HIGROMAS FRONTALES PDF

Higroma subdural traumático: a propósito de cinco casos com modificação de The CT scan on the 9th day showed bilateral frontal subdural hygroma, mainly. The CSDHs are usually on the most curved frontal or occipital convexity. Bilateral CSDH is common in patients with symmetrical frontal and occipital cranial vault. Results 1 – 14 of 14 Download Higromas frontales pdf: ?file=higromas +frontales+pdf Read Online Higromas frontales pdf.

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Chronic subdural hematoma CSDH is one of the most common neurosurgical conditions. There is lack of uniformity in the treatment of CSDH amongst surgeons in terms of various treatment strategies. Clinical presentation may vary from no symptoms to unconsciousness. CSDH is usually diagnosed by contrast-enhanced computed tomography scan. Magnetic resonance imaging MRI scan is more sensitive in the diagnosis of bilateral isodense Higromzs, multiple loculations, intrahematoma membranes, fresh bleeding, hemolysis, and the size of capsule.

Although definite history of trauma could be obtained in a majority of cases, some cases may be secondary to coagulation defect, intracranial hypotension, use of anticoagulants and antiplatelet drugs, etc.

Burr-hole evacuation is the treatment of choice for an uncomplicated CSDH. Most of the recent trials favor the use of drain to reduce recurrence rate. Craniotomy and twist drill craniostomy also play a role in the management. Dural biopsy should be taken, especially in recurrence and thick outer membrane. Nonsurgical management is reserved for asymptomatic or high operative frontwles patients. The steroids and angiotensin converting enzyme inhibitors may also play a role in the management. Single management strategy is not appropriate for all the cases of CSDH.

Better understanding of the nature of the pathology, rational selection of an ideal treatment strategy for an individual patient, and identification of hifromas merits and limitations of different surgical techniques could help in improving the prognosis.

The preferred surgical method continues to attract debate. There is lack of uniformity about the treatment strategies, such as the role of burr hole, twist drill, craniotomy, etc. There is also disagreement about the use of drain, irrigation, and steroid. The annual incidence of CSDH is about This higrimas is based on last 21 years search upto May on Pubmed and Google. The presentation of CSDH could vary from no symptoms to headache, seizures, decreased memory, and confusion.

Patients could have difficulty in speech, swallowing, and walking. There may be weakness or numbness of arms, legs, and face. The CSDHs are usually characterized by history of head trauma, which is usually a trivial trauma.

Some cases could be secondary to defective coagulation, after lumbar puncture LPetc. CSDH should be taken into account higroma an important differential diagnosis in reversible dementia.

The differentiation between CSDH and dementia could be difficult when it is associated with the hallucinations. CSDH generally occurs in elderly although it may present in young patients.

Traumatic subdural hygroma: five cases with changed density and spontaneous resolution

It may rarely be seen in infants. The presence of bilateral CSDH in an infant raises the suspicion of non-accidental trauma and presents a difficult diagnostic challenge because of the legal and social implications. Glutaric aciduria type 1 should be considered in the differential diagnosis of bilateral CSDHs in infants. Some CSDHs of infancy may have a congenital etiology. higrkmas

The CSDHs are usually on the most curved frontal or occipital convexity. Bilateral CSDH is common in patients with symmetrical frontal and occipital cranial vault.

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In asymmetrical cranium, CSDHs are usually on the side of the most curved frontal or occipital convexity frkntales is more frequently on the left side. Isolated third nerve palsy may also be seen in CSDH. Movement disorders such as choreoathetoid and parkinsonism could be associated with subdural hematomas SDHs.

Pressure effects, neurotransmitter abnormality, and ischemia have been postulated as reasons for this type of presentation. Elderly people suffering from subacute progressive parkinsonism should undergo computed tomography CT studies to differentiate it from primary parkinsonism. This parkinsonism is usually completely cured after successful evacuation of the hematomas. Resolution of the blepharospasm has been observed after evacuation of CSDH.

CSDH can cause voiding dysfunctions with small bladder capacity and high-amplitude overactive detrusor contractions with an intact sphincteric response. Hematomas are usually hypodense, but isodense or mixed density lesions are also observed. Although these are usually concavo-convex, rarely they may mimic acute epidural hematomas. These CSDHs could be globular, rarely, due to severe craniocerebral disproportion secondary to associated thin cerebral mantle.

Huge hemispheric CSDH, bigromas whole cerebral hemisphere and compressing the falx with almost complete obliteration of ipsilateral lateral ventricle, has been reported.

The calcified CSDHs, though rare, could mimic calvarial mass. Contrast images are essential to find out any associated primary or metastatic dural disease.

This method could underestimate some CSDH. This is a simple, precise, and convenient method for the estimation ihgromas volume in all the types of hematomas. MRI could help in making the diagnosis of such lesions. Fresh bleeding, hemolysis, and hemoglobin changes can also be observed by MRI. Drontales diffusion tensor imaging can examine anisotropic changes of the pyramidal tracts displaced by CSDH. These anisotropic changes are considered to be caused by a reversible distortion of neuron and vasogenic edema by the hematoma.

These changes in the affected pyramidal tract correlate to motor weakness in CSDH. Contrast-enhanced MRI could detect neomembranes, thick and extensive membranes, or solid fronhales. SDH could be seen in association with primary dural diseases or metastasis.

Such lesions could be missed and could be the cause of recurrence in CSDH. A contrast-enhanced brain CT scan is recommended to diagnose dural metastases. This disease is an uncommon, benign systemic histioproliferative disease characterized by massive lymphadenopathy, particularly in the head and neck region, and is often associated with extranodal involvement. CSDH can also develop in multifocal fibrosclerosis MFS which is a rare disorder of unknown etiology, characterized by chronic inflammation with dense fibrosis and lymphoplasmacytic infiltration into the connective tissue fronrales various organs.

The mechanism of the formation of Frontalez is presumed to involve reactive granular membrane together with subdural collection. On the hjgromas hand, the extramedullary erythropoiesis within CSDH can be confused with metastatic malignant tumors, such as lymphoma, carcinoma, and malignant melanoma.

Although majority of the CSDHs are due to trauma, intracranial hypotension and defective coagulations could also be responsible. Frontxles history of trauma could be higrkmas in majority of the cases.

Post-Traumatic Subdural Higroma: A Case Report

higroams Majority of these cases have mild head injury, although moderate to severe injury could be the causative factor in some cases. This injury could be trivial and may go unnoticed. Some cases could occur after neurosurgical operations.

The thin walls of bridging veins, circumferential arrangement of collagen fibers, and a hitromas of outer reinforcement by arachnoid trabecules contribute to the more fragile nature of bridging vein in the subdural portion as compared to the subarachnoid portion. Repeated injury on the head during play may be the cause of CSDH in children.

Bilateral subdural hygroma | Radiology Case |

Rupture of bridging veins, bleeding from the hygroma wall due higromws neocapillaries, vascular hyperpermeability, increased fibrinolysis, and increasing protein content in the hygroma are some of the explanations of the pathogenesis of traumatic SDE evolving into CSDH. Spontaneous intracranial hypotension could be the cause of CSDH, especially in young to middle-aged patients, without preceding trauma or hematological disorders.

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MRI frontsles of the spine and radionuclide cisternography are useful in the evaluation of intracranial hypotension. The possibility of an intracranial SDH as a complication of puncture of the dura mater should be suspected, especially in post LP headache of more than 1 week. Neuroimaging is necessary after 1 week of LP if the patient continues to have headache.

CSDH should be considered when postpartum patients, who have received epidural anesthesia, present with mild to severe, persistent, and non-postural headache. CSDH can develop due to intracranial frntales secondary to sudden decompression of intracranial pathologies, such as suprasellar arachnoid cyst fenestration and endoscopic third ventriculostomy.

CSDH could develop in the presence of potential hemorrhagic diathesis due to the deficiency of clotting factors. FXIII activity should be investigated because it may predict rebleeding events after treatment. CSDH consists of an outer membrane, hematoma cavity, and an inner membrane. Hematoma fluid is usually liquid that does not clot. Usually hematomas are liquefied, but mixed lesions with solid components are also seen. The fibrinolytic factors appear to be associated with evolution in CSDHs with heterogeneous density.

Usually there is no infection in these hematomas, but the CSDH is a potential site for bacterial infection.

The possibility of infected SDH should be considered when a patient has features of infection. The developing hematoma capsule shows gradual changes in cellular and vascular organization with progression in hematoma age.

Initial changes include angiogenic and aseptic inflammatory reactions. It is followed by fibroblasts-proliferation and development of collagen fibrils. Young hematomas days after trauma show numerous capillaries, suggesting formation of new blood vessels.

Older hematomas 40 days after trauma usually show numerous capillaries and thin-walled sinusoids accompanied frontalex patent, larger diameter blood vessels. Blood vessels are frontalee occluded by clots in the fibrotic outer membrane of 60 or more days old hematoma.

CSDHs cause decrease in the blood flow in the underlying brain.

The drainage of the hematoma results in the improvement of cerebral blood flow and clinical recovery. The pathology of the enlargement fdontales the CSDH is very complex. It is likely that multiple factors are responsible for the maintenance and enlargement of the CSDH, the relative importance of which varies from case higromae case.

There is a great variety of subdural fluid types, ranging from bright red liquid through to thick engine oil to light serous fluid. Similarly, some CSDHs contain a very thick outer membrane, whereas in others the membrane is hardly visible with the naked eye. The complex nature of CSDH pathology can be explained by the recurrence of hematoma even after complete removal of hematoma and outer membrane where as even the partial removal of the clot can lead to complete resolution of the hematoma and the membrane.

Rebleeding, exudates from the outer membrane, osmotic theory, and rapid enlargement due to CSF entrapment are considered as possible causes of expansion of hematomas. The CSDH enlarges from recurrent bleeding in the subdural space, caused by local angiogenesis, inflammation, defective coagulation, and ongoing fibrinolysis.

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