Modern neurological intensive care began with the use of respiratory care principles established during European poliomyelitis epidemics and expanded into the wider field that encompassed all acute and critical aspects of neurological and neurosurgical disease. Since the foundation of the Neurocritical Care Society (NCS) in 2003 and publication of the journal Neurocritical Care in 2004, papers in this medical subspecialty has increased explosively. The NCS is composed of multiprofessional healthcare providers that are dedicated to improve the care and outcomes of patients with life-threatening neurological illnesses by promoting quality patient care, professional collaboration, research, training and advocacy. The neurointensivist defragments and harmonizes the care of his or her patients by taking responsibility for basic elements of intensive care that might otherwise be provided by multiple subspecialists. In the United States, over 100 neurological intensive care units (neuro-ICUs) have been established. Detailed core curriculum for neurointensivists is prepared under formal recognition and acceptance by the United Council of Neurologic Subspecialties. Commonly managed conditions in neuro-ICUs include stroke, neurotrauma, seizures and epilepsy, neuromuscular diseases, infections, inflammatory and demyelinating diseases, encephalopathies, neuroendocrine disorders, movement disorders, various clinical syndromes, perioperative neurosurgical care, neurorehabilitation, and pharmacotherapeutics. Expertise in neurological intensive care involves procedural skills and proficiency with standard forms of intensive-care monitoring as well as specialized forms of neurological monitoring (i.e., intracranial pressure and continuous electroencephalograph monitoring) and interventions (i.e., therapeutic hypothermia and thrombolytic reperfusion therapy). Recent meta-analysis on neuro-ICUs indicated statistically significant reduction in mortality and an increased proportion of patients with a favorable outcome. Both the stroke care unit and neuro-ICU manage severe stroke patients, the latter being more rational in treating various kinds of critically ill neurological conditions including stroke mimics. A standard educational program for neurointensivists to establish sophisticated neuro-ICUs is now warranted in Japan.

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The etiology of acid-base disorder in acute kidney injury (AKI) and the mechanism of its correction using continuous renal replacement therapy (CRRT) were analyzed using the Stewart approach. AKI patients exhibited acidemia because of metabolic acidosis. This acidemia was mostly secondary to a decreased strong ion difference apparent, hyperphosphatemia, and elevated strong ion gap (SIG). These acidifying effects were offset by hypoalbuminemia. CRRT corrected the metabolic acidosis in AKI patients by reducing SIG, phosphate, and chloride. CRRT using lactate-buffered fluid resulted in an increase in the plasma lactate level with the lactate load. However, CRRT with bicarbonate-buffered fluid might decrease the plasma lactate level without the lactate load and with the removal of lactate, exerting an alkalizing effect. Moreover, caution is needed because high-volume hemofiltration with lactate-buffered fluid can induce hyperlactatemia, leading to temporally metabolic acidosis.

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Extubation criteria in adult patients with acute respiratory failure are reviewed. Oxygenation, ventilatory ability, and airway patency must be assessed to predict the possibility of successful extubation of the tracheal tube. Combined assessment of two or more parameters is more useful to predict ventilatory ability. However, prediction of airway patency after extubation is so difficult that aspiration, airway obstruction, and insufficient clearance of sputa are well known as the main reasons for reintubation. Although many extubation criteria have been proposed, none of these can perfectly predict a successful extubation. Therefore, we must remain prepared for reintubation, while attempting extubation of the tracheal tube.

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Objectives: We assessed the safety and efficacy of application of an enteral nutrition (EN) protocol in post-esophagectomy patients who required intensive care for more than 7 days. Methods: There was no EN protocol for 24 patients who underwent esophagectomy in 2006. The initiation and adjustment of feeding in those patients were decided by attending physicians once a day without any target goal of EN. An EN protocol was used in 27 patients in 2007. In those patients, EN was initiated on postoperative day 2 or 3, and the feeding dose was increased by 20 kcal/hr in the morning and evening toward 100% of basal energy expenditure (E100) calculated by Harris-Benedict formula. Results: The median durations to achieve EN administration of E100 was 3 days with the protocol, which was significantly shorter than the 6-day period for patients without the protocol (P < 0.001). There was no significant difference in the incidence of diarrhea and residual volumes between the two groups. The use of parenteral feeding was significantly less frequent in patients with the protocol than in patients without the protocol (0% vs. 16.7%, P = 0.03). Conclusions: Our simple EN protocol makes the duration to achieve the target goal of EN significantly shorter without any harmful side effects.

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Endovascular aneurysm repair (EVAR) for abdominal aortic aneurysms (AAA) is becoming the predominant technique compared with open repair (OR). However, limited data are available regarding the effect of EVAR on renal function. We studied the characteristics of acute kidney injury (AKI) in EVAR and OR. We retrospectively investigated 147 adults who underwent infrarenal AAA surgery (EVAR; 70, OR; 77) from 2006 to 2008. We analyzed the incidence and outcomes of AKI following AAA surgery. AKI was diagnosed according to the RIFLE criteria, which was defined as the maximum postoperative increase in serum creatinine level from the preoperative baseline ( ΔsCr). In the EVAR group, we observed that the patients were older and that the duration of operation, mechanical ventilation, ICU and hospital stay, fluids and blood products requirements, use of diuretics and cross clamping of the renal artery were significantly less than the OR group. However, there was no significant difference in the incidence of postoperative AKI between the two groups (P = 0.28). Neither hospital mortality nor the requirements for postoperative renal replacement therapy were significantly different. The preoperative sCr level was significantly higher in the EVAR group. The period that the ΔsCr was over 0.5 mg/dl was significantly longer in the EVAR group. In the comprehensive risk analysis in the both of EVAR and OR groups, intraoperative cross clamping of the renal artery increases the risk of AKI by 5 folds, and postoperative AKI increases the risk of postoperative mechanical ventilation by 6 folds. While AKI occurred at a similar frequency after either EVAR or OR, EVAR-AKI was more prolonged than OR-AKI. This is likely due to the advanced age and renal dysfunction in the EVAR group.

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Objectives: Patients with sepsis complicated by disseminated intravascular coagulation (septic DIC) have poor outcomes. Thrombomodulin-α (TM-α) is marketed as an anti-DIC drug in Japan. It has been reported that TM-α has also anti-inflammatory effects on sepsis by neutralizing high mobility group box 1 (HMGB1) in basic researches. The aim of this study was to investigate treatment effects of TM-α in patients with septic DIC. Methods: A historical cohort study was performed in a single tertiary emergency center. Patients with septic DIC were classified based on the period of admission. In the TM-α group (n = 30), all patients with septic DIC received TM-α with or without synthetic protease inhibitors (sPI) and/or antithrombin (AT). In the non-TM-α group (n = 23), all patients received sPI and/or AT without TM-α. The primary endpoint was 30-day survival rate. Secondary endpoints included DIC resolution rate at day 7. Results: Demographics, severity of illness, and interventions other than anti-DIC drugs were similar between the groups. The TM-α group had a significantly higher 30-day survival rate compared with the non-TM-α group [90.0% (27/30) vs. 65.2% (15/23), P = 0.041]. In the TM-α and non-TM-α groups, DIC resolution rates were 50.0% (15/30) and 34.8% (8/23) (P = 0.268), respectively. The rate of change in HMGB1 was -48.1% (-66.1 to 97.0) in the TM-α group (n = 7) and 213% (-6.55 to 473) in the non-TM-α group (n = 6) (P = 0.086). The rate of change in interleukin-6 (IL-6) was similar between the groups. Conclusion: TM-α had a positive treatment effect in patients with septic DIC as assessed by 30-day survival rate. The mechanism of this effect may not only be through anti-DIC action, but also an anti-inflammatory effect through reduction of HMGB1

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We report two cases of extracorporeal membrane oxygenation (ECMO) catheter misplacement in the ascending lumbar vein from the femoral vein. One case was a man in his thirties undergoing venoarterial ECMO because of shock-resistant ventricular fibrillation. The other case was a woman in her fifties undergoing venovenous ECMO for severe hypoxia. In both cases, the venous cannulation site for the drainage catheter was the right femoral vein. Although anteroposterior abdominal radiographs did not indicate the catheter malposition, abdominal CT showed that the drainage catheters were placed in the right ascending lumbar vein instead of the inferior vena cava. It is difficult to distinguish on anteroposterior abdominal radiographs whether the catheter is placed in the inferior vena cava or the ascending lumbar vein, but it is reported that lateral abdominal radiographs are useful for detection of catheter malposition. The use of a J-type guidewire rather than a straight or angle-type guidewire to insert the venous catheter may avoid misplacement in the ascending lumbar vein.

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Peripartum cardiomyopathy (PPCM) shows a sudden onset in the last month of pregnancy or in the months following delivery in women without a history of cardiovascular disease. It is a potentially fatal condition. A 40-year-old primigravida underwent Cesarean delivery because of pregnancy-induced hypertension and had an uncomplicated postoperative course. On the postoperative day 8, she was intubated for sudden dyspnea and oxygen desaturation (SpO₂ 60% under room air). Chest radiography showed bilateral infiltrative shadows. Echocardiography revealed an estimated ejection fraction of 25%. Acute pulmonary edema because of PPCM was diagnosed. The left ventricular systolic function improved after infusion of carperitide and dobutamine. On the 3rd day of ICU admission, she was extubated. On the 4th day, she was discharged from the ICU. Earlier diagnosis of PPCM is difficult because symptoms such as shortness of breath appear in healthy pregnant women. Our patient had a good outcome because she received prompt intensive care.

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The patient was a 62-year-old man who had been previously hospitalized eight times for cellulitis associated with varicose veins of the legs. He was admitted with the same diagnosis on this occasion. Soon after admission, he suddenly lost consciousness in the presence of a nurse, but regained consciousness soon thereafter. However, ventricular fibrillation occurred six times during the following hour or so. He was admitted to the ICU, where ventricular fibrillation did not occur following sedative administration and tracheal intubation, and the tube was removed on the second day of hospitalization. His body temperature on admission to the ICU was 41°C, and characteristic coved-type ST-segment elevation was observed in leads V₁ and V₂. Although the ST-segment elevation subsequently improved, the patient was diagnosed as having Brugada syndrome, and an implantable cardioverter defibrillator was inserted at a later date. No Brugada-type findings were present on electrocardiogram (ECG) under normal conditions, and although mild ST-segment elevation had been present on a previous ECG when the patient had a fever, it was considered impossible to have diagnosed Brugada syndrome. There have been sporadic reports of Brugada syndrome diagnosed during fever, and this condition should be borne in mind by ICU physicians who have frequent opportunities to examine febrile patients.

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The subject was a 32-year-old man who presented with burns to over 85% of the body surface (almost 2nd degree) after from falling into potash lye. We immediately washed the wound with water for 2 hr 15 min. Conservative therapy was then performed in ICU. On day 7, the patient developed septic shock and acute respiratory distress syndrome (ARDS), which were initially improved with antibiotics. However, ARDS subsequently exacerbated and the patient died on day 14. Lung findings on autopsy showed diffuse alveolar damage. These findings were consistent with ARDS, which in turn was suspected to have been caused by the burn itself or infection of the wound. Skin findings on autopsy showed deep burns exceeding the depth diagnosed on clinical assessment. These results raise the possibility that the window of opportunity for surgical treatment might have been missed. Other techniques for diagnosing burn depth must be taken into account when dealing with severe alkaline burns.

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The patient was a 31-year-old man in whom toxic shock syndrome was suspected based on refractory hypotension and oliguria. Polymyxin B immobilized fiber column direct hemoperfusion was performed. Approximately 2 hours after initiating this treatment, ST-segment elevation and chest pain suddenly occurred, and elevation of myocardial markers was also observed. However, echocardiography revealed no clear regional wall motion abnormalities, and coronary angiography did not show significant stenosis. Subsequently, the electrocardiographic changes diminished and then normalized. His general condition also improved. The patient was discharged in good condition after 10 days of treatment. The mechanisms underlying ST-segment elevation and chest pain may include coronary microcirculation failure and septic cardiac dysfunction due to eicosanoid produced by a staphylococcal exotoxin.

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We report a case of acquired hemophilia associated with pemphigoid. A 63-year-old male patient with pemphigoid developed acute onset of anemia because of retroperitoneal hematoma. Despite repeated embolization and abdominal surgery to control hemorrhage, anemia gradually progressed and the patient required transfusion frequently. Seventeen days after the onset, several hemostasis-related laboratory tests showed only prolongation of activated partial thromboplastin time (APTT). Further examinations for coagulation factors were carried out. The activity of factor eight was decreased to 1% and the presence of factor eight inhibitor was found in patient’s blood. A diagnosis of acquired hemophilia was therefore made. Administration of factor-eight concentrates and a large dose of methylpredonisolone was not effective for treatment of the bleeding tendency. Therefore, a factor eight inhibitor bypassing activity (FEIBA) agent was finally administered, and bleeding tendency was successfully controlled and did not recur thereafter. Although acquired hemophilia is a rare disease, the presence of this disease should be strongly suspected in patients with bleeding tendency of unknown cause and sole prolongation in APTT. This case suggested that administration of an FEIBA agent is a potential option for treatment of acquired hemophilia complicated with uncontrollable bleeding episodes.

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Heparin-induced thrombocytopenia (HIT) can develop due to the repeated administration of heparin after cardiovascular surgery, and therefore close attention must be paid. Surgical ascending aortic replacement was performed for an acute aortic dissection diagnosed by enhanced computed tomography. The patient received continuous hemodiafiltration (CHDF) and hemodialysis (HD) with the administration of nafamostat mesilate for acute renal failure after surgery. On post-operative day (POD) 11, nafamostat mesilate was changed to low molecular weight heparin during HD, and several hours after that, the patient suddenly fell into a state of shock. On POD 40, he was diagnosed with positive for HIT antibodies, suggesting that an administration of heparin during surgery may have led to the development of HIT and the repeated administration of heparin triggered the onset of a state of shock.

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Non-bacterial thrombotic endocarditis (NBTE) is a well-described pathological condition caused by hypercoagulability due to an inflammatory state including malignancy. While NBTE causes vegetation on heart valves and induces life-threatening systemic thromboembolism, valvular dysfunction is rarely considered as an indication for surgery. Therapy for NBTE consists of systemic anticoagulation and the control of underlying disease. Here, we describe a patient with a perivalvular abscess that might have been induced by NBTE from an abdominal tumor. A two-stage operation was scheduled for the tumor. After the cardiac valve operation, the patient was in a temporary lull, but died from disseminated intravascular coagulation. We missed the opportunity to perform surgical intervention of the abdominal mass. NBTE may be the background in the pathogenesis of infective endocarditis (IE). In order to choose an appropriate multidisciplinary treatment, the clinical features of NBTE should be considered when treating a patient with NBTE accompanied by chronic inflammatory process.

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Group G Streptococcus (GGS) is associated with severe invasive soft tissue infection and toxic shock syndrome. A 38-year-old man was admitted for swelling of the right leg and fever. He presented with septic shock, acute renal failure, and disseminated intravascular coagulation. GGS (Streptococcus dysgalactiae subsp. equisimilis) was detected on culture of a swab from the skin of the right leg. Lower-limb amputation was performed because the serum level of CK was 16,863 IU/l. Antimicrobial susceptibility tests revealed no resistance to ampicillin (ABPC) or clindamycin (CLDM) but strong resistance to clarithromycin (CAM), levofloxacin (LVFX), and minocycline (MINO). We analyzed the results of 99 antimicrobial susceptibility tests for GGS performed between 2005 and 2009 in our hospital, and found that there was marked resistance to CAM (30.3%), LVFX (26.3%), and MINO (44.4%). Some of the strains tested showed strong resistance to ABPC and cephalosporins (7.1%). It is necessary to consider the existence of GGS resistant to macrolide derivatives or new quinolone derivatives when using these antibiotics for severe GGS infection.

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A previously healthy 12-year-old boy was admitted to our hospital with distributive shock, liver failure, and non-oliguric renal failure. Initially, we suspected septic shock on the basis of laboratory studies, which showed high WBC, CRP, procalcitonin, and cytokine levels. However, echocardiography performed within 24 hr revealed decreased cardiac function, which led to the diagnosis of Kawasaki disease (KD). KD has been reported in all pediatric age groups, although 85% of patients were younger than 5 years. KD is a cytokine-associated disease, i.e., a systemic inflammatory response syndrome. The possibility of KD must be considered even when the patient's symptoms indicate distributive shock, as in this case.

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Introduction: We describe a case of toxic epidermal necrolysis presumably induced by streptococcal infection. Case: A 38-year-old man received some medication for systemic rash that developed 2 days before hospitalization. In addition to the rash, he was hospitalized for redness of the mucous membranes of his eyes and lips. He was diagnosed with Stevens-Johnson syndrome on the same day. A short-course treatment with methylprednisolone was initiated. On the 3rd day, he developed toxic epidermal necrolysis because of exacerbation of the rash and was admitted to ICU. Plasma exchange was performed, and immunoglobulin and antibiotics were administered for the streptococcal skin infection. We transiently controlled his skin lesion for 3 consecutive days by performing plasma exchange. However, we decided to perform plasma exchange 3 more times because of the rapidly progressing skin lesion, and we successfully treated the skin lesion. Conclusion: Our case is rare because in our patient, toxic epidermal necrolysis was presumably induced by streptococcal infection without the administration of specific medication before hospitalization.

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