The efficacy and safety of burr-hole craniotomy without continuous drainage for chronic subdural hematoma and subdural hygroma in children under 2 years of age.

PURPOSE: Various treatment modalities have been used in the management of chronic subdural hematoma and subdural hygroma (CSDH/SDHy) in children. However, few studies have examined burr-hole craniotomy without continuous drainage in such cases. Here, we retrospectively evaluated the efficacy and safety of burr-hole craniotomy without continuous drainage for CSDH/SDHy in children under 2 years old. We also aimed to determine the predictors of CSDH/SDHy recurrence. METHODS: We conducted a retrospective chart review of 25 children under 2 years old who underwent burr-hole craniotomy without continuous drainage for CSDH/SDHy at a pediatric teaching hospital over a 10-year period. We analyzed the relationship between CSDH/SDHy recurrence and factors such as abusive head trauma, laterality of CSDH/SDHy, and subdural fluid collection type (hematoma or hygroma). RESULTS: CSDH/SDHy recurred in 5 of the 25 patients (20 %), requiring a second operation at an average of 0.92 ± 1.12 months after the initial procedure. The mean follow-up period was 25.1 ± 28.6 months. There were no complications related to either operation. None of the assessed factors were statistically associated with recurrence. CONCLUSIONS: Burr-hole craniotomy without continuous drainage for CSDH/SDHy appears safe in children aged under 2 years and results in a relatively low recurrence rate. No predictors of CSDH/SDHy recurrence were identified. Advantages of this method include avoiding external subdural drainage-related complications. However, burr-hole drainage may be more effective for CSDH, which our data suggests is more likely to recur than SDHy, providing the procedure is performed with specific efforts to reduce complications.

Nonconvulsive Status Epilepticus Associated with Cerebral Hyperperfusion Syndrome after Carotid Endarterectomy: A Case Report.

We report a case of a 73-year-old man who developed nonconvulsive status epilepticus as a complication of cerebral hyperperfusion syndrome after carotid endarterectomy for carotid artery stenosis. On postoperative day 1, the patient experienced headaches and vomiting. Resting N-isopropyl-p-[123I] iodoamphetamine single-photon emission computed tomography showed increased cerebral blood flow to the entire right hemisphere, and the patient was diagnosed with cerebral hyperperfusion syndrome. He was treated with antihypertensive and antiseizure medications, sedated using propofol, intubated, and placed under mechanical ventilation. On postoperative day 3, computed tomography perfusion imaging showed a reduction in hyperperfusion, and propofol sedation was terminated on postoperative day 4. However, the patient exhibited prolonged impaired awareness and roving eye movements, and long-term video electroencephalographic monitoring revealed electrographic seizures. The patient was diagnosed with nonconvulsive status epilepticus. Propofol sedation was resumed, and the antiseizure medication dose was increased. Subsequently, the state of hyperperfusion in the right hemisphere diminished, and electroencephalographic findings improved, allowing sedation to be terminated on postoperative day 7. The findings from this case suggest that when clinical subtle symptoms, such as impaired awareness and roving eye movements, are observed during treatment of cerebral hyperperfusion syndrome, video electroencephalography should be performed to detect electrographic seizures.

A Case of Acquired Factor XIII Deficiency with Systemic Lupus Erythematosus Diagnosed after Repeated Intracerebral Hemorrhages.

We present a case of autoimmune-acquired factor XIII deficiency associated with systemic lupus erythematosus, which was diagnosed as a cause of repeated intracerebral hemorrhage. An intracerebral hemorrhage occurred in a 24-year-old female patient. Craniotomy was performed to remove the hematoma, but rebleeding occurred at the same site on days 2 and 11, respectively. Detailed blood tests revealed that factor XIII activity decreased. Although autoimmune-acquired factor XIII deficiency is a very rare disease, it can sometimes be fatal when intracerebral hemorrhage occurs. If there is repeated intracerebral hemorrhage, factor XIII activity should be confirmed.

Nonocclusive Mesenteric Ischemia Is a Potentially Lethal Complication Just after Stroke Onset: Report of Six Case Studies.

Nonocclusive mesenteric ischemia (NOMI) is a rare but life-threatening post-stroke complication. This is the first case series report of NOMI after stroke, describing its characteristics and the difficulty of diagnosis. We retrospectively reviewed 367 stroke patients from April 2018 to May 2019 in our hospital. We identified six patients (1.6%) with NOMI after stroke and described their clinical presentation, including characteristics, vital signs, laboratory parameters, treatment, and outcomes. The mean interval between stroke onset and diagnosis of NOMI was 4.6 days (range, 3-10 days). Five patients had disturbance of consciousness caused by stroke, and therefore the major complaints and symptoms associated with NOMI were nonspecific, possibly resulting in delayed diagnosis and treatment. All patients had a high respiratory rate (≥22 breaths/min). C-reactive protein and lactate levels were high (mean, 21.6 mg/L and 2.4 mmol/L, respectively). All patients underwent emergent abdominal operations. Four patients were discharged with modified Rankin Scale scores ≥4, and two patients died. NOMI can be a fatal post-stroke complication and is challenging to diagnose. Further investigations should be conducted to determine the most efficient way to diagnose NOMI after stroke.

Rapid De Novo Aneurysm Formation after Rathke Cleft Cyst Rupture.

BACKGROUND: Spontaneous rupture of a Rathke cleft cyst is very rare, and rapid de novo aneurysm formation associated with pituitary apoplexy is rare. CASE DESCRIPTION: A 66-year-old woman experienced severe left temporal pain. Magnetic resonance imaging showed a Rathke cleft cyst, and transsphenoidal surgery was planned. However, the patient suddenly developed severe headache, vomiting, visual disturbance, and a lowered level of consciousness about 3 weeks after the first onset. The clinical course and neuroradiologic characteristics suggested Rathke cleft cyst rupture. The patient received hormone replacement, and the visual abnormalities resolved. However, subsequent neuroradiologic evaluation demonstrated that a de novo aneurysm in the cavernous sinus portion of the internal carotid artery had formed within 8 days after rupture of the Rathke cleft cyst. This de novo aneurysm was not apparent on initial magnetic resonance angiography. CONCLUSIONS: This case features a rare clinical presentation of rapid de novo aneurysm formation after Rathke cleft cyst rupture. The severe inflammation around the vasculature after rupture of the Rathke cleft cyst might have been involved in aneurysm formation.