Coagulation studies were performed in 31 patients with blunt head injury who were divided into three groups according to their clinical course and outcome (Group I: obeyed to commands within two weeks of head injury; Group II; unconsciousness more prolonged than in Group I; and Group III: died). Thrombin-antithrombin III complex (TAT), plasmin-α₂plasmin inhibitor complex (PIC) and D dimer (DD), in addition to the usual parameters, including antithrombin III (AT III), plasminogen (PLG), α₂ plasmin inhibitor (α₂PI), platelet count (PLT), prothrombin time (PT), partial thromboplastin time (APTT), fibrinogen (FBG) and fibrin/fibrinogen degradation products (FDP), were measured on admission. Glasgow coma scale (GCS) and intracranial pressure (ICP) were used for assessment of severity, while neuron-specific enolase (NSE) was used as a quantitative marker of brain destruction. The following results were obtained: (1) TAT, PIC, and DD were elevated in the mild (Group I) and moderate (Group II) cases, in whom the usual parameters were normal. (2) The degree of hemostatic abnormality, in particular TAT, which is a marker of hypercoagulative states, correlated well with the severity of head injury on admission and the outcome of the patients. (3) Serum NSE concentration showed a significant correlation with TAT, PIC and DD. (4) Despite the marked elevation of TAT (more than 1, 000ng/ml), AT III, a main inhibitor, was not decreased. (5) The hypercoagulative state, as indicated by TAT, PIC and DD values, showed rapid improvement within a day without failure of the coagulation system. These results suggest that TAT, PIC and DD on admission are useful markers of the severity and the outcome of patients with head injury. Also, these results indicate that head injury patients rapidly develop a hypercoagulative state, which is followed by fibrinolysis, and that the hypercoagulative state, which rapidly returns to normal within a day without leaving effects on the coagulation system, is caused by tissue factors released from damaged brain tissue.

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Disordered states of coagulation and fibrinolysis differ according to various diseases. In this study, TAT and PIC of 123 patients in grave states of various diseases were measured, and the results from these measurements were compared according to the representative diseases. Moreover, other parameters of coagulation and fibrinolysis, including PT, AT III, α₂-PI, plasminogen, fibrinogen, FDP-E and D-dimer, were also examined daily. Then, relationships between these examined-values, and relationships between APACHE II and TAT, APACHE II and PIC, and characteristics and differences of the various diseases were analysed. A total of 114 cases were enrolled in the present study. They consisted of 7 cases of MOF, 8 cases of liver failure, 6 cases of fulminant hepatitis, 14 cases of sepsis, 6 cases of thrombosis, 6 cases of aneurysm, 3 cases of gynecologic disease, 7 cases of burn, 27 cases of trauma, 2 cases of APL and 28 cases of other diseases. Thirty-eight cases among them were diagnosed as having DIC. No significant relationships were observed between any combinations except for that between TAT and Ddimer. Moreover, there were no relationships between APACHE II and TAT, and APACHE II and PIC. The average values of TAT and PIC were 11.0ug/l and 0.8ug/ml in MOF, 11.5 and 3.1 in liver failure, 26.6 and 6.3 in fulminant hepatitis, 15.0 and 1.6 in sepsis, 25.3 and 7.1 in thrombosis, 29.3 and 2.6 in aneurysm, 43.1 and 5.7 in gynecologic disease, 23.8 and 1.3 in burn, 36.0 and 2.7 in trauma, 162.9 and 10.9 in APL and 13.6 and 1.8 in other diseases, respectively. High TAT and PIC values were observed in all patients. According to results reflecting the variety of disorders in coagulation and fibrinolysis among indivisual diseases, we tried to categorize these diseases in 5 groups. Many disordered states of coagulation and fibrinolysis were observed in the grave states of various diseases. Furthermore, it was suggested that DIC is not only a disordered state of coagulation and fibrinolysis, but also represents deterioration in the grave state of various disordered states of coagulation and fibrinolysis of certain diseases.

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Cerebral and systemic metabolic changes after cardiac arrest are complex and unclear. We postulate that post-arrest monitoring of arterial, systemic and cerebral mixed venous oxygen (O₂), lactate (L), and glucose (G) contents might help guide life support. We used our standardized dog model with ventricular fibrillation (VF), 12.5min of no flow, brief (2∼3min) cardio-pulmonary bypass (CPB), and controlled ventilation for 24hr (n=8). We monitored systemic and cerebral pressure variables including cardiac output (CO), intracranial pressure (ICP), arterial (a) and sagittal sinus (ss) O₂, L, and G, and pulmonary arterial (pa) O₂. CO was stable except for a 30% reduction at 4hr post-arrest. ICP remained normal for 24hr. The cerebral a-v O₂ content difference (Ca-ssO₂) was almost doubled at 1∼24hr post-arrest (worst at 4hr), whereas the systemic a-v difference (Ca-PaO₂) was only slightly increased at 4∼12hr. These results implied the mismatching of cerebral metabolism/blood flow. Calculated cerebral O₂ extraction ratio (OER) was 0.34 pre-arrest; decreased transiently to 0.06 during hyperemia; and increased post-arrest during hypoperfusion to a peak of 0.74 at 4hr. Simultaneous systemic OER was 0.16 pre-arrest, and changed little post-arrest. Cerebral a-vG values (a-ssG) were not consistent. Cerebral v-a values for L (a-ssL) were increased from reperfusion to 2hr. Oxygen glucose, lactate glucose, and lactate oxygen indices (OGI, LGI, LOI) were calculated. OGI and LGI varied considerably between dogs. LOI was more consistent; it reflected severe cerebral lactacidosis between 0∼2hr post-arrest. Post-arrest cerebral O₂ deprivation seemed more severe than systemic deprivation in this model. Monitoring LOI early and CeOER early and late might be valuable for clinically guiding post-arrest therapy.

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Clinical predisposition to respiratory failure was investigated retrospectively in 393 trauma patients who were treated in Chiba Emergency Medical Center during a 6-year period from 1984 to 1990. Patients were classified into 4 groups according to the site of injury, namely, an extremity and pelvic injury group (144 cases, Group I ), an abdominal injury group (71 cases, Group II ), a thoracic injury group (98 cases, Group III) and a brain injury group (80 cases, Group IV). Location and severity of injury, shock index, duration of shock and amount of blood transfused were analyzed. The results were as follows: (1) The rate of development of respiratory failure was 18.1% in Group I, 26.8% in Group II, 46.9% in Group III and 10.0% in Group IV. (2) In Groups I, II and III, there were statistically significantly higher ISS's, TI's and APACHE II's in cases with respiratory failure. (3) In Groups I and II, there were statistically significantly higher shock indices in cases with respiratory failure. (4) In Groups I, II and III, when the duration of shock exceeded 2 hours, the rate of respiratory failure increased remarkably. (5) In Group I, the amount of blood transfused significantly affected the rate of respiratory failure. (6) In Group I, a fall in GCS was associated with a significantly higher rate of respiratory failure. (7) In Group IV, no potential predisposition was related to the development of respiratory failure.

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The authors reviewed retrospectively 174 cases of acute cholecystitis between 1982 and 1991. They were classified into the following three groups and were compared as to their clinical data: 1) early surgery group (operated on within 3 days of onset), 2) intermediate surgery group (operated on between 4 days and 29 days of onset), 3) delayed surgery group (operated on after 30 days of onset). There were no differences in the distribution of age or sex, operation time, intraoperative bleeding, or morbidity. The total hospital stay was significantly shorter in the early group. This suggests that in acute cholecystitis early surgery is safe and can reduce hospital stay.

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Protective helmets are believed to reduce the number of injuries from motorcyle accidents and lessen the severity of head injuries. This study was intended to investigate the mechanism of head injuries in helmeted motorcyclists. One hundred twenty helmets involved in motorcycle accidents were collected with information from the scene and examined. Helmets consist of two major components, the shell and the liner. Deformation of each component was inspected to grade the damage to the helmet. The severity of the head injury was evaluated according to the J-AIS code in each case. Head injuries were classified into three main groups, skull fracture, focal brain damage, and diffuse brain damage. The reports from the scene obtained from accident report forms enabled the cases to be divided into “wearing” cases, in which the helmet was secured to the motorcyclist's head throughout the accident, and “uncapping” cases, in which the helmet was knocked off by the initial impact. The severity of head injury was higher in “uncapping” cases. The “uncapping” cases showed a higher rate of skull fracture and focal brain damage. An analysis of the correlations between types of head injury and helmet damage disclosed the following results: motorcyclists wearing helmets were likely to sustain diffuse axonal injury when receiving an upper region impact. The assumption that diffuse axonal injury is produced by coronal plane angular acceleration is widely accepted. It seems reasonable to suppose that an impact to the upper region of the helmet would produce angular acceleration based on a consideration of the center of gravity of the head. The results of our study support this hypothesis. Motorcyclists who suffer brain damage, such as acute subdural hematoma, cerebral contusion or diffuse axonal injury, would die at the site if they had accidents without helmets. Again, we emphasize the beneficial effects of protective helmets.

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The authors report an analysis of 85 patients with sudden death due to central nervous system diseases over a 10 year period. All cases had vascular disease, i.e. 34 cases (40.0%) had intracerebral hemorrhage, 47 cases (55.3%) had subarachnoid hemorrhage and 4 cases (4.7%) had cerebral infarction. Cases of sudden death are usually reported in the cardiovascular field. In this paper we examined the characteristics of sudden death due to central nervous system disease. Ninety-five percent of the cases had a bleeding vascular disease. Many of the patients who died within 2 hours of the attack had brain-stem infarction, subarachnoid hemorrhage or cerebellar hemorrhage.

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A 49-year-old man with pulmonary edema and cardiogenic shock due to acute inferior myocardial infarction was successfully treated with percutaneous transluminal coronary angioplasty supported by percutaneous cardiopulmonary bypass. Emergency diagnostic coronary angiography revealed nearly complete obstruction in segment (seg) 2 of the right coronary artery (RCA), 99% stenosis with delayed filling of contrast medium in seg 6 of the left anterior descending artery (LAD), and hypoplasty of the circumflex artery except in seg 12 with 75% stenosis. Both the LAD and seg 12 arteries provided fairly good collateral circulation to segs 3 and 4, while the septal branches of the LAD were poorly perfused by the conus branch of the RCA. The shock in this case was pathophysiologically characterized as pump failure of the functioning heart due to multivessel disease, which affected the infarcted but stunned inferior myocardium and the severely acute ischemic anterior myocardium. Percutaneous cardiopulmonary bypass support was instituted because of poor left ventricular function revealed by echocardiogram (ejection fraction≤30%) and the high risk of hemodynamic collapse during angioplasty in segs 2 and 6 even with the combined use of intraaortic balloon counterpulsation and administration of cathecholamine. It is concluded that cardiopulmonary bypass can safely be instituted percutaneously to hemodynamically stabilize a patient in cardiogenic shock and facilitate potentially life-saving emergency complex coronary angioplasty.

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Three patients with clinical and investigative features suggestive of septic cavernous sinus thrombosis are reported. Case 1: A 53-year-old woman developed headache, severe edema of the conjunctiva, proptosis and ophthalmoplegia with high fever following respiratory tract infection. CSF examination showed pleocytosis (11, 842/cmm; 49% polymorphs) and its culture revealed Streptococcus milleri. In spite of vigorous antibiotic treatment, she had hemiparesis and personality change as a sequela. Case 2: A 37-year-old man with a three-month history of dental infection developed high fever, proptosis and severe edema of the conjunctiva, and fell into coma. The spinal fluid contained 13, 672 white cells/cmm (91% polymorphs) with no sugar. He died on the 5th hospital day. Carotid angiograms of cases 1 and 2 demonstrated narrowing of the intracavernous portion of the internal carotid artery. Case 3: A 42-year-old man with a history of paranasal sinusitis developed headache, high fever, blephaloptosis and ophthalmoplegia. Plain skull radiograph showed opacity of the sphenoid sinus. The spinal fluid contained 764 white cells/cmm (49% polymorphs). In spite of antibiotic treatment, he died on the 13th hospital day. At autopsy the brain showed severe edema and the cavernous sinus contained pus. Culture of the pus revealed α-Streptococcus. We propose early diagnosis and aggressive antibiotic treatment of this disease.

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We present a case of traumatic dissecting aneurysm of the vertebral artery associated with fracture of the cervical spine. The patient was a 73-year-old man who received head and neck injuries in an automobile accident. He was immediately brought to our hospital by ambulance following a short period of unconsciousness. The patient became alert and was orientated at the time of admission. Slight swelling on the left side of the neck was noted. Neurological examination revealed left Wallenberg's syndrome and swallowing disturbance. Roentgenograms and cervical CT confirmed transverse fracture of the axis. CT scan showed no intracranial lesion and angiography demonstrated a dissection of the left vertebral artery. T2-weighted MRI indicated a high intensity area in the left lateral medulla. Ten days later, angiography was carried out again and showed complete occlusion of the left vertebral artery at the origin of the dissection. The patient's condition was stable during observation and anticoagulation therapy was carried out. He became asymptomatic after a few weeks. Traumatic dissecting aneurysm of the vertebral artery is rare, and its diagnosis is quite difficult. When cerebrovascular disorder is suspected after trauma, early diagnosis and proper treatment should be conducted prior to the onset of semi permanent neuro-deciduation.

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We describe a case of acute subdural hematoma, successfully treated by burr-hole opening and subdural tapping. The patient was a 55-year-old man who fell from the third floor of his house and suffered a head injury. On admission, he was semicomatose, and a computed tomography (CT) scan showed a right acute subdural hematoma and brain contusion. During preparation for the craniotomy, the patient's neurological state deteriorated. Transcranial Doppler (TCD) examination showed a decrease in mean flow velocity (MFV) in the right middle cerebral artery (MCA) and an increase in the pulsatility index (PI), which means an increase in intracranial pressure and a decrease in cerebral perfusion pressure. The patient was therefore subjected to burr-hole opening and subdural tapping in the right parietal region on the spot, and about 100ml of semiliquid subdural hematoma was drained off. At this time, the both MFV and PI according to TCD had improved. A craniotomy was then performed, and the subdural hematoma was totally evacuated. A postoperative CT scan revealed a contralateral epidural hematoma. Therefore a second craniotomy was performed, and the epidural hematoma was totally evacuated. After surgery, the patient's neurological condition improved to a confused state. Our experience in this case suggests that assessment of intracranial pressure by TCD and subdural tapping in the emergency room prior to craniotomy in the operating room, are beneficial in emergency cases of acute subdural hematoma.

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