Abdominal compartment syndrome (ACS) is a life-threatening disorder caused by rapidly increasing intraabdominal pressure. ACS can result in multiorgan failure and carries a mortality of 60~70%. The treatment of choice in ACS is surgical decompression. There are very few reports of ACS and experience in Korea. We report 12-year-old male patient who developed an abdominal compartment syndrome due to traffic-accident-induced retroperitoneal hematomas, Which was successfully treated by performing a bedside emergency surgical decompression with open linea alba fasciotomy with intact peritoneum. When patients do not respond to medical therapy, a decompressive laparotomy is the last surgical resort. In patients with severe abdominal compartment syndrome, the use of a linea alba fasciotomy is an effective intervention to lower intra-abdominal hypertension (IAH) without the morbidity of a laparotomy. Use of a linea alba fasciotomy as a first-line intervention before committing to full abdominal decompression in patients with abdominal compartment syndrome improves physiological variables without mortality. Consideration for a linea alba fasciotomy as a bridge before full abdominal decompression needs further evaluation in patients with polytrauma abdominal compartment syndrome.
Child ; Decompression, Surgical ; Emergencies ; Health Resorts ; Hematoma ; Humans ; Intra-Abdominal Hypertension ; Korea ; Laparotomy ; Lower Body Negative Pressure ; Male ; Peritoneum

T-type calcium channels are low voltage-activated calcium channels that evoke small and transient calcium currents. Recently, T-type calcium channels have been implicated in neurodevelopmental disorders such as autism spectrum disorder and neural tube defects. However, their function during embryonic development is largely unknown. Here, we investigated the function and expression of T-type calcium channels in embryonic neural progenitor cells (NPCs). First, we compared the expression of T-type calcium channel subtypes (CaV3.1, 3.2, and 3.3) in NPCs and differentiated neural cells (neurons and astrocytes). We detected all subtypes in neurons but not in astrocytes. In NPCs, CaV3.1 was the dominant subtype, whereas CaV3.2 was weakly expressed, and CaV3.3 was not detected. Next, we determined CaV3.1 expression levels in the cortex during early brain development. Expression levels of CaV3.1 in the embryonic period were transiently decreased during the perinatal period and increased at postnatal day 11. We then pharmacologically blocked T-type calcium channels to determine the effects in neuronal cells. The blockade of T-type calcium channels reduced cell viability, and induced apoptotic cell death in NPCs but not in differentiated astrocytes. Furthermore, blocking T-type calcium channels rapidly reduced AKT-phosphorylation (Ser473) and GSK3β-phosphorylation (Ser9). Our results suggest that T-type calcium channels play essential roles in maintaining NPC viability, and T-type calcium channel blockers are toxic to embryonic neural cells, and may potentially be responsible for neurodevelopmental disorders.
Apoptosis ; Astrocytes ; Autism Spectrum Disorder ; Brain ; Calcium ; Calcium Channels ; Calcium Channels, T-Type* ; Cell Death ; Cell Survival ; Embryonic Development ; Female ; Neural Tube Defects ; Neurodevelopmental Disorders ; Neurons ; Pregnancy ; Stem Cells*