Cases reported "Hematoma, Subdural, Acute"

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1/11. Cranial nerve palsy and intracranial subdural hematoma following implantation of intrathecal drug delivery device.

    BACKGROUND AND OBJECTIVES: Complications related to cerebrospinal fluid (CSF) leak and low CSF pressure can occur following placement of an intrathecal drug delivery device. methods: A 58-year-old man with chronic, intractable lower back pain underwent implantation of an intrathecal drug delivery device. On the fourth postoperative day, he developed a postural headache and diplopia with findings compatible with left sixth cranial nerve palsy. The headache subsequently became constant and nonpostural. Cranial magnetic resonance imaging was obtained that showed the presence of a posterior subdural intracranial hematoma. Conservative treatment for postdural puncture headache did not improve the symptomatology. Therefore, an epidural blood patch was performed that produced rapid improvement and eventual resolution of symptoms. CONCLUSIONS: Intrathecal catheter implantation can result in CSF loss that might not resolve promptly with conservative therapy. In this case, epidural blood patch proved to be a safe and effective form of treatment.
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2/11. Cranial subdural haematoma associated with dural puncture in labour.

    A 23-yr-old primagravida sustained a dural puncture during epidural catheter insertion and developed a headache that settled with oral diclofenac and codydramol. On the third day after delivery, she convulsed twice without warning. As plasma urate was increased, the putative diagnosis of an eclamptic fit was made, and magnesium therapy was started. A contrast CT scan revealed that the cause of the patient's symptoms was a subdural haematoma with raised intracranial pressure. A coincidental arteriovenous malformation was noted. This case emphasises the need to consider the differential diagnoses of post-partum headache. The management of acute intracranial haematoma is described.
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3/11. Kernohan's notch phenomenon: a case study.

    In a patient suffering from brain herniation due to a right-sided subdural hematoma, a neurological examination should show left-sided deficits, known as localizing signs, and a decreased level of consciousness. However, false localizing signs may be present, attributed to pressure on Kernohan's notch. A case study demonstrates these false localizing signs, known as Kernohan's notch phenomenon.
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4/11. Single burr hole evacuation for traumatic acute subdural hematoma of the posterior fossa in the emergency room.

    A 57-year-old man and a 55-year-old man presented with acute subdural hematoma of the posterior cranial fossa due to trauma. Both were comatose preoperatively. Emergent single burr hole evacuation in the posterior cranial fossa was performed in the emergency room immediately after computed tomography. Neurological symptoms improved dramatically just after initiating the burr hole evacuation in both patients. A 57-year-old man became alert and could walk unassisted 1 month after surgery. The other could walk with assistance 4 months after surgery, although psychic disturbance resulting from cerebral contusion remained. Single burr hole evacuation in the emergency room is a useful treatment for acute subdural hematoma of the posterior cranial fossa because the procedure can be performed easily and rapidly, thus achieving reduction of intracranial pressure. Progressing neurological deterioration, reversibility of brainstem function by mannitol administration and the sign of brainstem compression and noncommunicating hydrocephalus are good indicators for this treatment.
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5/11. Acute subdural hematoma after lumboperitoneal shunt placement in patients with normal pressure hydrocephalus.

    Acute subdural hematoma (SDH) is a rare but disastrous complication after lumboperitoneal shunt placement. Four of 206 adult patients with normal pressure hydrocephalus (1.9%) who underwent lumboperitoneal shunt placement suffered acute SDH following head trauma. The interval between shunt placement and acute SDH was one month to 7 years. Two patients had subdural effusion on computed tomography (CT) at 2- and 6-month follow up. All four patients required assistance in their daily activities before acute SDH onset. The traumatic event was a fall. On admission, CT revealed a large SDH that required surgical removal in two patients, of whom one had manifested subdural effusion after shunt placement. The other two patients had a small SDH. None of the four patients had cerebral contusions. patients with lumboperitoneal shunts, especially those not capable of independent daily activities, are at risk for acute SDH after even minor head trauma.
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6/11. Bedside biochemical monitoring of the penumbra zone surrounding an evacuated acute subdural haematoma.

    We describe a penumbra zone with increased biochemical vulnerability in cerebral cortex underlying an evacuated acute subdural haematoma. Two microdialysis catheters were placed in this zone and one catheter was placed in the opposite, less injured hemisphere. The microdialysis perfusates were analysed bedside for glucose, pyruvate, lactate, glutamate, and glycerol. In the penumbra zone, but not in the opposite hemisphere, energy metabolism was seriously disturbed with signs of cell membrane degradation. During an adverse event (decrease in haemoglobin level, systemic blood pressure and cerebral perfusion pressure) the perturbation of energy metabolism increased in this zone. energy metabolism recovered and the signs of cell membrane degradation disappeared after normalization of the physiological parameters. We use the term biochemical penumbra zone to describe an area with signs of energy failure and cell membrane degradation, which has a capacity to regain a normal metabolic pattern but also an increased vulnerability to secondary insults.
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7/11. Human kluver-bucy syndrome following acute subdural haematoma.

    We present a rare case of complete human kluver-bucy syndrome (KBS) following recovery from transtentorial herniation caused by acute subdural haematoma (ASDH). A 17-year-old right-handed high school boy got into stupor within five minutes after 3-rounds of sparing at boxing. Emergency computed tomographic (CT) scan showed right cerebral hemispheric ASDH, which was evacuated following intentional decompressive craniectomy. After recovery of consciousness, he developed emotional changes (placidity with loss of normal fear and anger), psychic blindness, aberrant sexual behaviour, excessive oral tendencies, increased appetite, and hypermetamorphosis in order of mention, which were observed with waxing and waning from 17th to 28th hospital day. Peri-operative CT scaning and magnetic resonance imaging showed lesions of the right temporal lobe and right-dominant orbitofrontal regions including bilateral rectal and medial orbital gyri, and the intact left temporal lobe. Two pathogeneses can be thought of and the whole picture of KBS following ASDH can arise even though one (left in this case) temporal lobe is preserved, 1) in which associated orbitofrontal lesions of the frontal lobes may correlate with occurrence of KBS, or 2) cerebral blood hypoperfusion of both temporal lobes due to increased intracranial pressure and/or compression of both posterior cerebral arteries at the edge of the tentorium cerebelli occurs.
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8/11. Bilateral acute epidural hematoma after evacuation of acute subdural hematoma: brain shift and the dynamics of extraaxial collections.

    Acute epidural hematoma following supratentorial decompressive craniectomy is a very seldom described but serious complication. The occurrence of intraoperative brain swelling may suggest the development of a contralateral hematoma. A unique case of bilateral acute epidural following decompressive craniectomy and evacuation of acute subdural hematoma is presented. awareness of unexplained elevation of intracranial pressure is of paramount importance when routine immediate postoperative computed tomography is not performed. This case provides insight into the well-known but poorly understood dynamic process of brain shift and extraaxial collections.
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9/11. Coexistence of rapidly resolving acute subdural hematoma and delayed traumatic intracerebral hemorrhage.

    Rapid resolution of acute subdural hematoma is rare. Delayed traumatic intracerebral hematomas following medical or surgical treatment of increased intracranial pressure have also been reported. Coexistence of a quickly resolving acute subdural hematoma and a delayed traumatic intracerebral hemorrhage has not been reported before. A 13-month-old boy was admitted to our emergency department after a car accident. On CT, a thin acute subdural hematoma on the right frontotemporal region and a small epidural hematoma on the left frontal region could be seen. On 24-hour follow-up CT, the right subdural hematoma was found to be less dense but larger than it had been before. At 36 h after hospitalization, CT showed that the right acute subdural hematoma had completely disappeared; however, a delayed traumatic intracerebral hematoma on the left occipital region was identified. We think that the mechanism involved in the development of a delayed intracerebral hematoma in our case was similar to the one causing delayed traumatic intracerebral hematoma after treatment for increased intracranial pressure.
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10/11. Acute subdural hematoma originating from the lacerated intracranial internal carotid arteries--case report.

    A 51-year-old male presented with laceration of the bilateral intracranial internal carotid arteries (ICAs) manifesting as acute subdural hematoma (SDH) after a fall of 3 m. brain computed tomography showed acute SDH appearing as irregular mixed high and low density and causing midline shift. During the operation, massive liquiform hematoma flowed out from the deep portion around the cranial base and systemic blood pressure decreased abruptly. hemostasis was impossible and he died soon after the operation. autopsy revealed skull fractures in the bilateral sphenoidal, orbital, temporal, frontal, parietal, and occipital bones, and laceration of the bilateral ICAs in the cavernous sinuses at the fracture sites. Acute SDH can be caused by laceration of the ICA.
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