Reasons for failing to save acute aortic dissection (AAD) patients include critical, sudden complication associated with AAD and limited examination feasible in critical condition. Computed tomography and angiography are occasionally unfeasible. Considering it most important to comprehend the pathology at bedside in real time, we introduced transesophageal echocardiography (TEE) to manage AAD. Subjects were 27 consecutive patients--15 men 35 to 68 years old and 12 women 51 to 84 years old. A biplace TEE (Hitachi, Co., Tokyo) was used. TEE included: 1) diagnosis of dissection; 2) extent of dissection; 3) site of entry; 4) diagnosis of complications (cardiac workup tamponade, hemothorax, etc); 5) thrombosis in false lumen; 6) perfusion in branch arteries; 7) intraoperative changes in pathology; and 8) navigation of treatment. Surgical intervention was indicated in 24 and conservative theraphy in 3. We had 3 operative deaths and overall survival of 88.9%. The occurrence of subclinical changes that could be diagnosed only with TEE was not rare. Information provided by TEE has enabled definite diagnosis, elimination of possible pathologies, comprehension of altered conditions, monitoring of intraluminal events, guidance of therapeutic procedures, and immediate assessment of surgical procedures in the operating room. TEE was advantageous in obtaining abundant information less invasively at bedside and in real time and in using it as an eye in various procedures. Disadvantages of TEE include semiinvasiveness in awake patients, presence of a learning curve, and possible damage to esophageal mucosa (although none was encountered in this series). Although arch branch vessels and abdominal visceral arteries were “blind zone” for TEE, we developed techniques for visualizing these vessels, enabling us to recognize extended dissection into these arteries and perfusion in them. While computed tomography is still the gold standard in diagnosing AAD, useful information is provided by using TEE complimentarily. We concluded that TEE is useful for recognizing pathologies and dealing with them in patients with unusual clinical courses of AAD.

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Background: Superantigens are potent stimulators of T cells that lead to the overexpression of proinflammatory cytokines. Although superantigens have been implicated in the pathophysiology of a wide variety of human diseases, solid evidence for their role is confirmed only in toxic shock syndrome and some other cases. We determined whether circulating superantigens were detected in an intensive care unit (ICU) population and studied the relationship between superantigen detection and infection severity. Methods: Plasma samples (n=474) were serially collected from 78 ICU patients whose primary diagnoses were cardiovascular (n=4), respiratory (n=11), abdominal (n=27), and neurological disorders (n=2); trauma (n=10); burns (n=10); and others (n=14). Plasma concentrations of superantigens, i.e., staphylococcal enterotoxin A (SEA), SEB, and SEC; toxic shock syndrome toxin-1 (TSST-1); and streptococcal pyrogenic exotoxin A (SPEA); were measured by a newly developed enzyme-linked immunosorbent assay for specific detection and quantitation of these superantigens. Results: Significant levels of plasma superantigens were detected in 16 patients (21%). Four species of superantigens were detected in 1, 3 species in 2, 2 species in 1, and a single species in 12 patients. SEA was detected in 7, SEB in 4, SEC in 2, TSST-1 in 6, and SPEA in 5. The detection of superantigens was 6% (1/17) in patients who did not show systemic inflammatory response syndrome (SIRS), 0% (0/21) in SIRS patients without infection, 31% (5/16) in septic patients without shock, and 42% (10/24) in septic shock patients. In septic patients who had obvious staphylococcus aureus or streptococcus pyogenes infection, the rate of detecting at least 1 superantigen in plasma was 48% (12/25). Conclusions: Superantigens were detected in the circulation of ICU patients and detection of superantigens was higher in septic than nonseptic patients.

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Purpose: We clarified the effects of triiodothyronine on proinflammatory cytokines in a septic rat model. Materials and Methods: Sprague-Dawley rats weighing 320-420g underwent cecal ligation and puncture (CLP) to induce sepsis and were grouped randomly as (1) control group: CLP only, (2) L group: CLP/T₃ 3ng/hr, and (3) H group: CLP/T₃ 15ng/hr. T₃ was administered subcutaneously by osmotic pump. Blood samples were obtained 24 hours after laparotomy from abdominal aorta and IL-1β, TNF-α, IL-6, IL-8, and free T₃ were measured. Results and Discussion: Proinflammatory cytokine production was suppressed by T₃ administration especially in the L group. Free T₃ was also maintained within the normal range by T₃ administration. All animals survived in the L and H groups, whereas 3 died in the control group. We concluded that T₃ replacement offers a good outcome in a septic rat model because it suppresses proinflammatory cytokines.

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A 76-year-old man who had suffered subarachnoid hemorrhage about 10 years ago did not undergo surgery but other details were not clear. When admitted to our hospital, his consciousness level was 3-1-5 (Glasgow coma scale) and right hemiparesis was apparent. In the computed tomography (CT) scan, a cerebral hematoma (64×43×60mm) and subarachnoid hemorrhage appeared in the left frontotemporal area and a circular low-density area was observed in the cerebral hematoma. Enhanced CT enhanced the low-density area. In magnetic resonance (MR) and cerebral angiography, a cerebral aneurysm (8×7×7mm) was observed at the bifurcation of the M1-M2 and cystic expansion (17×13×15mm) adjoined the aneurysm. We considered pseudoaneurysm or thrombosed giant aneurysm. We conducted coil embolization of the aneurysm using Guglielmi electrolytically detachable coils, then evacuated cerebral hematoma by stereotactic aspiration surgery. V-P shunt was conducted for normal pressure hydrocephalus after 23 days. Follow-up MRI and cerebral angiography showed thrombosis of aneurysm and disappearance of the cerebral hematoma. We discuss neuroimaging features of the giant aneurysm and pseudoaneurysm.

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Traumatic biliary stricture is a relatively rare path ologic condition developing after abdominal trauma. We treated 2 patients with traumatic biliary stricture who differed in the mechanism of injury, organs simultaneously injured, and treatment principles. Patient 1 had steering wheel trauma, with surgery indicated mainly for stricture of the pancreatic duct. However, since biliary stricture developed and was diagnosed preoperatively, choledochoduodenostomy was conducted following Letton and Wilson's procedure, and the patient was discharged 54 days after injury (44 days after onset). Patient 2 underwent emergency laparotomy for duodenal perforation and retroperitoneal bleeding due to seatbelt injury. Biliary stricture developed 14 days postoperatively and was treated by percutaneo-transhepatic cholangiole drainage (PTCD). This patient had to remain hospitalized 95 days after injury (81 days after onset). For traumatic biliary stricture, nonoperative treatment may be the first choice despite onset time and the mechanism of injury, but long hospitalization is difficult to avoid. As in patient 1, when laparotomy is conducted for coexisting injury, diversion of the biliary tract may be useful.

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We reported a case of fatal cardiac conduction disturbance induced by blunt chest trauma, “commotio cordis.” A 67-year-old man experienced thoracic impact and complete A-V block on hospital arrival, then complete A-V block without escaped beats 1.5 hours after admission. He was resuscitated by cardiopulmonary resuscitation (CPR) including transcutaneous/transvenous pacing. No obvious myocardial damage showing structural injury due to trauma was seen in echocardiographic or biochemical surveys. Electrophysiological studies indicated that preexisting cardiac incapability (right bundle branch block) was not responsible for this posttraumatic episode of fatal arrhythmia. Commotio cordis, fatal cardiac conduction disturbance induced by relatively minor chest wall impact should be taken into consideration under intense monitoring in a trauma center setting and warrants further investigation.

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Neuroleptic malignant syndrome (NMS) occurs suddenly in patients treated with neuroleptic agents and involves high mortality. We report a case of NMS due to intramuscular injection of haloperidol decanoate. A 29-year-old man with paranoia schizophrenia since the age of 19 years was treated with neuroleptics. From 4 months ago, he was treated with haloperidol decanoate (50mg i.m. monthly), increased to 100mg/month. On the day before admission, he took an overdose of neuroleptics (include chlorpromazine hydrochloride 4.2g). He was transfered to our hospital due to drug intoxication. After admission, he developed NMS. After onset, haloperidol decanoate and all other neuroleptics were stopped. He was treated with dantrolene, bromocriptine, muscle relaxants, and intensive care including assisted ventilation, but his clinical condition and laboratory data did not improved for 25 days. In this case, we studied drug concentration in muscles undergoing haloperidol decanoate injection to determine the possible muscle resection for decreasing the blood concentration of the drug, but the patient recovered without muscle resection.

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