is described as having a “crank case oil” appearance. The prognosis is guarded, and there is substantial risk of recurrent subdural hematoma that necessitates further surgery. Figure 103-2 shows bilateral chronic subdural hematomas. Subdural hematoma may have both acute and chronic components if there is ongoing bleeding in the subdural space. The presence of a mixed acute and chronic subdural hematoma is readily identified on CT (Figure 103-3). View chapterPurchase book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323033541501073 Spinal Cord Vascular DiseaseJoseph Jankovic MD, in Bradley and Daroff's Neurology in Clinical Practice, 2022 Spinal Epidural and Subdural HemorrhageSpinal epidural hemorrhage (SEH) occurs more frequently than spinal subdural hemorrhage (SSH). SEH is more commonly observed in men and has a bimodal distribution, with peaks during childhood andthe fifth and sixth decades of life. Cervical lesions are more common in childhood, whereas thoracic and lumbar lesions predominate in adults. Hemorrhages can be spontaneous but often occur following exertion or trauma. SEH is a complication of both lumbar puncture and epidural anesthesia and is more likely in anticoagulated patients. Other causes include blood dyscrasia, thrombocytopenia, neoplasms, trauma, and vascular malformations. Pregnancy also appears to increase risk for SEH. SSH is most common in women. It may occur at any age but tends to predominate in the sixth decade. Most occur in the thoracic and lumbar regions. Hemorrhagic diatheses, including treatment with anticoagulants, blood dyscrasias, and thrombocytopenia, are the precipitating factors most commonly associated with SSH. Other factors include trauma, lumbar puncture, vascular malformation, and spinal surgery. The clinical presentations of SEH and SSH are indistinguishable. The initial symptom is severe back pain at the level of the bleed. Myelopathy or cauda equina syndrome, with motor and sensory findings corresponding to the level of the lesion, develops over hours to days. The diagnosis should be suspected in patients with disorders of coagulation who have undergone recent lumbar puncture and develop back pain or signs of spinal cord or root dysfunction. Patients with a rapidly decreasing platelet count or less than 40,000 platelets/μL are at particular risk of developing SEH or SSH as a complication of lumbar puncture and should receive a platelet transfusion prior to the procedure. Clotting studies and a platelet count are important in the initial evaluation. In SEH and SSH, the CSF may be normal or xanthochromic and may contain increased protein. MRI can delineate the size and location of the hematoma. In addition, gadolinium-enhanced MRI and MRA may show an underlying vascular malformation. In patients unable to tolerate MRI or where it is unavailable in the acute phase of the illness, myelography with computed tomography (CT) scanning provides an alternative. Myelography can reveal a partial filling defect or complete blockage to the flow of contrast material at the level of the lesion. However, the myelographic appearances of SEH and SSH may be indistinguishable. Both SEH and SSH are surgical emergencies. Operative treatment is directed toward relief of local pressure and repair of any underlying defect. Laminectomy with evacuation of the clot should be performed as soon as possible to minimize the risk of permanent neurological dysfunction. The prognosis for recovery is better when the preoperative deficits are not severe; timing of surgery appears less important. The complete reference list is available online athttps://expertconsult.inkling.com/.View chapter on ClinicalKey Brain and Spinal CordRay N. Conley, Gary A. Longmuir, in Clinical Imaging (Third Edition), 2014 BackgroundSubdural hematomas are caused more frequently by venous rather than arterial damage and are often self-limiting because of the slow bleeding process. However, if the hematoma is large, mass pressure effect may take place, shifting cerebral structures and causing edema in the parenchyma of the brain, resulting in a poor clinical outcome. In addition, the possibility of herniation exists with large subdural hematomas or with hematomas that continue to enlarge after injury. Subdural hematomas arise deep to the dura but external to the arachnoid membrane, and the untreated hematoma may become subacute or chronic. Acute subdural hematoma is more common in older age groups because the veins are less resilient and more easily damaged. Patients taking anticoagulants and patients with alcoholism are also prone to acute subdural hematoma.139,224,275,281 View chapterPurchase book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323084956000336 Neuroimaging Part ISandra Rincon, ... Thomas Ptak, in Handbook of Clinical Neurology, 2016 Subdural hematomaSubdural hematomas are seen in 10–20% of patients with head trauma (Young and Destian, 2002). A subdural hematoma results from the stretching and tearing of bridging cortical veins in the subdural space, a potential space between the pia arachnoid and the dura (Figs 22.10–22.13). The bridging cortical veins rupture because of trauma-induced rotational movement of the brain, which shears the cortical veins where they are fixed and drain into the adjacent dural sinus. About 95% of subdural hematomas occur in the frontoparietal regions because of the tearing of these bridging veins. Approximately 10–15% of subdural hematomas are bilateral. Fig. 22.10. Axial noncontrast computed tomography image shows a large acute right cerebral convexity subdural hematoma and smaller left cerebral convexity subdural hematoma. Fig. 22.11. Axial noncontrast computed tomography image shows a left cerebral convexity subdural hematoma with associated mass effect on the left cerebral hemisphere, effacement of the left lateral ventricle and mild midline shift. Fig. 22.12. Axial noncontrast computed tomography image shows bilateral acute subdural hematomas extending along the tentorium cerebelli. Fig. 22.13. (A–C) Axial noncontrast computed tomography images show a small acute subdural hematoma along the posterior aspect of the falx and left tentorial leaflet. Use of an intermediate window width may enhance the sensitivity for detecting a small SDH, which can be difficult to differentiate from the adjacent calvarium (Fig. 22.14). Using “subdural windows” should be a routine part of every head CT evaluation for increased conspicuity of subtle subdural hematomas. Fig. 22.14. (A, B) Axial noncontrast computed tomography images show a small subdural hematoma along the right cerebral convexity. The subdural hematoma is better visualized on image (B) because of subdural windows. Subdural hematomas are seen in approximately 30% of patients with severe closed head trauma (Grossman and Yousem, 2003). They may or may not be associated with a brain parenchymal injury. When associated with a brain parenchymal injury, a subdural hematoma is associated with a 35–50% mortality rate (Grossman and Yousem, 2003). Subdural hematomas may also be seen in the setting of minor trauma, particularly in the elderly. In older patients, a subdural hematoma tends to be larger because of generalized parenchymal volume loss. In some patients, a history of trauma may be lacking. The appearance of a subdural hematoma on CT varies with clot age and organization of the hemorrhage. Acute subdural hematomas are usually hyperdense, typically crescent-shaped, are not limited by the cranial sutures, but are limited by dural reflections, such as the falx cerebri, tentorium, and falx cerebelli. Up to 40% of acute subdural hematomas have a heterogeneous appearance with both hyperattenuating and hypoattenuating areas that reflect acute unclotted blood, serum extruded during clot retraction, or mixing with CSF from an arachnoid tear (Fig. 22.15). Fig. 22.15. Axial noncontrast computed tomography image shows an acute heterogeneous subdural hematoma with significant mass effect on the left cerebral convexity, effacement of the left lateral ventricle, and subfalcine herniation. In the hyperacute phase, a subdural hematoma may appear isodense to the adjacent cortex, with a swirled appearance due to a mixture of serum with clotted and unclotted blood (Brant and Helms, 2007). A subacute subdural hematoma may appear isodense or hypodense to the adjacent brain and may be apparent only by the attendant mass effect (Figs 22.16 and 22.17). On imaging, an isodense subdural hematoma may result in effacement of the ipsilateral sulci, inward displacement of the cortical veins and gray–white matter junction, effacement of the ventricles, and midline shift. Identification of isodense subdural hematomas may be difficult, especially if they are bilateral. Fig. 22.16. Axial noncontrast computed tomography image shows an isodense subacute left cerebral convexity subdural hematoma and chronic right frontal subdural hematoma. Fig. 22.17. Axial noncontrast computed tomography image shows a large isodense subacute left cerebral convexity subdural hematoma with associated mass effect on the left cerebral hemisphere, effacement of the left lateral ventricle, and minimal midline shift. A chronic subdural hematoma is usually hypodense on CT. It typically appears as a crescent-shaped, multiseptated extra-axial collection encapsulated by enhancing membranes. A subdural hygroma, by contrast, is a CSF collection in the subdural space caused by an arachnoid tear. A subdural hygroma will have no evidence of hemorrhage and no enhancing membranes. A subdural hygroma, however, can be indistinguishable from a chronic subdural hematoma on imaging. An acute on chronic subdural hematoma refers to acute hemorrhage into a pre-existing chronic subdural hematoma. It typically appears as a hypodense extra-axial collection with a dependent hematocrit level (Fig. 22.18). A recurrent, mixed-density subdural hematoma in a child raises suspicion for nonaccidental trauma and shaking injury. MRI is extremely useful in the evaluation of children suspected of nonaccidental trauma, because it can better characterize blood products of different ages. The MRI appearance of a subdural hematoma is variable and changes with the age of the blood products, as described earlier in the chapter (Fig. 22.19). Fig. 22.18. (A–C) Axial noncontrast computed tomography images show an acute on chronic right cerebral convexity subdural hematoma with a layering hyperdense component representing acute hemorrhage. There is also a large isodense subacute left cerebral convexity subdural hematoma with associated mass effect on the left cerebral hemisphere and left lateral ventricle. Fig. 22.19. Coronal T1-weighted magnetic resonance image shows T1 hyperintense subdural hemorrhage along the right cerebral convexity, falx, and right tentorial leaflet, consistent with subacute hemorrhage. View chapterPurchase book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780444534859000222 Pediatric Neurosurgical AnesthesiaCraig D. McClain, Sulpicio G. Soriano, in A Practice of Anesthesia for Infants and Children (Sixth Edition), 2019 Subdural HematomaSubdural hematomas are usually associated with cortical damage resulting from direct parenchymal contusion or laceration of venous blood vessels. Acute subdural hematomas are almost always traumatic and are frequently a result of abuse, such as shaking of small children, particularly those younger than 1 year of age. Shaken baby syndrome occurs when an infant is shaken so vigorously that significant neuronal disruption occurs and tears in the cortical bridging veins cause subdural hematomas.151–153 These infants suffer brain damage complicated by episodes of apnea and further hypoxic insult. Subdural hematomas occasionally result from birth trauma within the first hours of life. Vitamin K deficiency, congenital coagulopathies, and disseminated intravascular coagulation are considerations in these situations. Great force is required to produce a subdural hematoma, whether by direct impact, laceration of blood vessels, or traumatic separation of the brain and overlying dura. Cerebral edema, uncontrolled intracranial hypertension, and persistent neurologic deficits often characterize the postoperative course. Chronic subdural hematomas or effusions may also develop in infancy, although these children do not usually present with acute symptoms. Children are often diagnosed because they are irritable and vomiting or have an increased head circumference. Chronic subdural hematomas can increase in size, causing slow but significant increases in ICP. Although a craniotomy is sometimes performed, most children undergo some form of hematoma drainage or shunting procedure as definitive treatment. How does a subdural hematoma cause ICP?As a subdural hematoma expands in the subdural space, it raises the ICP and deforms the brain. The rise in ICP is initially compensated by efflux of cerebrospinal fluid (CSF) toward the spinal axis and compression of the venous system, expediting venous drainage through the jugular veins.
What is the first signs of increased intracranial pressure?These are the most common symptoms of an ICP: Headache. Blurred vision. Feeling less alert than usual.
Which nursing action should be implemented in the care of a patient who is experiencing increased ICP?If a patient is suspected of having increased ICP, immediate interventions should include securing the airway, maintaining adequate oxygenation and ventilation, and providing circulatory support as needed.
How should you position a patient with increased intracranial pressure?In most patients with intracranial hypertension, head and trunk elevation up to 30 degrees is useful in helping to decrease ICP, providing that a safe CPP of at least 70 mmHg or even 80 mmHg is maintained. Patients in poor haemodynamic conditions are best nursed flat.
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