FGF23-secreting sinonasal tumour presenting with acute subdural haemorrhage and tumour-induced osteomalacia.

A female in her 50s developed a headache, collapsed and was noted to have an acute atraumatic subdural haemorrhage (SDH) requiring surgical evacuation and intracranial pressure-directed therapy. Her background included recurrent epistaxis, severe generalised bone pain and multiple insufficiency fractures and an undifferentiated autoimmune connective tissue disease. Chronic hypophosphataemia, elevated alkaline phosphatase and raised fibroblast growth factor 23 (FGF23) were also noted. An MRI head and subsequent 68Ga CT/positron emission tomography scan demonstrated an intensely avid tumour in the right ethmoid sinus, extending intracranially. Phosphate was aggressively replaced, and alfacalcidol was initiated to circumvent the effects of FGF23 on her kidneys and bone minerals. The tumour was biopsied and then definitively resected via combined endonasal and craniotomy approaches, resulting in good clinical improvement. FGF23 titre and serum phosphate both normalised leaving the diagnosis of a phosphaturic mesenchymal tumour-secreting FGF23, leading to tumour-induced osteomalacia.

Decompressive craniectomy in trauma: What you need to know.

ABSTRACT: Decompressive craniectomy (DC) is a surgical procedure in which a large section of the skull is removed, and the underlying dura mater is opened widely. After evacuating a traumatic acute subdural hematoma, a primary DC is typically performed if the brain is bulging or if brain swelling is expected over the next several days. However, a recent randomized trial found similar 12-month outcomes when primary DC was compared with craniotomy for acute subdural hematoma. Secondary removal of the bone flap was performed in 9% of the craniotomy group, but more wound complications occurred in the craniectomy group. Two further multicenter trials found that, whereas early neuroprotective bifrontal DC for mild to moderate intracranial hypertension is not superior to medical management, DC as a last-tier therapy for refractory intracranial hypertension leads to reduced mortality. Patients undergoing secondary last-tier DC are more likely to improve over time than those in the standard medical management group. The overall conclusion from the most up-to-date evidence is that secondary DC has a role in the management of intracranial hypertension following traumatic brain injury but is not a panacea. Therefore, the decision to offer this operation should be made on a case-by-case basis. Following DC, cranioplasty is warranted but not always feasible, especially in low- and middle-income countries. Consequently, a decompressive craniotomy, where the bone flap is allowed to "hinge" or "float," is sometimes used. Decompressive craniotomy is also an option in a subgroup of traumatic brain injury patients undergoing primary surgical evacuation when the brain is neither bulging nor relaxed. However, a high-quality randomized controlled trial is needed to delineate the specific indications and the type of decompressive craniotomy in appropriate patients.

A rare case of herpes simplex virus encephalitis from viral reactivation following surgically treated traumatic brain injury.

OBJECTIVE: Herpes simplex virus encephalitis (HSVE) is associated with significant morbidity and mortality. Here, we present the occurrence of HSVE in a 36-year-old immunocompetent patient following craniotomy for a traumatic acute subdural hematoma (ASDH). METHODS: Imaging after four days of progressive headache following a fall with head-strike demonstrated a 1 cm thick left holohemispheric ASDH with significant cerebral compression, edema, and 8 mm of left-to-right midline shift, and an emergent craniotomy and ASDH evacuation were performed, with additional treatment needed for reaccumulation. Postoperatively, the patient developed a worsening leukocytosis, became febrile, and was hypotensive requiring vasopressor support. RESULTS: Despite empiric antibiotics, the patient remained persistently febrile with significant leukocytosis. Repeat head CT showed a new left insular hypodensity and a subsequent viral encephalitis panel was positive for HSV-1. The patient was then started on intravenous acyclovir, with progressive neurological exam improvement. Of note, the patient was noted to have a positive serum HSV-1 IgG antibody titer, indicative of prior infection. CONCLUSIONS: Given the known systemic immunosuppression in brain injury and the high prevalence of HSV seropositivity, clinicians should consider the possibility of HSVE from HSV reactivation in TBI patients with persistent fever, leukocytosis, and/or neurological deficits without an obvious etiology.

The Effect of Targeted Hyperoxemia on Brain Immunohistochemistry after Long-Term, Resuscitated Porcine Acute Subdural Hematoma and Hemorrhagic Shock.

Epidemiological data suggest that moderate hyperoxemia may be associated with an improved outcome after traumatic brain injury. In a prospective, randomized investigation of long-term, resuscitated acute subdural hematoma plus hemorrhagic shock (ASDH + HS) in 14 adult, human-sized pigs, targeted hyperoxemia (200 < PaO2 < 250 mmHg vs. normoxemia 80 < PaO2 < 120 mmHg) coincided with improved neurological function. Since brain perfusion, oxygenation and metabolism did not differ, this post hoc study analyzed the available material for the effects of targeted hyperoxemia on cerebral tissue markers of oxidative/nitrosative stress (nitrotyrosine expression), blood-brain barrier integrity (extravascular albumin accumulation) and fluid homeostasis (oxytocin, its receptor and the H2S-producing enzymes cystathionine-ß-synthase and cystathionine-γ-lyase). After 2 h of ASDH + HS (0.1 mL/kgBW autologous blood injected into the subdural space and passive removal of 30% of the blood volume), animals were resuscitated for up to 53 h by re-transfusion of shed blood, noradrenaline infusion to maintain cerebral perfusion pressure at baseline levels and hyper-/normoxemia during the first 24 h. Immediate postmortem, bi-hemispheric (i.e., blood-injected and contra-lateral) prefrontal cortex specimens from the base of the sulci underwent immunohistochemistry (% positive tissue staining) analysis of oxidative/nitrosative stress, blood-brain barrier integrity and fluid homeostasis. None of these tissue markers explained any differences in hyperoxemia-related neurological function. Likewise, hyperoxemia exerted no deleterious effects.

Importance of repeated computed tomography on pediatric traumatic acute posterior fossa subdural hematoma: A case study.

Traumatic acute posterior fossa subdural hematoma (PFSDH) is a rare and potentially fatal condition in which the progressed hematoma compresses the brainstem or causes secondary hydrocephalus. Hence, vigilant monitoring of clinical and radiological findings is crucial to detect the typical sudden deterioration, which can occur in the early stages. However, managing pediatric PFSDHs poses additional challenges due to risks associated with radiation exposure from repeat computed tomography (CT) examinations, potentially impeding crucial diagnostic insights. Here, we present a rare pediatric case of fatal acute traumatic PFSDH. Despite undergoing a timely initial CT scan that indicated the presence of PFSDH, the patient experienced sudden deterioration 15 h later and eventually died. No follow-up CT examinations were conducted during this critical period. This case underscores the challenges in managing pediatric PFSDHs, particularly concerning the benefits of repeated CT examinations in initially stable patients.

Pearls & Oy-sters: What Came First, the Bleed or the Fall?: An Aneurysmal Subdural Hemorrhage.

Acute subdural hemorrhages are a common emergency presentation often associated with trauma. However, in the absence of significant trauma, it is important to consider alternative causes. In this case, a 58-year-old woman with trivial trauma after a sudden collapse had bilateral subdural hemorrhages on CT. CT-angiogram revealed anterior communicating artery aneurysm, which had ruptured. This case explores intracerebral aneurysms as a rare cause of subdural hemorrhage that is important to consider in the absence of significant trauma.

Traumatic Falcine Artery Aneurysm Resulting in Intracranial Hemorrhage.

A 50-year-old man presented with mild unconsciousness after a fall-induced head injury. Initial imaging revealed a left-sided acute subdural hematoma. After transportation to our hospital, his condition deteriorated, leading to the discovery of a new hemorrhage and an anterior falcine artery aneurysm upon further examination. The patient underwent successful decompressive craniectomy and endovascular occlusion. This case, the first reported of a traumatic anterior falcine artery aneurysm, suggests the initial injury caused both the hematoma and aneurysm. The aneurysm's specific location near the crista galli likely contributed to the formation of the traumatic aneurysm, and the compression of the left frontal lobe by the acute subdural hematoma caused the subsequent hemorrhage. This case highlights the importance of considering traumatic aneurysms in atypical postinjury hemorrhages and adds to the understanding of traumatic intracranial aneurysms' mechanisms.

Kernohan-Woltman Notch Phenomenon Following Acute Subdural Hematoma.

A 72-year-old right-handed female patient was operated on for left-sided acute subdural hematoma responsible for coma. Two weeks afterward, her neurological status had improved with a Glasgow Coma Scale score of 14 and a paradoxical left-sided hemiparesis. The brain magnetic resonance imaging displayed a diffusion-restricting, hyper fluid-attenuated inversion recovery lesion of the right cerebral peduncle facing the tentorial notch, and the patient was diagnosed with Kernohan-Woltman notch phenomenon. This allowed to focus the neurological rehabiliation on the ipsilateral motor deficit as well as the hemineglect.

Acute Traumatic Subdural Hematoma in the Elderly and Associated Factors that May Influence Chronicity.

Traumatic acute subdural hematomas (TASDH) is by far the most common traumatic brain injury in adult patients with blunt trauma, who presented to the Emergency Department (ED). One of the serious sequale of TASDH is the development of Chronic Subdural Hematomas (CSD) with associated deterioration in mental status and convulsion.1,2 Studies to identify the risk factors that favors development of chronicity of TASDH are few and inconclusive. As seen in our prior initial study, there were few factors which were common in those who developed chronicity of their TASDH, and we elected to expand our pool of patients to include those admitted between the years of 2015 and 2021 with ATSDH and identify the common factors associated with development of CSD.

Pure retroclival subdural hemorrhage secondary to ruptured posterior communicating artery aneurysm.

Approximately 3% of intracranial aneurysm ruptures result in an associated subdural hematoma (SDH). SDH from intracranial aneurysm rupture without radiographic evidence of SAH, however, is rare. We report a case of an isolated retroclival SDH secondary to an intracranial aneurysm rupture.

Giant cell glioblastoma multiforme presents as acute pathological nontraumatic subdural haematoma.

We describe a case of giant cell glioblastoma multiforme (GBM) that presented with a non-traumatic acute subdural haematoma (NASDH). A 57-year-old male had a sudden onset headache and rapid deterioration in conscious level with Glasgow Coma Scale (GCS) of 5 and dilated unreactive left pupil. CT of the head revealed a left acute subdural haematoma with mass effect and a left parietal lesion. Our literature review revealed that glioblastoma presenting as an acute subdural haematoma is extremely unusual. To our knowledge, we report the second case. We propose an invasion of the arachnoid and cortical veins by the aggressive tumour as a possible underlying mechanism.

Infective Arteritis Manifesting as an Acute Subdural Hematoma.

We encountered a 60-year-old man who had been diagnosed with heart failure of valvular disease and infective endocarditis; he was being treated with intravenous antibiotics and diuretics. On the 12th hospital day, he suddenly lost consciousness; computed tomography showed a right-sided huge subdural hematoma (SDH) with brain herniation. He died after invasive care was discontinued. A massive SDH was noted at autopsy, and microimaging demonstrated ruptured infective arteritis, without aneurysm, on the surface of the culprit lobe. Acute SDH usually occurs after head trauma, but an area of nonsaccular aneurysmal arteritis can also result in acute SDH.