Aortic valve-sparing operation versus Bentall and mechanical aortic valve replacement--midterm results.

OBJECTIVES: The primary aim of this retrospective study was to evaluate short-term (one-to-six months) and mid-term (six-to-forty-eight months) results of aortic valve-sparing procedures. The second endpoint was to compare the results with the group of patients undergoing mechanical aortic valve replacement during the same period. METHODS: Between April 2008 and May 2012 at our institution, we treated 76 patients either with ascending aorta/root aneurysm/dissection or with isolated aortic regurgitation. A total of seventy-six patients undergoing aortic valve surgery. RESULTS: Analyzed parameters were divided into two parts as function of time. In the first part, i.e. during hospitalization, the mortality, duration of hospitalization, duration of extra corporeal circulation (ECC), and duration of cardiac arrest (CA) were compared and assessed. In the second part, i.e. during monitoring of the patients after their discharge from hospital (one-to-six months, and six-to-forty-eight months), the grade of postoperative AR aimed mainly at the group of aortic valve-sparing operations (subgroups A1, A2, A3), postoperative peak gradient, presence of thromboembolic and bleeding complications, postoperative endocarditis and need for reoperation or hospitalization due to cardiac reasons were analyzed. CONCLUSION: Based on our first experience, we believe that in spite of higher technical difficulty, the aortic valve-sparing operations can be possibly performed with the same or respectively lower rate of postoperative morbidity and mortality. Presented results show that compared with the aortic valve replacement, the aortic valve-sparing operation is a promising method, and an interesting therapeutic alternative for patients. After proper indications, we consider it to be a method of choice (Tab. 6, Fig. 7, Ref. 28).

[Quiscent trophoblastic disease]. / Neinvazivní trofoblastická nemoc.

TYPE OF STUDY: Case report. SETTING: Center for trophoblastic disease in Czech Republic, Institute for care of mother and child, 3rd Faculty of Medicine of Charles University Prague. METHODS: The autors present a case of quiscent trophoblastic disease diagnosed at 27 years old primipara, secundigravida after previous molar pregnancy. The patient had low levels of serum hCG present for more than 18 months after the termination of pregnancy. After this period there was a malignant transformation associated with rapid elevation of hCG levels with need for chemotherapy which was succesfully completed. CONCLUSION: Quiscent (dormant, noninvasive) trophoblastic disease is a recently described unit defined by low levels of hCG present in patients serum and urine samples without any evidence of trophoblastic tumour or other source of hCG production. Quiscent trophoblastic disease is associated with high risk of malignant transformation.

[New diagnostic approach to different hydatidiform mole types, hydropic abortions and relevant clinical management]. / Nové diagnosticki prístupy k ruzným typum hydatidózních mol, hydropickým abortum a príslusné klinické postupy.

OBJECTIVE: To describe new diagnostic approach to complete hydatidiform mole, immature complete hydatidiform mole, partial hydatidiform mole, proliferative mole and hydropic abortion. TYPE OF STUDY: Original research. SETTING: Trophoblastic Disease Center in the Czech Republic (TDC-CZ), Institute for the Care of Mother and Child, Prague. METHODS: Our study consists of 1321 partial hydatidiform moles, 805 complete hydatidiform moles, 524 proliferative moles, and over 2500 hydropic abortuses diagnosed and treated at theTDC-CZ, besides which 2896 of these lesions were examined at the TDC-CZ by referral. The material was examined by routine histopathological methods, which in selected cases was supplemented by immunohistological examination and correlated with cytogenetic and molecular genetic results and clinical features. RESULTS: The study describes the diagnostic procedures enabling the differential diagnosis between mature complete hydatidiform mole, immature complete hydatidiform mole, partial hydatidiform mole, proliferative mole and hydropic abortion. Fourteen histological parameters have been defined which are most common, individually or in combination, in various types of hydatidiform moles and hydropic abortions. Warning is given to errors in histological diagnosis correlated with cytogenetic and molecular genetic results. Proposed reliable method of eliminating the influence of these errors on the possible development of trophoblastic disease. CONCLUSION: The study describes differential diagnosis of complete hydatidiform mole, immature complete hydatidiform mole, partial hydatidiform mole, proliferative mole, hydropic abortion and relevant clinical management.

[Histological differential diagnosis of hydatidiform moles and hydropic abortions]. / Histologická diferenciální diagnostika hydatidózních mol a hydropických abortu.

OBJECTIVE: To describe the diagnostic methods enabling histological differential diagnosis of complete hydatidiform mole, immature complete hydatidiform mole, partial hydatidiform mole, proliferative mole and hydropic abortion. METHODS: Our study consists of 1321 partial hydatidiform moles, 805 complete hydatidiform moles, 524 proliferative moles, and over 2500 hydropic abortuses diagnosed and treated at the Trophoblastic Disease Center in the Czech Republic (TDC-CZ), Institute for the Care of Mother and Child, plus 2896 of these lesions examined at the TDC-CZ by referral. The material was examined by routine histopathological methods, which in selected cases were supplemented by immunohistological examination and correlated with cytogenetic and molecular genetic results and clinical features. RESULTS: The study describes the diagnostic procedures enabling differential diagnosis between mature complete hydatidiform mole, immature complete hydatidiform mole, partial hydatidiform mole, proliferative mole and hydropic abortion. Fourteen histological parameters have been defined which are most common, individually or in combination, in various types of hydatidiform moles and hydropic abortions. Warning is given to errors in histological diagnosis, correlated with cytogenetic and molecular genetic results. We propose a reliable method of eliminating the influence of these errors on the possible development of trophoblastic disease. CONCLUSION: The study describes a histological differential diagnosis of complete hydatidiform mole, immature complete hydatidiform mole, partial hydatidiform mole, proliferative mole and hydropic abortion.

[Persistent trophoblastic disease in Trophoblastic Disease Center in the Czech Republic in 1955--2007]. / Perzistující trofoblastická nemoc v Centru pro trofoblastickou nemoc v CR v letech 1955--2007.

OBJECTIVE: To define persistent trophoblastic disease as a clinical entity of gestational trophoblastic disease. To describe its classification, treatment and follow-up. TYPE OF STUDY: Retrospective analysis. SETTING: Trophoblastic Disease Center (TDC) in the Czech Republic TDC-CZ, Institute for the Care of Mother and Child, Prague. METHODS: This study analyzes data from the Trophoblastic Disease Center consisting of 396 choriocarcinomas, 512 proliferative moles, 798 complete hydatid moles, 1299 partial hydatid moles, and 2105 persistent trophoblastic invasions treated at the TDC up to the year 2007. The study includes also 2615 cases of trophoblastic disease which documented by gynecologists and pathologists of the Czech Republic and registered in the TDC-CZ. RESULTS: Persistent trophoblastic disease was defined and described in detail as follows: 1. Differentiating autothonic hCG, produced by the gestational trophoblast, from so-called "phantom hCG," hypophyseal hCG and hCG during PLL-Q and PLL-U syndrome. 2. Evaluating the level and length of persistence of hCG relevant for the diagnosis of persistent trophoblastic disease. 3. Identifying three types of persistent trophoblastic disease: A. Non-metastatic B. Metastatic low-risk C. Metastatic high-risk 4. Described treatment, indications, and choice of various chemotherapeutic protocols in individual types of persistent trophoblastic disease as well as its follow-up. CONCLUSION: This study enables the differentiation of persistent trophoblastic disease in general gynecologic and obstetric clinical practice, by evaluating the presence, level, and length of persistence of hCG, and thus allowing for timely referral of the patient to the Trophoblastic Disease Center in the Czech Republic.

Pulmonary artery pressure and alveolar gas exchange in man during acclimatization to 12,470 ft.

Pulmonary hemodynamics and gas exchange were studied in four physicians during 72 hr acclimatization to 12,470 ft. Pulmonary catheters were left in three subjects for 72 hr. Resting mean pulmonary arterial pressure (PAP) rose progressively during the first 24 hr from 10.3 +/-1.0 to 21.1 +/-4.0 torr and remained at this level. During this same 24 hr period cardiac output increased from 7.1 +/-1.4 to 8.4 +/-2.0 liters/min and total pulmonary resistance rose from 122 +/-16 to 209 +/-40 dynes.sec/cm(-5). Excercise at 60 w after 24 hr of hypoxia increased PAP to 28.8 +/-5.1 torr and decreased total pulmonary resistance to 155 +/-25. Shunt fractions were 11 +/-3.8% after 24 hr at altitude and fell to 7 +/-0% after 72 hr. Alveolar to arterial O(2) difference (P(A-a)(O2)) breathing oxygen fell from 116 +/-10.8 to 92 +/-33.3 torr during the same period of acclimatization, whereas dead space to tidal volume ratio (V(D)/V(T)) rose from 33 +/-4.0% to 40 +/-5.3% and P(A-a)(O2) breathing ambient air rose from 8 +/-2.6 to 11 +/-3.0 torr. Inspiratory static lung compliance decreased significantly from a control of 176 +/-8 to 141 +/-8 ml/cm H(2)O after 72 hr of hypoxia. After 4-7 days at altitude, further deterioration in gas exchange was observed after a 5 mile, 1800 ft climb to the summit (14,255 ft) and return. P(A-a)(O2) on air rose from 2.5 +/-2.1 just before starting, to 16.3 +/-2.8 at the summit (rested), and was still 9.0 +/-2.2 several hours after returning. The O(2)-breathing values paralleled these, whereas dead space appeared to fall. We speculate that the hypoxic pulmonary hypertension which develops over 24 hr in some way may be responsible for a reduction of compliance and deterioration in oxygen exchange efficiency, possibly representing a sub-clinical form of pulmonary edema of high altitude. The increased alveolar to arterial O(2) difference induced by hypoxic exercise persists for several hours of hypoxic rest.

Misoprostol for induction of labor with a live fetus.

Induction of labor is common in clinical practice. Many different medical and mechanical methods have been used, but the current gold standard is vaginal dinoprostone. Misoprostol has been used for the induction of labor since 1987. In early studies with large misoprostol doses (e.g. 200 microg) there were high rates of uterine hyperstimulation. Cochrane meta-analysis, however, shows that when used in low doses it is as effective as vaginal dinoprostone and with no excess of hyperstimulation. 25 microg vaginal misoprostol 4-hourly, 50 microg oral misoprostol 4-hourly or 20 microg oral misoprostol solution 2-hourly are all safe and effective regimens. Reports of uterine rupture in women with previous cesarean sections mean that it remains contraindicated in this group.

[Syndrome of persistent low levels of human chorionic gonadotrophin (hCG)]. / Syndrom perzistujících nízkých hladin humánních choriových gonadotropinu (hCG) etiologie, klasifikace, diagnostika, postupy.

OBJECTIVE: To analyze the syndrome of persistent low levels of hCG in terms of its etiology, classification, diagnosis, and management. DESIGN: Retrospective analysis. SETTING: Center for Trophoblastic Disease in Czech Republic, Institute for Care of Mother and Child, Prague, Institute of Postgraduate medical education, IPVZ, Prague METHODS: An analysis of the syndrome of persistent low levels of hCG recorded in CTN in 29 women in the years 1979-2005 by the immunoluminesence method which can quantitatively assess variable levels of hCG in blood and urine. A comparison was made of our findings with results of a similar studies having been done in England and USA. RESULTS: Persistent low levels of hCG (PLL) can be differentiated according to cause. 1. PLL-F False positive, also known as Phantom hCG, often caused by heterogenous antibodies. 2. PLL-H Of hypophysial origin, mainly in perimenopause and menopause. 3. PLL-Q Quiescent with trophoblastic disease in history, of trophoblastic origin. 4. PLL-U Undetermined, in history without trophoblastic disease, but in the past with physiological or pathological pregnancy. Assuming also to be of trophoblastic origin. All types of PLL lead in practice to the wrong diagnosis of trophoblastic disease and to a high percentage (40-80%) of needless chemotherapy and operations. In no case of PLL did chemotherapy or operations have an effect on PLL and thus are contraindicated. PLL-Q and PLL-U require continuous clinical and laboratory monitoring and repeated examinations with sophisticated visualization methods. The percentage of developing malignant trophoblastic tumors after PLL-Q and PLL-U is unclear. Extreme incidence was established in 7-25%. PLL-Q and PLL-U are considered as a marker of persistent trophoblastic invasion. Its detection by visualization methods in any organ localization before it turns into a limited solid tumor is excluded by it microscopic dissociative structure. CONCLUSION: The syndrome of persistent low levels of hCG (PLL) lately affects all gynecological and obstetrical workplaces. According to cause it can be divided into: 1. PLL false positive, 2. PLL of hypophysial origin, 3.PLL quiescent with trophoblastic disease in the history, 4. PLL undetermined, in history without trophoblastic disease. In the last two items mentioned above we assume to be of trophoblastic origin. Their morphological base is persistent trophoblastic invasion. The syndrome of PLL often leads to the wrong diagnosis of trophoblastic disease and to needless chemotherapy and operations. In this work was described the diagnosis of PLL, its classification, cause, and management. The percentage of PLL turned into malignant trophoblastic disease is unknown and ranges from 7-25% and requires monitoring in an accredited, national center for trophoblastic disease.

[Guideline for gynecological malignant tumors I. Standard--a complex therapy of ovarian epithelial malignant tumors]. / Guideline gynekologických zhoubných nádoruu I. Standard--komplexní lécba ovariálních epiteliálních zhoubných nádoru.

OBJECTIVE: Elaboration of guideline for primary and secondary treatment of ovarian cancer. DESIGN: Review, consensus between proposers and opponents. METHOD: A retrospective review of published data, analysis of Czech statistics and consensus between proposers and opponents. RESULTS: We underline importance of comprehensive approach in therapy of ovarian cancer. We notice importance of expert ultrasound and CA 125 level in diagnostic algorithm. Extension of surgery depends on result of frozen section. All departments which want to perform surgery for ovarian resistance must have possibility to do peroperative histopathology. We can perform conservative fertility sparing surgery in patient with wishing of pregnancy and low stage disease. The effort of maximal debulking with radical surgery including lymphadenectomy is the standard procedure. When we diagnose ovarian cancer during laparoscopy, we have to convert on laparotomy procedure. We define the role of the neoadjuvant chemotherapy followed by surgery after 3-4 cycles of chemotherapy. We define adequate surgery treatment, indication for adjuvant chemotherapy and indication for second line therapy. CONCLUSION: Guideline for the treatment of epithelial ovarian cancer should become directions for clinicians and others, who participate in the process of treatment of the ovarian cancer. The guidelines include all parts of the process from diagnosis, treatment to follow up. All topics of the guidelines arose from a voting of the proposers and opponents.

Outcome model of asphyxial cardiac arrest in rats.

An outcome model with asphyxial cardiac arrest in rats has been developed for quantifying brain damage. Twenty-two rats were randomized into three groups. Control group I was normal, was conscious, and had no asphyxia (n = 6). Sham group II had anesthesia and surgery but no asphyxia (n = 6). All 12 rats in groups I and II survived to 72 h and were functionally and histologically normal. Arrest group III (the model; n = 10) had light anesthesia and apneic asphyxia of 8 min, which led to cessation of circulation at 3-4 min of apnea, resulting in cardiac arrest (no flow) of 4-5 min. All 10 rats had spontaneous circulation restored by standard external cardiopulmonary resuscitation. Nine rats survived controlled ventilation for 1 h and observation to 72 h, while one rat died before extubation. All nine survivors were conscious at 72 h, with neurologic deficit scores (0% = best; 100% = worst) of 7 +/- 6% (2-16%). All brain regions at five coronal levels were examined for ischemic neurons. The prevalence of ischemic neurons in five regions was categorically scored. The average total brain histopathologic damage score in group III (n = 9) was 2.1 (p < 0.05 vs. group I or II). A reproducible outcome model of cardiac arrest in rats was documented. It provides a tool for investigating pathophysiological mechanisms of neuronal death caused by a transient global hypoxic-ischemic brain insult.

Mild cerebral hypothermia during and after cardiac arrest improves neurologic outcome in dogs.

We previously found mild hypothermia (34-36 degrees C), induced before cardiac arrest, to improve neurologic outcome. In this study we used a reproducible dog model to evaluate mild hypothermia by head cooling during arrest, continued with systemic cooling (34 degrees C) during recirculation and for 1 h after arrest. In four groups of dogs, ventricular fibrillation (no flow) of 12.5 min at 37.5 degrees C was reversed with cardiopulmonary bypass and defibrillation in less than or equal to 5 min, and followed by controlled ventilation to 20 h and intensive care to 96 h. In Study A we resuscitated with normotension and normal hematocrit; Control Group A-I (n = 12) was maintained normothermic, while Treatment Group A-II (n = 10) was treated with hypothermia. In Study B we resuscitated with hypertension and hemodilution. Control Group B-I (n = 12) was maintained normothermic (6 of 12 were not hemodiluted), while Treatment Group B-II (n = 10) was treated with hypothermia. Best overall performance categories (OPCs) achieved between 24 and 96 h postarrest were in Group A-I: OPC 1 (normal) in 0 of 12 dogs, OPC 2 (moderate disability) in 2, OPC 3 (severe disability) in 7, and OPC 4 (coma) in 3 dogs. In Group A-II, OPC 1 was achieved in 5 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.001), OPC 3 in 1, and OPC 4 in 0 dogs. In Group B-I, OPC 1 was achieved in 0 of 12 dogs, OPC 2 in 6, OPC 3 in 5, and OPC 4 in 1 dog. In Group B-II, OPC 1 was achieved in 6 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.05), and OPC 3 or 4 in 0 dogs. Mean neurologic deficit and brain histopathologic damage scores showed similar significant group differences. Morphologic myocardial damage scores were the same in all four groups. We conclude that mild brain cooling during and after insult improves neurologic outcome after cardiac arrest.

Brain enzyme levels in CSF after cardiac arrest and resuscitation in dogs: markers of damage and predictors of outcome.

Levels of brain creatine kinase (CK), aspartate aminotransferase (ASAT), and lactate dehydrogenase (LD) in CSF after cardiac arrest were studied in dog models. Ventricular fibrillation cardiac arrest lasting 10 min or asphyxiation cardiac arrest lasting 0-10 min was followed by cardiopulmonary resuscitation and 96-h intensive care. Outcome was scored as neurologic deficit (0% = normal, 100% = brain death) and overall performance category (1 = normal, 5 = death). Both measures correlated with EEG return time after asphyxiation cardiac arrest, but not after ventricular fibrillation cardiac arrest. Peak activity of enzymes in CSF at 48-72 h post arrest correlated with outcome, and CK was the best predictor. Brain histopathologic damage score at autopsy 96 h post arrest correlated with CK level in CSF (r = 0.79, n = 39) and neurologic deficit (r = 0.70, n = 50). Ischemic neuronal changes occurred after ventricular fibrillation cardiac arrest of 10 min, and neuronal changes plus microinfarcts occurred after asphyxiation cardiac arrest of 1.5-10 min. Brain enzymes were decreased at 6 h post arrest in regions with worst histologic damage (gray matter of neocortex, hippocampus, caudate nucleus, cerebellum). Brain CK decreased further, ASAT remained low, and LD increased at 72 h after arrest. The temporal changes in CK level paralleled the temporal ischemic neuronal changes in the brain, and time to peak activity was unaffected by the severity of the ischemic insult. Peak activity of individual enzymes in CSF was determined predominantly by the brain concentration, but was also influenced by rate of decomposition. This "chemical brain biopsy method" represents a useful adjunctive tool to predict permanent, severe brain damage during comatose states after cardiac arrest and resuscitation.

Amelioration of brain damage after 12 minutes' cardiac arrest in dogs.

To determine the efficacy of cerebral microcirculation promoting therapy in postischemic brain failure, 11 dogs awakening from methohexital sodium anesthesia were subjected to 12 minutes of reversible circulatory arrest by ventricular fibrillation. Physiological variables were controlled for six hours after resuscitation, and the dogs were observed for seven days. Six dogs without the special postresuscitative therapy did not awaken, and either died within 36 hours or remained comatose for seven days. In five dogs, a combination of the following measures was applied: (1) mean arterial pressure was raised to 150 to 180 mm Hg with norepinephrine for six hours; (2) heparinization; (3) rapid intra-aortic injection of dextran 40 (10 ml/kg body weight); and (4) normovelemic hemodilution with dextran 40 to a hematocrit reading of 25% to 30%. All five treated dogs awakened within 24 hours and appeared normal on the seventh day. Therapy enhanced constriction of pupils and normalization of the electroencephalogram (P less than .05). Postischemic neurological deficit is at least partially due to impaired reperfusion and can be ameliorated or prevented by blood flowing-promoting therapy.

Intracranial pressure: monitoring and normalization therapy in children.

The clinical course of 42 children with intracranial pressure monitoring was reviewed. Intracranial hypertension was documented in a variety of diagnostic categories. Therapy was titrated to maintain a baseline intracranial pressure of less than 15 torr (mm Hg), and to decrease the frequency of spontaneous and reactive pressure waves. Ventricular drainage, controlled hyperventilation, intravenous glycerol osmotherapy, therapeutic hypothermia, and barbiturate loading were employed as needed to achieve those goals. Survival was significantly related to average and peak intracranial pressure levels and to the degree of serum hyperosmolality that developed during therapy.

Hypothermia and hyperthermia in children after resuscitation from cardiac arrest.

OBJECTIVE: In experimental models of ischemic-anoxic brain injury, changes in body temperature after the insult have a profound influence on neurologic outcome. Specifically, hypothermia ameliorates whereas hyperthermia exacerbates neurologic injury. Accordingly, we sought to determine the temperature changes occurring in children after resuscitation from cardiac arrest. STUDY DESIGN: The clinical records of 13 children resuscitated from cardiac arrest were analyzed. Patients were identified through the emergency department and pediatric intensive care unit arrest logs. Only patients surviving for > or =12 hours after resuscitation were considered for analysis. Charts were reviewed for body temperatures, warming or cooling interventions, antipyretic and antimicrobial administration, and evidence of infection. RESULTS: Seven patients had a minimum temperature (T min) of < or =35 degrees C and 11 had a maximum temperature (T max) of > or =38.1 degrees C. Hypothermia often preceded hyperthermia. All 7 patients with T min < or =35 degrees C were actively warmed with heating lamps and 5 of 7 responded to warming with a rebound of body temperatures > or =38.1 degrees C. None of the 6 patients with T min >35 degrees C were actively warmed but all developed T max > or =38.1 degrees C. Six patients received antipyretics and 11 received antibiotics. Fever was not associated with a positive culture in any case. Conclusion. Spontaneous hypothermia followed by hyperthermia is common after resuscitation from cardiac arrest. Temperature should be closely monitored after cardiac arrest and fever should be managed expectantly.

Gut damage during hemorrhagic shock: effects on survival of oral or enteral interleukin-6.

It has been reported that oral interleukin (IL)-6, without deleterious systemic side effects, prevents bacteremia and gut epithelial apoptosis after hemorrhagic shock (HS) in rodents. The goal of this study was to explore potential benefit of oral or enteral IL-6 on the gut and, consequently, on survival in a long-term outcome model of HS in rats. In Study A, 20 rats (control and IL-6, n = 10 per group) were anesthetized by spontaneous breathing of halothane and N2O. The left femoral vein and artery were cannulated. HS was initiated with withdrawal of 3 mL of blood per 100 g body weight over 15 min, and mean arterial pressure was maintained at 40 to 50 mmHg for another 75 min (total HS 90 min) by blood withdrawal or infusion of Ringer's solution. At HS 90 min, resuscitation included reinfusion of shed blood and additional Ringer's solution to restore normotension for 30 min. After awakening at resuscitation time 30 min, the rats received either 300 units IL-6 or the same volume of vehicle (controls) injected into the stomach via a feeding cannula. In Study B, 20 rats (control and IL-6, n = 10 per group), fasted overnight, were prepared and treated as in Study A, except that HS was initiated with withdrawal of 2 mL blood per 100 g over 10 min, and mean arterial pressure was maintained at 35-40 mmHg. IL-6 rats received 3,000 units IL-6 in 5 mL of normal saline injected directly into the ileum lumen 20 min after induction of shock and again at resuscitation time 60 min. Control rats received normal saline alone. In both studies, survival was observed to 72 h. In Study A, 7 of 10 rats in the control group and 5 of 10 in the IL-6 group survived to 72 h (NS). Macroscopic assessment of gut injury was not different between the two groups. In Study B, 6 of 10 rats survived to 72 h in each group. Frequency of bacteria growth in liver tissue of 72 h survivors was not different between the two groups. IL-6, administered into the stomach or directly injected into the small intestine lumen, did not protect the gut from ischemic injury, nor did it improve survival following severe HS in rats.

Continuous positive airway pressure without tracheal intubation in spontaneously breathing patients.

Indications for the use of therapy with continuous positive airway pressure (CPAP) in spontaneously breathing patients are increasing in number. The value of this technique without tracheal intubation was investigated in 14 patients with acute respiratory distress. In most patients (eight patients, or 57 percent) the technique was successful, as evidenced by avoidance of the necessity for tracheal intubation and improvements in clinical appearance, arterial oxygen pressure, and chest x-ray films. Complications were observed in three patients, but these necessitated discontinuation of therapy in only one. The use of this technique allows avoidance of endotracheal intubation and mechanical ventilation, with their attendant risks.

Moderate hypothermia for 48 hours after temporary epidural brain compression injury in a canine outcome model.

In a previous study with this dog model, post-insult hypothermia of 31 degrees C for 5 h prevented secondary intraventricular pressure (IVP) rise, but during 35 degrees C or 38 degrees C, one-half of the dogs developed delayed IVP rise to brain death. We hypothesized that 31 degrees C extended to 48 h would prevent brain herniation. Using epidural balloon inflation, we increased contralateral IVP to 62 mm Hg for 90 min. Controlled ventilation was to 72 h and intensive care to 96 h. Group 1 dogs (n = 10) were normothermic controls (37.5 degrees C). Group 2 dogs (n = 10) were surface-cooled from 15 to 45 min of balloon inflation and maintained at moderate hypothermia (31 degrees C) to 48 h. Rewarming was from 48 to 72 h. Four additional dogs of hypothermia Group 2 had to be excluded from analysis for pneumonia and/or bleeding diathesis. After balloon deflation, IVP increased to 20 mm Hg or greater at 154 +/- 215 (range 15-720) min following the insult in Group 1 and at 1394 +/- 1191 (range 210-3420) min in Group 2 (p = 0.004), still during 31 degrees C but without further increase during hypothermia. Further IVP rise led to brain death in Group 1 in 6 of 10 dogs at 44 +/- 18 (range 21-72) h (all during controlled ventilation); and in Group 2, in 6 of 10 dogs at 87 +/- 11 (range 72-96) h (p = 0.001), all after rewarming, during spontaneous breathing. Survival to 96 h was achieved by 4 of 10 dogs in Group 1, and by 7 of 10 dogs in Group 2 (NS). Three of the six brain deaths in Group 2 occurred at 96 h. The macroscopically damaged brain volume was only numerically smaller in Group 2. The vermis downward shift was 6.8 +/- 3.5 mm in Group 1, versus 4.7 +/- 2.2 mm in Group 2 (p = 0.05). In an adjunctive study, in 4 additional normothermic dogs, hemispheric cerebral blood flow showed post-insult hypoperfusion bilaterally but no evidence of hyperemia preceding IVP rise to brain death. In conclusion, in this model, moderate hypothermia during and for 48 h after temporary epidural brain compression can maintain a low IVP during hypothermia but cannot prevent lethal brain swelling after rewarming and may cause coagulopathy and pulmonary complications.

Isoflurane improves long-term neurologic outcome versus fentanyl after traumatic brain injury in rats.

Despite routine use of fentanyl in patients after traumatic brain injury (TBI), it is unclear if it is the optimal sedative/analgesic agent. Isoflurane is commonly used in experimental TBI. We hypothesized that isoflurane would be neuroprotective versus fentanyl after TBI. Rats underwent controlled cortical impact (CCI) and received 4 h of N2O/O2 (2:1) and either fentanyl (10 microg/kg i.v. bolus, 50 microg/kg/h infusion) or isoflurane (1% by inhalation) with controlled ventilation. Shams underwent identical preparation, without CCI. Functional outcome (beam balance, beam walking, Morris water maze [MWM] tasks) was assessed over 20 days. Lesion volume and hippocampal neuron survival were quantified on day 21. Additional rats underwent identical CCI and anesthesia with intracranial pressure (ICP) monitoring, and brain water content was assessed. Motor and MWM performances were better in injured rats treated with isoflurane versus fentanyl (p < 0.05). CA1 hippocampal damage was attenuated in isoflurane-treated rats (p < 0.05). Fentanyl-treated rats had higher mean arterial blood pressure after injury (p < 0.05); however, ICP and brain water were similar between groups. Isoflurane improved functional outcome and attenuated damage to CA1 versus fentanyl in rats subjected to CCI. Isoflurane may be neuroprotective by augmenting cerebral blood flow and/or reducing excitotoxicity, not by reducing ICP or brain water content. Alternatively, fentanyl may be detrimental. Isoflurane may mask beneficial effects of novel agents tested in TBI models. Additionally, fentanyl may not be optimal early after TBI in humans.

Glucose plus insulin infusion improves cerebral outcome after asphyxial cardiac arrest.

Hyperglycemia before ischemia worsens cerebral outcome. The aim of this study was to determine the cerebral effects of giving glucose with or without insulin after asphyxial cardiac arrest. Rats underwent 8 min of asphyxial cardiac arrest. After arrest, Group 1 received NaCl; Group 2, insulin; Group 3, glucose; and Group 4, glucose plus insulin, all intravenously. Neurological deficit (ND) scores were 14+/-10%, 22+/-12%, 12+/-10% and 2+/-2% in Groups 1-4, respectively, 72 h after reperfusion. Overall histological damage (HD) scores were 4, 2, 3 and 1, respectively. Group 4 fared significantly better than group 1 on both scores. Glucose after asphyxial cardiac arrest in rats produces no increased brain damage while glucose plus insulin improves cerebral outcome.