While congenital heart disease is not uncommon, cyanotic congenital heart disease (CCHD) accounts for a minor fraction of them. However, when cyanosis is present, it usually indicates a severe or critical illness. Tetralogy of Fallot (TOF) is one of the common CCHDs, representing 7-10% of all congenital cardiac malformations. Double-outlet right ventricle (DORV) is another CCHD similar to the TOF and associated with decreased pulmonary flow, ventricular septal defect (VSD), and aorta receiving blood from both ventricles. Reduced oxygen arterial saturation and increased viscosity by polycythemia induce focal cerebral ischemia, often in the area supplied by the middle cerebral artery leading to brain abscess. Brain abscesses require craniotomy, which is a major surgery. These patients also often show features of sepsis and increased intracranial pressure. The presence of CCHD further complicates the situation, making perioperative management even more challenging. There are studies in the literature on the management of similar cases, and they report successful management in most of them. However, not all such cases need intensive postoperative management. We present four pediatric cases who had either TOF or DORV and had to undergo craniotomy for brain abscess or ventriculoperitoneal shunt placement. We describe case management and highlight the critical features and cases that require prolonged postoperative critical care management.

We report a unique case of delayed brain swelling following craniectomy that improved rapidly after cranioplasty, and discuss the potential mechanism underlying this delayed and reversible brain swelling. A 22-year-old woman developed surgical site infection after removal of a convexity meningioma. Magnetic resonance imaging revealed an epidural abscess around the surgical site. Subsequently, the abscess was evacuated, and the bone flap was removed. Later, brain edema around the skull defect emerged and progressed gradually, despite resolution of the infection. The edematous brain developed focal swelling outward through the bone defect without ventricle dilatation. Because we suspected that the edema and swelling were caused by the state of the bone defect, we performed a cranioplasty 10 weeks after the bone flap removal, and brain edema improved rapidly. We hypothesized that the brain edema was initially caused by surgical stress and inflammation, followed by compression of cortical veins between the dural edge and brain tissue, leading to disruption of venous return and exacerbation of brain edema. When delayed focal brain edema and external swelling progress gradually after bone flap removal, after excluding other pathological conditions, cranioplasty should be considered to improve cortical venous congestion caused by postsurgical adhesion.

Pseudohypoxic brain swelling (PHBS) is known to be an uncommon event that may occur during and following an uneventful brain surgery, when negative suction drainage is used. The cerebrospinal fluid loss related to suction drainage can evoke intracranial hypotension that progress to PHBS. The main presentations of PHBS are sudden unexpected circulatory collapses, such as severe bradycardia, hypotension, cardiac arrest, consciousness deterioration and diffuse brain swelling as seen with brain computerized tomography (CT). We present a stuporous 22-year-old patient who underwent cranioplasty under general anesthesia. The entire course of the general anesthesia and operation progressed favorably. However, the time of scalp suture completion, sudden bradycardia and hypotension occurred, followed by cardiac arrest immediately after initiation of subgaleal and epidural suction drainage. After successful resuscitation, the comatose patient was transferred to the neurosurgical intensive care unit and PHBS was confirmed using brain CT.

We give a case study demonstration, using aqueductal cerebrospinal fluid (CSF) stroke volume quantification with phase-contrast magnetic resonance imaging, of a large opening in the rigid cranium by a decompressive craniectomy and its subsequent closure by bone flap repositioning resulted in the arrest and subsequent restoration of aqueductal CSF flow.

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