We present a case of Marfan's syndrome with acute aortic dissection during the trimester of her pregnancy, who underwent a Bentall operation 2 days after emergency cesarean section. A 24-year-old woman during the 31st week of pregnancy visited our emergency room due to sudden onset of chest and back pain, though she had no abnormality until this event. Because of her tall height, spider fingers, positive wrist sign, visual disorder and scoliosis, she was given a diagnosis of Marfan's syndrome. Enhanced CT and cardiac ultrasonography revealed that she was suffering from acute aortic dissection with annulo-aortic ectasia. Since it was difficult for her to continue with her pregnancy, she underwent emergency cesarean section and gave birth to a male baby weighted 1, 706g. Although there was little likelifood of early thrombus formation in the false lumen or significant aortic regurgitation indicating an emergency operation, fear of massive bleeding from her uterus and the exfoliated surface of the placenta after cesarean section required an observation period of 2 days. We performed a Bentall operation successfully after careful sedation, ventilation and blood pressure control for 2 days.

Protein C (PC) deficiency is an inherited thrombotic disorder with a prevalence of 0.19% among the general population. PC deficiency is associated with an increased risk of thrombosis when other risk factors are present, such as trauma, surgery, or infection, and is an important cause of mechanical valve thrombosis. We performed tricuspid valve replacement with a 29mm Carpentier-Edwards Perimount valve in a 20-year-old man with PC deficiency. The patient had corrected transposition of the great vessels with severe tricuspid insufficiency, as well as a history of cerebral infarction. In the perioperative period, we used only heparin sodium as the anticoagulant. When we restarted administration of warfarin, changing over from heparin, transient increases of serum plasmin inhibitor-plasmin complex (PIC) and thrombin antithrombin complex (TAT) levels were observed. Despite an increased dose of heparin, an appropriate activated partial thromboplastin time (APTT) was not obtained. This suggested a hypercoagulatory state, but the postoperative course was uneventful. Management of perioperative anticoagulation, prevention of late thrombotic events, and prosthetic valve selection in this particular situation are discussed.

Infected aortic aneurysm is very difficult to treat and is associated with a high mortality rate. A 78-year-old man had been scheduled to undergo selective endovascular repair for distal aortic arch aneurysm. While standby, however, he was admitted to our emergency room because of hemoptysis. Rapid dilatation of the aneurysm shown on serial CT and elevated of inflammatory reactions yielded a diagnosis of infected aortic aneurysm. Because the aneurysm had ruptured into the left lung, emergency surgery was performed. Six days after the first operation, critical bleeding due to anastomotic disruption of the distal aorta caused by infection and subsequent cardiac arrest occurred. We immediately started open chest massage and controlled the bleeding manually in the ICU, while an operating room was prepared. In the redo operation, anastomotic disruption was repaired using the visceral pleura under deep hypothermic circulatory arrest. Anastomotic bleeding is a potentially life-threatening condition, therefore extremely prompt measures are vital. Appropriate management based on the assumption of anastomotic bleeding was very important in the postoperative course of this case of infectious aortic aneurysm.

A 56-year-old woman suffering from mitral stenosis had underwent PTMC (percutaneous transvenous mitral commissurotomy) at age 46. After she developed congestive heart failure, mitral valve replacement (MVR) with Carbomedics 29M and tricuspid annuloplasty (TAP) was carried out. Four hours after admission to the ICU, massive bleeding was noticed. Cardiopulmonary bypass was restarted in the operating room. Laceration and hematoma were found at the posterolateral wall of the left ventricle. Under cardiac arrest with removal of the prosthetic valve, an internal tear was detected about 2cm below the anterolateral commissure (Miller Type III). The tear was covered with a horse pericardial patch (2×3cm) using 6-0 running sutures with reinforcement with gelatin-resorcine-formaline (GRF) glue between the laceration and the patch. MVR sutures in the annulus above the ventricular tear were first passed through the annulus, the pericardial patch and then the prosthetic cuff. Additionally, an epicardial tear was covered and reinforced with the fibrin sheet, GRF glue and pericardial patch in turn. Cardiopulmonary bypass was weaned easily without bleeding. The patient was intentionally on respiratory support with sedation for 3 days. The subsequent postoperative course was uneventful.

It was reported that nerve fibers were present in the inner part of lumbar intervertebral discs from patients with discogenic pain. Because there are no nerve fibers in the inner part of annulus fibrosus in normal condition, this finding suggests nerve ingrowth into the disc may be a cause of discogenic pain. Disc degeneration is often asymptomatic, thus, to understand the differences between symptomatic and asymptomatic disc, it is necessary to understand the pathogenesis of discogenic pain. We recently revealed that over 90% of the nociceptive dorsal root ganglion (DRG) neurons innervating the disc are sensitive to nerve growth factor (NGF), which is related to inflammatory pain. This indicates that discogenic pain is closely related to inflammation and NGF may play a key role. The increase of inflammatory mediators in symptomatic discs has been reported; we therefore studied the effects of disc inflammation and found that it induces sensitization of disc-innervating neurons and nerve ingrowth into the disc. More recently, it was shown that annular rupture induces nerve ingrowth, an increase of inflammatory mediators in the disc, and upregulation of calcitonin gene-related peptide, a pain-related molecule in DRGs. These findings led us to believe that annular rupture triggers inflammation and nerve ingrowth, inflammatory mediators then further promote nerve ingrowth into the disc and sensitization of disc-innervating neurons, and discogenic pain finally becomes chronic. NGF, found in symptomatic discs, may act as a key factor in generating chronic discogenic pain by sensitizing disc-innervating neurons and stimulating nerve ingrowth into the disc.
Calcitonin Gene-Related Peptide ; Diagnosis-Related Groups ; Ganglia, Spinal ; Humans ; Inflammation ; Intervertebral Disc ; Intervertebral Disc Degeneration ; Nerve Fibers ; Nerve Growth Factor ; Neurons ; Rupture ; Up-Regulation