This review article covers recent advances in the pathophysiologic and therapeutic considerations of SMOF. Bacterial and/or endotoxic translocation plays an important role in the development of severe infection in the critically ill. As to pathophysiology, generalized overwhelming inflammatory responses (systemic inflammatory response syndrome: SIRS) to infection and impaired tissue oxygen metabolism are considered to be two central mechanisms of the development of organ failure in a septic critically ill patient. The generalized overwhelming inflammation is caused by activation of a network involving various humoral mediators. In the mediator network, cytokines such as tumor necrosis factor and interleukin-1, elastase and oxygen free radicals released by primed neutrophils which accumulate in vital organs through the so-called “second attack theory”, and nitric oxide released by vascular endothelium plays a central role. In the impairment of tissue oxygen metabolism, delivery-dependent oxygen consumption and decreased oxygen uptake are pathological features. As for the therapeutic considerations, an SMOF patient should receive critical care in the ICU. For multidisciplinary treatment, curative treatment for infection, various artificial supports including continuous blood purification, nutritional support including immunonutrition, immunomodulation or immunotherapy, cellular support through countermeasures for the impaired tissue oxygen metabolism and causative humoral mediators are fundamental. Among these treatments, cellular support is the most important. The recent tremendous advances in molecular biology, including introduction of the concept of “apoptosis” in the cellular pathogenesis of SMOF, hold promise that new prophylactic or therapeutic approaches in this field become clinically available in the near future.

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To clarify the mechanisms underlying myocardial damage in aneurysmal subarachnoid hemorrhage (SAH), 494 SAH patients, admitted within 24 hours of the onset, were studied. Forty-eight patients had left ventricular asynergy (LV ASYN) on 2-dimensional echocardiogram (group A) and were compared to 446 patients without LV ASYN (group B). All patients received neurological examination, X-rays of the chest and computed tomographic (CT) brain scans on admission. We measured serum CK and plasma catecholamines in both groups, and assessed hemodynamics using a Swan-Ganz catheter in group A. LV ASYN was detected in 9.7% of all patients in the acute phase of SAH, and developed more frequently in female than in male patients. LV ASYN associated with SAH was related to the initial level of neurologic severity, as assessed by the WFNS grade, but was not related to the amount of subarachnoid blood visualized on the initial computed tomogram. The incidence of pulmonary edema was significantly higher in group A than in group B (42 vs 12%; p<0.001). Serum CK (MB-CK) and plasma levels of norepinephrine and epinephrine were higher in group A than in group B [550±500 (7.0±3.7) vs 310±320IU/l (1.9±1.5%); p<0.001 (p<0.001), 1, 690±1, 600 vs 670±450pg/ml; p<0.001, and 1, 250±1, 190 vs 310±300pg/ml; p<0.001, respectively]. In group A, pulmonary arterial pressure, mean pulmonary capillary wedge pressure, cardiac index and left ventricular ejection fraction were 33±6/19±4mmHg, 18±5mmHg, 2.6±0.71/min/m² and 37±13% on admission, respectively. These parameters improved to 28±6 (p<0.01)/11±4mmHg (p<0.001), 10±3mmHg (p<0.001), 4.6±0.91/min/m² (p<0.001) and 65±9% (p<0.001) within 15 days (6±4 days) after admission, respectively. In conclusion, SAH patients with LV ASYN had cardiac dysfunction and damage with myocardial necrosis, and LV ASYN was thought to be related to the subsequent development of pulmonary edema. Elevation of plasma norepinephrine and epinephrine levels may play an important role in the origin of LV ASYN associated with SAH.

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The emegency patient transport system in Japan is inferior to the American system because of the higher numbers of dead on arrival (DOA) patients. To examine the present system and appraise the possibility of improving survival rate by introducing a doctor's car system in Japan, doctors in the department of critical care medicine investigated the patient transport system in the district assigned to the Nagoya City, Naka Ward Fire Department Emergency Section for 10 days. The number of total requests was 55, including one mistaken request. Thirty-three patients were male and 21 were female. The average age was 44.5±21.3 years old. Fifty-two patients were transported. Eight patients were hospitalized, including 1 patient who required emergency intervention by a doctor. In one patient, heart beat and respiration had stopped. Thirty-seven patients were treated with some procedure at the scene and in the ambulance. Total transport time was 22.2±9.0min, response time was 4.8±2.2min, scene time was 8.4±6.2min and time in ambulance was 9.0±6.0min (data are means±SD). The total transport time at night was longer than in the daytime. The severer the patient's condition, the longer the total transport time. Total transport time was correlated with both the ambulance time and scene time (p<0.0005). Total transport time was more closely correlated with the time in the ambulance than scene time (p<0.05). Few of the patients required emergency procedures or transportation. These were 5 or 6 requests a day. These results suggest it would be inefficiently to employ this type of doctor's car in this area. To employ the docotor's car system in this area, the following would be required: (1) the district assigned to one doctor's car should be larger, (2) the doctor should be able to arrive at the patient's site within 15min, (3) doctors and receiving hospitals should be ensured for this system. Prolonged ambulance time represents difficulty in finding a receiving hospital or long distance transportation. People who need emergency information are just the patients who need urgent treatment. Thus, emergency information centers should be able to provide fast accurate information about receiving hospitals to these patients at all times.

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To determine the diagnostic value of coagulation and fibrinolytic molecular markers in patients with clinically suspected pulmonary thromboembolism (PE), we conducted a prospective pilot study in the emergency department with the general ICU. Fifteen patients with clinically suspected PE participated and 7 cases were diagnosed as PE -positive. After the diagnosis of PE, urokinase was administered followed by heparin therapy. Plasma plasmin antiplasmin complex (PAC) and cross-linked fibrin degradation product (D-dimer) were measured before the treatment. In the PE-positive patients, the levels of both molecular markers the normal range prior to the treatment were above, and were significantly higher than those in the PE-negative patients. If the cut off points of PAC and D-dimer were set at 1.0μg/ml and 500ng/ml, respectively, both markers had a high sensitivity, a highly negative predictive value and a moderate specificity. We conclude that the PAC and D-dimer levels measured in this study are useful for PE screening. Since the sample was small, these data are preliminary. Further study, involving a large number of patients and the application of medical decision analysis, is necessary to confirm these results.

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To study endothelial cell injury in multiple organ failure (MOF), we measured plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (t-PA) in the plasma of 25 patients who were randomly chosen among patients admitted to our ICU. Eight cases were trauma patients, 4 were burn patients, 8 were postoperative patients, and there were 5 other cases. Eight patients developed MOF and 6 died. We analyzed the time course of PAI-1 and t-PA levels. PAI-1 levels were significantly higher in the plasma of MOF patients than in those of non-MOF patients. No difference was found in t-PA levels between MOF and non-MOF patients. A significant difference was found between the two in platelet count, FDP value, CRP value and APACHE II score. The result was the same between survivors and non-survivors as that between MOF and non-MOF patients. Some non-MOF patients showed high PAI-1 levels on admission, but these subsequently returned to normal in all cases. Among MOF patients, survivors showed the same pattern as non-MOF patients, but in nonsurvivors PAI-1 levels gradually increased on the following days. The PAI-1 level correlated well with platelet count and FDP value, but no correlation was found between the t-PA level and CRP value. Although further studies are needed to determine whether PAI-1 is an “alarm hormone” that reflects endothelial cell injury, these findings suggested that endothelial cell injury including a change in PAI-1 release might be involved in the pathogenesis of MOF.

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A 37-year-old, previously healthy man, with no history of serious infection, sustained a contusion on the flexor side of his right thigh. Severe pain and swelling at the wound area were present the following day. He had fever, hypotension, anuria, stupor and right leg ischemia, and was admitted on the 3rd post-injury day. Although incisions were twice made in the swollen portion of his thigh for decompression, shortly after admission, the skin around the incision became necrotic on the 4th day. At the same time, adult respiratory distress syndrome, disseminated intravascular coagulation, and profound hypotension developed rapidly, and cathecolamine infusion, mechanical ventrilation, hemodialysis and debridement of the necrotizing skin and muscle were needed. However, erythema with blisters extended to both legs, the lower abdomen and bilateral chest, and he died due to circulatory collapse on the 6th day. Group A streptococcal organisms were isolated from the necrotizing skin, muscles and blood. The serotype of this strain was M22, which produces exotoxins type B and C in vitro.

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The authors report a case of distal anterior cerebral artery (ACA) aneurysm presenting as acute subdural hematoma (ASDH). The clinical incidence of SDH complications is reported to be 0.5-7.9% of all ruptured aneurysms. Moreover, cases of SDH caused by distal ACA aneurysm are rare, with only 15 cases, including ours, having been described in detail. Ruptured distal ACA were located in the bifurcation of the pericallosal artery and callosomarginal artery in 5 cases, pericallosal artery and frontopolar artery in 2 cases and azygos artery in 2 cases. The prognosis is poor: 7 of 15 patients died, and most of them were accompanied with brain herniation in the initial stage. However, the outcome of some cases not accompanied with brain herniation was relatively good. Therefore, we need to differentiate it from traumatic SDH, and perform emergency treatment.

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We report a case of severe PE treated by thrombolytic therapy using tissue plasminogen activator (t-PA) and preventional insertion of a bird's nest inferior vena cava filter (BNF). A 48-year-old woman suffered sudden dyspnea. Pulmonary angiogram revealed massive bilateral pulmonary embolism. Heparin and urokinase were administered immediately, but no relief was obtained. She was transferred to our department because her pulmonary artery pressure (PA) did not decrease and she had begun to suffer renal and liver dysfunction. We started thrombolytic therapy using t-PA; her PA pressure decreased from 96/72mmHg to 57/11mmHg after 5 hours and her oxygenation was remarkably improved. Soon thereafter, we inserted the BNF via the right internal jugular vein to prevent recurrent pulmonary embolism. No thrombi were detected by venography in the deep veins of the lower legs and pelvis; however, giant myoma uteri was found. On the 25th hospital day the myoma uteri was resected. The patient showed no complications and was discharged from our hospital on the 39th hospital day. We believe that thrombolytic therapy using t-PA is very effective for severe pulmonary embolism, and that early insertion of an inferior vena cava filter is very useful for the prevention of recurrent pulmonary embolism.

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A 39-year-old man sustained an orbital fracture due to an intraorbital metallic foreign body. We successfully removed the foreign body and repaired the orbital fracture via a frontotemporal craniotomy and the microscopic extradural approach. There are several surgical approaches to the orbit. We used the frontotemporal craniotomy and the microscopic extradural approach. This approach provides an adequate operative field for a large intraorbital foreign body.

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Hemopericardial effusion is a common complication after blunt cardiac injury, especially in the acute phase. On the other hand, delayed (more than 7 days) hemopericardial effusion is relatively uncommon in the literature. We report two cases with delayed hemopericardial effusion. The first case, a 44-year-old male, suffered blunt cardiac injury and perforations of the stomach and diaphragm as well. On the 7th hospital day, pericardial effusion was found, and the patient developed circulatory shock due to cardiac tamponade on the 10th hospital day. The second case, a 21-year-old female, had blunt chest trauma. On the 10th hospital day, increasing pericardial effusion was detected by USG and chest X-ray. On the 12th hospital day, she developed shock as a complication. Both patients recovered from shock, with pericardial drainage of bloody discharge, and had no further complications. We want to stress the importance of close monitoring of patients with blunt cardiac injury for more than one week to prevent circulatory shock due to delayed hemopericardial effusions.

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