Surgical treatment and anticoagulant therapy for liver injury due to cardiopulmonary resuscitation with lethal pulmonary embolization: A case report.

INTRODUCTION: Cardiopulmonary resuscitation (CPR) can sometimes induce organ injury, however, such an occurrence is rare. We herein report a case of liver injury due to CPR with life-threatening pulmonary embolization (PE) that required the patient to undergo surgical hemostasis and antithrombotic therapy. PRESENTATION OF CASE: A woman in her 70s fell off her bicycle. She suffered cardiopulmonary arrest and underwent CPR. She was diagnosed with PE and underwent catheter treatment and anticoagulant therapy; however, her blood pressure did not increase. Contrast-enhanced computed tomography revealed injury to the liver and inferior phrenic artery. Hemostasis could not be completely achieved by transcatheter arterial embolization alone. She was therefore transferred to our hospital and underwent damage control surgery (DCS). Definitive surgery (DS) performed 33 h after DCS showed right hepatic subcapsular hematoma and left hepatic subcapsular hematoma. We cut away the capsules and removed the hematomas. There were lacerations and oozing under the capsule in the left lobe. We sutured the laceration. At 72 h after undergoing DS, antithrombotic therapy was started. On day 19, the patient was discharged home by herself without any neurological damage. DISCUSSION: For a case of liver injury due to CPR with life-threatening PE, treatment with both hemostasis and antithrombotic therapy should be performed. Antithrombotic therapy was started appropriately in this case by accurately identifying the liver laceration and suturing it. CONCLUSION: Hemostasis following both DCS and DS with appropriate anticoagulant therapy was effective for the management of liver injury due to CPR with life-threatening PE.

A case of hemorrhagic shock due to intercostal artery injury that occurred during initial trauma care with multiple displaced rib fractures and traumatic head injury.

Rib fractures can cause injury to some organs. We herein report a case of hemorrhagic shock due to intercostal artery injury that occurred during initial trauma care (ITC) treated by resuscitative thoracotomy (RT) and transcatheter arterial embolization (TAE) with multiple displaced rib fractures (RFs) and traumatic head injury (THI). A man in his 50s who was injured in a traffic accident was transferred to our institution by helicopter for emergency medical treatment. He underwent left thoracic drainage on site. On admission, he was diagnosed with multiple RF, THI, pelvic fracture and right humerus fracture. His D-dimer and fibrin degradation products (FDP) level were extremely elevated. However, contrast enhance CT (CECT) revealed no extravasation. At 2 h after arrival, massive hemorrhaging from his thoracic tube suddenly occurred and his blood pressure decreased to approximately 40s mmHg. CECT performed after volume resuscitation and massive transfusion revealed extravasation from the intercostal artery. Because his blood pressure could not be maintained by massive transfusion, we performed RT and TAE followed by RT. He then received intensive care and several surgical procedures were performed, including craniotomy for removal of hematoma, rib fixation and humerus fixation. He was transferred to another hospital for rehabilitation on day 63, with a GCS of 15. Hemorrhagic shock due to intercostal artery injury may occur at any time from arrival in cases with displaced RF, especially when complicated by THI.

[A Case of Carcinomatous Meningitis Due to Gastric Cancer].

A 43-year-old man was diagnosed with gastric cancer with diaphragm invasion and multiple lymph node metastases and underwent total gastrectomy. The histological diagnosis was por2>tub2, ypT4b(diaphragm), int, INF c, ly1, v1, ypN3, yp Stage ⅢC. Three months postoperatively, computed tomography showed recurrence in the peritoneum and multiple lymph nodes, and he received chemotherapy(RAM plus PTX). After initiating the third course of chemotherapy, he was hospitalized due to loss of appetite and fatigue. On the third day of hospitalization, he lost consciousness and had a temporary convulsion seizure. Thereafter, he complained of headache and nausea. Brain magnetic resonance imaging and cerebrospinal fluid examination lead to a diagnosis of carcinomatous meningitis due to gastric cancer. An Ommaya reservoir was placed, and intrathecal infusion with methotrexate(MTX)and cytarabine(Ara-C)was planned; however, intrathecal infusion could not be administered because of hepatic injury due to acute obstructive cholangitis. He died 6 months postoperatively. Carcinomatous meningitis has a rapidly progressive course with very poor prognosis. Early diagnosis is important, and the treatment should be initiated as soon as possible. Moreover, an effective standard treatment for carcinomatous meningitis needs to be established.

A new hybrid sutureless patch repair utilizing chitosan for left ventricle rupture after myocardial infarction: A case report.

INTRODUCTION: There are many publications reporting the use of TachoSil sheets for sutureless repair. Trauma doctors have recently reported that chitosan-based sheets can efficiently achieve hemostasis for active bleeding. PRESENTATION OF CASE: An 85-year-old man was diagnosed with left ventricle free wall rupture that caused cardiac tamponade and cardiogenic shock. Extracorporeal membrane oxygenator (ECMO) was started immediately and surgical repair was planned. Bleeding occurred from a 1-cm tear in the center of the necrotic area in the territory of the left circumflex artery. The tear was treated with a chitosan-based HemCon Bandage. After hemostasis of the myocardium was achieved, the bandage was peeled off and a patch repair was performed using collagen fleece with fibrinogen-based impregnation. His condition subsequently improved. The tracheal tube was extubated and ECMO was removed 2days after the surgery. One month later, the patient had no complications at his postoperative follow-up visit. DISCUSSION: To our knowledge, this is the first report of a hybrid patch repair utilizing chitosan-based sheets for a left ventricle rupture after myocardial infarction. Further studies are necessary to evaluate the short- and long-term efficacy of this procedure, and these results must be compared with those of classical surgical repairs. CONCLUSION: The new hybrid sutureless patch utilizing chitosan was demonstrated as safe, easy and effective.

[Appropriate Biliary Drainage Methods for Unresectable Cholangiocarcinomas].

We investigated the efficacy of different biliary drainage methods for the treatment of unresectable cholangiocarcinomas. We performed a retrospective study of 28 patients with unresectable cholangiocarcinomas who underwent biliary drainage at our hospital between January 2008 and June 2014 to compare the incidence of post-drainage stent dysfunction (SD) and reintervention (RI) for SD according to primary drainage method, lesion site, and complication status (the presence or absence of cholangitis). The duration of stent patency was compared between the different stent types. No significant differences in the incidence of SD and RI were found according to primary drainage methods, lesion site, or the presence or absence of cholangitis. The mean durations of stent patency for plastic and metal stents were 2.7 months and 7.4 months, respectively, suggesting that metal stents should be selected when the estimated prognosis is ≥2 months. Furthermore, metal stent placement, rather than the additional placement of plastic stents, should be considered a feasible option in cases of SD.

Successful management of threatened aortic rupture late after rib fracture caused by blunt chest trauma.

A 62-year-old man was crushed in a car accident and diagnosed with a fractured left ninth rib, pulmonary and heart contusion, hemopneumothorax, and descending aortic injury based on a computed tomography scan. He underwent chest tube drainage and was intubated for mechanical ventilation because a bone fragment of the ninth rib threatened to penetrate the descending aorta. On the second posttrauma day, computed tomography showed the bone fragment of the ninth rib approaching the descending aorta. He underwent graft replacement of the injured portion of the descending thoracic aorta, and we removed the fractured left ninth rib.

[Strategy for the treatment of Stage IV gastric cancer with preoperative chemotherapy].

In 2007, we began using neoadjuvant chemotherapy for the treatment of Stage IV gastric cancer and then performing R0/1 surgery in patients in whom chemotherapy was effective. Here, we evaluate the use of this therapeutic strategy combining chemotherapy and surgery for the treatment of Stage IV gastric cancer. The subjects of our investigation were 46 patients with Stage IV gastric cancer treated from 2007 through 2012. We divided these patients into the NAC group (19 patients), in whom we performed R0/1 surgery after chemotherapy, and the Cx group (27 patients), who continued chemotherapy. We also included 79 patients with Stage IV gastric cancer treated from 2001 to 2006, divided into the OPE group (36 patients), in whom we performed R0/1 surgery without neoadjuvant chemotherapy, and the NC group (43 patients), in whom we performed R2 surgery. We plotted the survival curves of these 4 groups. The chemotherapy protocols used were S-1+cisplatin( CDDP) and S-1+docetaxel( DOC). The disease control rate of these chemotherapies was 72%, and R0/1 surgery was performed in 53.8% of patients with liver metastasis, 62.5% of those with paraaortic lymph node (PALN) metastasis, 29.4% of those with peritoneal metastasis, 100% of patients with T4N2 disease, and 0% of patients with distant metastasis. The 2-year survival rates of the NAC, OPE, Cx, and NC groups were 69%, 55%, 0%, and 20%, respectively. The 5-year survival rates of the NAC, OPE, Cx, and NC groups were 35%, 30%, 0%, and 5%, respectively.

Cellular toxicity of polyglutamine expansion proteins: mechanism of transcription factor deactivation.

The expression of polyglutamine-expanded mutant proteins in Huntington's disease and other neurodegenerative disorders is associated with the formation of intraneural inclusions. These aggregates could potentially cause cellular toxicity by sequestering essential proteins possessing normal polyQ repeats, including the transcription factors TBP and CBP. We show, in vitro and in cells, that monomers or small soluble oligomers of huntingtin exon1 accumulate in the nucleus and inhibit the function of TBP in a polyQ-dependent manner. FRET experiments indicate that these toxic forms are generated through a conformational rearrangement in huntingtin. Interaction of toxic huntingtin with the benign polyQ repeat of TBP structurally destabilizes the transcription factor, independent of the formation of insoluble coaggregates. Hsp70/Hsp40 chaperones interfere with the conformational change in mutant huntingtin and inhibit the deactivation of TBP. These results outline a molecular mechanism of cellular toxicity in polyQ disease and can explain the beneficial effects of molecular chaperones.

Molecular chaperones as modulators of polyglutamine protein aggregation and toxicity.

The formation of insoluble protein aggregates in neurons is a hallmark of neurodegenerative diseases caused by proteins with expanded polyglutamine (polyQ) repeats. However, the mechanistic relationship between polyQ aggregation and its toxic effects on neurons remains unclear. Two main hypotheses have been put forward for how polyQ expansions may cause cellular dysfunction. In one model neurotoxicity results from the ability of polyQ-expanded proteins to recruit other important cellular proteins with polyQ stretches into the aggregates. In the other model, aggregating polyQ proteins partially inhibit the ubiquitin-proteasome system for protein degradation. These two mechanisms are not exclusive but may act in combination. In general, protein misfolding and aggregation are prevented by the machinery of molecular chaperones. Some chaperones such as the members of the Hsp70 family also modulate polyQ aggregation and suppress its toxicity. These recent findings suggest that an imbalance between the neuronal chaperone capacity and the production of potentially dangerous polyQ proteins may trigger the onset of polyQ disease.

Co-translational folding of caspase-activated DNase with Hsp70, Hsp40, and inhibitor of caspase-activated DNase.

CAD (caspase-activated DNase) that causes chromosomal DNA fragmentation during apoptosis exists as a complex with ICAD (inhibitor of CAD) in proliferating cells. Here, we report that denatured CAD is functionally refolded with Hsc70-Hsp40 and ICAD. Hsc70-Hsp40 suppresses the aggregation of the denatured CAD, but cannot restore its enzymatic activity. In contrast, ICAD could not suppress the aggregation of CAD, but supported the CAD's renaturation with Hsc70-Hsp40, indicating that ICAD recognizes the quasi-native folding state of CAD that is conferred by Hsc70-Hsp40. Using an in vitro translation system, we then showed that during CAD translation, Hsc70-Hsp40 as well as ICAD bind to the nascent CAD polypeptide, while on ribosomes. These results indicate that ICAD together with Hsc70-Hsp40 assists the folding of CAD during its synthesis, and that the CAD*ICAD heterodimer is formed co-translationally.