Makoto Takaoka

Morbidity and mortality of hospitalized patients after the 1995 Hanshin-Awaji earthquake

The objective of this study was to provide an overview of the morbidity and mortality of hospitalized patients during the Hanshin-Awaji earthquake. Medical records of 6,107 patients admitted to 95 hospitals (48 affected hospitals within the disaster area and 47 back-up hospitals in the surrounding area) during the initial 15 days after the earthquake were analyzed retrospectively. Patient census data, diagnoses, dispositions, and prognoses were considered. A total of 2,718 patients with earthquake-related injuries were admitted to the 95 hospitals included in our survey, including 372 patients with crush syndrome and 2,346 with other injuries. There were 3,389 patients admitted with illnesses. Seventy-five percent of the injured were hospitalized during the first 3 days. In contrast, the number of patients with illnesses continued to increase over the entire 15-day period after the earthquake. The mortality rates were 13.4% (50/372), 5.5% (128/2,346), and 10.3% (349/3,389) associated with crush syndrome, other injuries, and illness, respectively. The overall mortality rate was 8.6% (527/6,107 patients). Morbidity as well as mortality rates increased with age in patients with both injuries and illnesses. In the initial 15-day period, there was an unprecedented number of patients suffering from trauma, and they converged upon the affected hospitals. Subsequently an increased incidence of illness was observed. This survey underscores the need for adequate disaster response in such an urban situation.

Analysis of 2,702 Traumatized Patients in the 1995 Hanshin-awaji Earthquake

BACKGROUNDnThis study was undertaken to define the factors that affected the final outcome of trauma patients in the Hanshin-Awaji earthquake.nnnMETHODSnMedical records of patients admitted to 95 hospitals within or surrounding the affected area during the first 15 days after the quake were reviewed.nnnRESULTSnThere were 2,702 traumatized patients. One-third of the patients were transported to hospitals in the surrounding area and had a mortality rate of 3%. The remainder, who were treated in the affected hospitals, showed a significantly higher mortality rate (8%; p < 0.05). Intensive care was provided for 513 patients, most of whom suffered from crush syndrome or from injuries to vital organs; these patients had a high mortality rate. Patients with other types of injuries had a lower mortality rate.nnnCONCLUSIONnCrush syndrome and injuries to vital organs were potentially life-threatening. We believe that early transportation of such patients to undamaged hospitals with the ability to provide intensive care would have improved the survival rate.

Fluid resuscitation and systemic complications in crush syndrome: 14 Hanshin-Awaji earthquake patients.

BACKGROUNDnCrush syndrome is a form of traumatic rhabdomyolysis characterized by systemic involvement, in which acute renal failure is potentially life-threatening.nnnMETHODSnClinical and laboratory data of 14 crush-syndrome patients transferred to a tertiary emergency department after the Hanshin-Awaji earthquake were analyzed. The patients were buried under collapsed houses for the average of 6.7 +/- 5.7 (SD) hours (range, 1 to 24 hours). They were referred to us 6 to 250 hours after the earthquake.nnnRESULTSnOf those who arrived at our institution within 40 hours, 25% (two of eight) developed renal failure, whereas all six patients who arrived after 40 hours developed renal failure. Peak serum creatine kinase ranged from 6,677 to 134,200 U/L (51,674 +/- 41,776). Renal failure was highly associated with massive muscle damage (serum creatine kinase above 25,000 U/L) and insufficient initial fluid resuscitation (below 10,000 mL/2 days).nnnCONCLUSIONSnPrompt and adequate, if not massive, fluid resuscitation is the key to preventing renal failure after such injury.

Characteristics of infection and leukocyte count in severely head-injured patients treated with mild hypothermia.

OBJECTIVEnThis study was designed to characterize the infectious complications and kinetics of leukocyte count in severely head-injured patients treated with mild hypothermia.nnnPATIENTS AND METHODSnWe retrospectively analyzed the incidence and severity of infectious complications as well as daily changes in leukocyte count in 41 severely head-injured patients treated with mild hypothermia (group H). They were retrospectively compared with 25 severely head-injured patients treated with high-dose barbiturates (group B) and to 25 other severely head-injured patients treated with no barbiturates (group N).nnnRESULTSnInitial intracranial pressure was significantly higher in group H than in the other groups. No significant differences existed in the incidence of pneumonia or meningitis among the three groups, whereas the incidence of bacteremia was significantly higher in group H than in the other two groups. Pneumonia was significantly more severe in group H than in the other groups. In six patients of group H, pneumonia spread fulminantly to become life threatening. Daily changes in total leukocyte count showed the same pattern, consisting of a peak, a nadir, and a second peak in all groups. Total leukocyte count was, however, significantly lower during the first 2 weeks in group H than in the other two groups. Lymphocyte and neutrophil counts were also lower in group H.nnnCONCLUSIONnInfectious complications were more severe and leukocyte counts were lower in patients treated with mild hypothermia, who also had the highest initial intracranial pressures, than in patients treated with conventional therapies. Measures against increased susceptibility to infection and leukocyte suppression should be explored.

Hypothermia suppresses nitric oxide elevation during reperfusion after focal cerebral ischemia in rats

We aimed to investigate effect of temperature on the jugular levels of nitric oxide (NO) at reperfusion after focal cerebral ischemia. Both nitrosyl hemoglobin (HbNO) (2.5 +/- 0.4 microM) and plasma nitrite plus nitrate levels (61 +/- 5 microM) in rats under normothermia (approximately 37 degrees C) after 30 min of reperfusion following 2 h of left middle cerebral artery occlusion were significantly high, compared with sham operated rats (1.3 +/- 0.1 microM, 40 +/- 4 microM, respectively). Both HbNO (1.5 +/- 0.3 microM) and nitrite plus nitrate levels (43 +/- 7 microM) under moderate hypothermia (approximately 32 degrees C) were significantly low, compared with normothermic rats. HbNO (2.8 +/- 0.8 microM) and nitrite plus nitrate levels (65 +/- 8 microM) under mild hyperthermia (approximately 39 degrees C) were not significantly high. These results firstly demonstrated that hypothermia suppresses the elevation in intrajugular NO after cerebral ischemia-reperfusion.

Granulocyte colony-stimulating factor ameliorates life-threatening infections after combined therapy with barbiturates and mild hypothermia in patients with severe head injuries.

OBJECTIVEnThe objective of this study was to clarify the effects of recombinant human granulocyte colony-stimulating factor (rhG-CSF) administration on infections in patients with severe head injuries after combined therapy with high-dose barbiturates and mild hypothermia.nnnPATIENTS AND METHODSnSince 1996, we have administered rhG-CSF to eight patients with severe head injuries for 5 days (group G). Their treatment results were compared with those of 22 patients cared for earlier without rhG-CSF treatment (group N). All patients in both groups met the criteria of total leukocyte count (TLC) less than 5,000/mm3, C-reactive protein (CRP) over 10 mg/dL, and the presence of an infectious complication. Changes in the TLC, CRP, respiratory index, intracranial pressure, and infectious condition were evaluated in both groups. In addition, the nucleated cell count and differentiation from bone marrow aspiration, neutrophil functions, serum concentrations of interleukin-6, and plasma concentration of leukocyte elastase were evaluated in group G.nnnRESULTSnIn group G, TLC, nucleated cell count, and neutrophil functions significantly increased, whereas CRP, respiratory index, and interleukin-6 decreased reciprocally. There was no deterioration of intracranial pressure and leukocyte elastase. Consequently, seven of the eight patients in group G recovered from life-threatening infections, and none of the eight patients died. However, in group N, CRP and respiratory index remained high and TLC did not increase as much as it did in group G. Infections continued after 5 days in 17 of the 22 patients, 7 of whom died from severe infections during hospitalization.nnnCONCLUSIONnAdministration of rhG-CSF ameliorated life-threatening infections without causing lung injury or increasing brain swelling in patients with severe head injuries who were treated with combined therapy involving high-dose barbiturates and mild hypothermia.

Pentoxifylline attenuates reperfusion injury in skeletal muscle after partial ischemia.

Leukocytes have been shown to contribute to ischemia-reperfusion injury in skeletal muscle. Pentoxifylline (PTXF), a xanthine-derived phosphodiesterase inhibitor, has received recent attention because of its action on leukocytes. To clarify the effects of PTXF in reperfusion injury, we measured the resting transmembrane potential difference ( E m) and evaluated postcapillary venule microcirculation using intravital microscopy in rat skeletal muscle during ischemia and reperfusion. The infrarenal aorta was clamped for 90 min and then reperfused for 60 min. Persistent depolarization of the resting E m was observed in an ischemia-reperfusion (IR) group and was significantly repolarized in a PTXF group during the reperfusion period. The tissue water content was significantly reduced in the PTXF group, although no difference was noted in the tissue lactate content. Flowing erythrocyte velocity and wall shear rate in the PTXF group were significantly higher than in the IR group during the reperfusion period but without significant differences in vessel diameter and hemoglobin oxygenation. Blood flow measured by laser-Doppler flowmeter was also significantly improved in the PTXF group. Furthermore, the adherent leukocyte count was significantly reduced in the PTXF group during this same period. These results indicate that PTXF attenuated reperfusion-associated membrane injury and tissue edema and that PTXF suppressed leukocyte adhesion and improved hindlimb blood flow during the reperfusion period.

Does growth hormone augment brain edema caused by brain injury? A study with a freeze brain injury model in the rat.

OBJECTIVEnBecause of the known sodium and water retention associated with growth hormone (GH) therapy, it is crucial to evaluate the safety of GH after brain injury. To clarify this issue, we investigated whether GH affects brain edema in a rat brain freeze-injury model.nnnMETHODSnMale Wistar rats (n = 29) were divided into four groups according to the substance injected (GH vs. normal saline) and whether the brain was injured or not. The subcutaneous injections of GH (0.8 IU/kg) or saline were given 24 hours apart. In the injury groups, after the second injection, an aluminum rod (4-mm diameter) cooled to -50 degrees C was placed on the exposed dura mater in the right parietal region for 4 minutes, under anesthesia. At 4 hours after the insult, brain and skeletal muscle were excised and their water content was measured by drying.nnnRESULTSnFreeze injury of the brain caused an increase in water and sodium content in skeletal muscle. GH injection augmented this edema in skeletal muscle. Freeze injury of the brain also caused an increase in water and sodium content in the injured hemisphere of the brain. GH injection did not exacerbate this edema in injured brain tissue. Neither freeze injury nor GH injection caused brain edema in the noninjured hemisphere or in the cerebellum.nnnCONCLUSIONnGH administration did not augment brain edema caused by brain injury in our model.