Arito Kaji

The impact of spontaneous ventilation on distribution of lung aeration in patients with acute respiratory distress syndrome: airway pressure release ventilation versus pressure support ventilation.

BACKGROUND: In this study, we sought to determine which mode, airway pressure release ventilation (APRV) or pressure support ventilation (PSV), decreases atelectasis more in patients with acute lung injury/acute respiratory distress syndrome (ARDS). METHODS: This was a retrospective study in the intensive care unit. Between 2006 and 2007, we identified 18 patients with acute lung injury/ARDS who received either APRV or PSV and had a helical computed tomography scan twice in 3 days. RESULTS: Computed tomography data from the APRV and PSV groups (n = 9 each) were analyzed for 3-dimensional reconstruction and volumetry. Aerated lung regions (normally aerated, poorly aerated, nonaerated, and hyperinflated) were identified by their densities in Hounsfield units. The Pao2/Fio2 ratio and alveolar-arteriolar oxygen gradient after ventilation were improved in both groups (P = 0.008); however, the improvements in the APRV group exceeded those in the PSV group when delivered with equal mean airway pressure (P = 0.018 and 0.015, respectively). Atelectasis decreased significantly from 41% (range, 17%–68%) to 19% (range, 6%–40%) (P = 0.008) and normally aerated volume increased significantly from 29% (range, 13%–41%) to 43% (range, 25%–56%) (P = 0.008) in the APRV group, whereas lung volume did not change in the PSV group. CONCLUSIONS: Spontaneous ventilation during APRV improves lung aeration by decreasing atelectasis. PSV for gas exchange is effective but not sufficient to improve lung aeration. These results indicate that APRV is more efficient than PSV as a mode of primary ventilatory support to decrease atelectasis in patients with ARDS.

Endovascular Treatment of Intractable Oronasal Bleeding Associated with Severe Craniofacial Injury

BACKGROUND Severe craniofacial injury may cause intractable oronasal bleeding, which is refractory to conventional treatments. This study will evaluate the efficacy of endovascular treatment for such oronasal bleeding. METHODS Nine males between the ages of 19 and 62 years who had intractable oronasal bleeding resulting from severe craniofacial injuries received treatments of transarterial embolization using Gelfoam pledgets, polyvinyl alcohol particles, or platinum coils. We then reviewed their clinical and neuroradiologic characteristics retrospectively. RESULTS In all but one case, angiography demonstrated bleeding points as extravasation. These bleeding points were multiple in seven cases. Except for bleeding from ethmoidal arteries, selective embolization was successful. In all cases, intractable oronasal bleeding was controlled. Patient survival was not directly related to oronasal bleeding, but rather was strongly correlated with associated brain injuries. CONCLUSION Endovascular treatment is an acceptable treatment for intractable oronasal bleeding associated with severe craniofacial injuries when conventional treatments have failed.

Effect of barbiturate therapy on phenytoin pharmacokinetics

To evaluate the effect of high-dose pentobarbital therapy on phenytoin pharmacokinetics. Design:A prospective, clinical study. Setting:The intensive care unit of a university hospital. Patients:Ten adult patients with cerebral lesions requiring anticonvulsants and control of intracranial pressure. Interventions:Each patient received phenytoin sufficient to maintain a plasma concentration at 15 μg/mL (60 μmol/L) both before and after barbiturate therapy. Plasma concentrations of total phenytoin, unbound phenytoin, and the major metabolite of phenytoin, 5-(phydroxyphenyl)-5-phenylhydantoin, were measured, and pharmacokinetic variables obtained before and after barbiturate therapy were compared. Measurements and Main Results:Plasma concentrations of total phenytoin remained within the therapeutic range during the 12-hr period preceding barbiturate therapy. After barbiturate therapy, plasma concentrations of both total and unbound phenytoin were significantly less than those concentrations before barbiturate therapy. For total phenytoin, maximum metabolic velocity was increased by 62% (1.09 ± 0.62 to 1.77 ± 0.52 mg/L/hr, 1.20 ± 0.68 to 1.95 ± 0.57 nmol/L/sec, p < .05), and area under the plasma concentration-time curve (0 to infinity) and mean residence time were each decreased by 73% (32.5 ± 20.0 to 8.7 ± 3.1 min-mg/ mL, 2.14 ± 1.25 to 0.57 ± 0.19 sec-mmol/L, p < .01, and 135,000 ± 69,000 to 37,000 ± 11,000 secs, p < .005, respectively) after barbiturate therapy. The plasma concentration of the principal metabolite of phenytoin, 5-(p-hydroxyphenyl)-5-phenylhydantoin, was significantly increased after barbiturate therapy. Conclusions:Phenytoin metabolism is increased by barbiturate therapy, and supplemental doses of phenytoin and frequent drug monitoring may be required after barbiturate therapy. (Crit Care Med 1993; 21:1514–1522)

Hemorrhagic shock and encephalopathy syndrome – the markers for an early HSES diagnosis

BackgroundThe hemorrhagic shock and encephalopathy syndrome (HSES) is a devastating disease that affects young children. The outcomes of HSES patients are often fatal or manifesting severe neurological sequelae. We reviewed the markers for an early diagnosis of HSES.MethodsWe examined the clinical, biological and radiological findings of 8 patients (4 months to 9 years old) who met the HSES criteria.ResultsAlthough cerebral edema, disseminated intravascular coagulopathy (DIC), and multiple organ failure were seen in all 8 cases during their clinical courses, brain computed tomography (CT) scans showed normal or only slight edema in 5 patients upon admission. All 8 patients had normal platelet counts, and none were in shock. However, they all had severe metabolic acidosis, which persisted even after 3 hours (median base excess (BE), -7.6 mmol/L). And at 6 hours after admission (BE, -5.7 mmol/L) they required mechanical ventilation. Within 12 hours after admission, fluid resuscitation and vasopressor infusion for hypotension was required. Seven of the patients had elevated liver enzymes and creatine kinase (CK) upon admission. Twenty-four hours after admission, all 8 patients needed vasopressor infusion to maintain blood pressure.ConclusionCT scan, platelet count, hemoglobin level and renal function upon admission are not useful for an early diagnosis of HSES. However, the elevated liver enzymes and CK upon admission, hypotension in the early stage after admission with refractory acid-base disturbance to fluid resuscitation and vasopressor infusion are useful markers for an early HSES diagnosis and helpful to indicate starting intensive neurological treatment.

Marked regional heterogeneity in venous oxygen saturation in severe head injury studied by superselective intracranial venous sampling: case report.

OBJECTIVE Continuous monitoring of jugular venous oxygen saturation (SjvO2) is useful in the management of severe head injury. Abnormally high SjvO2 values can be caused by increased cerebral blood flow, decreased cerebral metabolism, brain death, contamination from extracerebral venous blood, or traumatic arteriovenous fistula. CLINICAL PRESENTATION A 20-year-old man with severe head injury was diagnosed to have a traumatic dural carotid-cavernous sinus fistula on the day of trauma. Continuous left SjvO2 monitoring from Days 4 to 12 revealed oxygen saturation ranging between 85 and 98%. INTERVENTION Superselective intracranial and extracranial venous sampling on Day 5 demonstrated marked regional heterogeneity in venous oxygen saturation as follows: superior sagittal sinus, 95 to 97%; straight sinus, 88%; right transverse sinus, 94%; left transverse sinus, 74%; right SjvO2, 95%; left SjvO2, 89%; the basilar plexus, 99%; right internal jugular vein, 98%; the left internal jugular vein, 94%. Extremely high oxygen saturation in the superior sagittal sinus and basilar plexus was attributed to severe brain damage and carotid-cavernous sinus fistula, respectively. CONCLUSION Although jugular bulb oximetry is useful in the management of severe head injury, high oxygen saturation values should be interpreted with caution because they cannot show the intracranial heterogeneity of venous oxygen saturation.

Using transpulmonary thermodilution leads successful fluid resuscitation in early phase of septic shock

Purpose of the study: The reported incidence of rib and sternum fractures after unsuccessful cardiopulmonary resuscitation by manual chest compressions (manual CPR) in the twentieth century varied greatly, and it was generally considered that at least 1/3 of resuscitated patients sustained rib fractures and at least 1/5 sternum fractures. However, recent studies indicate amuch higher incidence of such injuries. Increasing use of the LUCASTM device (mechanical CPR) raises the question of whether it has any adverse effects. Our goal was to compare the incidence and number of rib and sternum fractures after manual and mechanical CPR. Materials and methods: This retrospective autopsy study included 946 patients (802 manual CPR and 144 mechanical CPR) resuscitated in the period 2011–2014, i.e., when Guidelines 2010 were applied. Results: At least one rib fracture was found in 86.9% of the patients resuscitated manually and in 88.9% of those resuscitated mechanically (p=0.512). Sternum fractures were found in 64.2% of the patients resuscitated manually and in 72.9% of those resuscitated mechanically (p=0.043). Either rib or sternum fractures or both were found in 88.8% of the patients in the manual CPR group and 93.1% of the patients in the mechanical CPR group (p=0.854). The average number of rib and sternum fractures per injured patient was 12.04 in the manual CPR group and 11.88 in the mechanical CPR group. Conclusion: In the studied population, mechanical CPR caused approximately 4% more rib and/or sternum fractures than manual CPR. However, the average number of fractures per injured patient was slightly lower in the mechanical CPR group.1,2

A missense mutation of the plasminogen gene in hereditary angioedema with normal C1 inhibitor in Japan

more toxic drugs in case of relapse. The study was approved by the Internal Review Board of the Clinic. The baseline features of the study patients along with the clinical response to the treatment are shown in Table 1. Seven of 14 patients (50%) showed an ongoing complete control of the disease (UAS7 < 6) despite halving the monthly dose of omalizumab. In the remaining seven patients, the dose reduction was associated with a worsening of the disease (UAS7 score between 7 and 21), although in no case, it returned to the baseline severity. The partial loss of response to the drug did not depend on disease duration, the presence of thyroid autoimmunity, or baseline ESR, CRP, or D‐dimer, whereas it was associated with the baseline severity of the disease (P < 0.05). Also, a history of angioedema was much more frequent among those who worsened following the reduction in omalizumab dosage (6/7, 86%) than in patients who maintained the control of the disease (2/7; 29%), but due to the small number of patients, the difference did not reach the statistical significance. Although studies on larger number of patients are needed to confirm these observations and despite the limitation of being nonrandomized, the present real‐life study suggests that it is possible to halve the costs of omalizumab maintenance treatment in about one half of patients with severe CSU showing a prompt response to the drug at the dose of 300 mg/mo without any loss of clinical efficacy. Patients who worsen with a reduced dosage of omalizumab are in general those showing a more severe diseases at baseline as well as those with a history of angioedema associated with the wheals. This is in keeping with previous observations that in patients with angioedema, only the dosage of 300 mg/month seems to be effective 2 Whether the reduction in omalizumab dosage as a maintenance therapy will work also in patients showing a delayed response to the drug remains to be established. In conclusion, this study confirms previous observations in a very small number of patients 10 that a maintenance monthly dose of 150 mg of omalizumab may be sufficient to guarantee an ongoing control of the disease in a large proportion of patients with CSU showing an early response to the drug.