Current trends in brain trauma.
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Biomedical subjects
Publications and source records attributed to J Cruz.
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Mechanical ventilation in acute traumatic coma is comprehensively approached, by means of comparatively reviewing the pertinent literature. Multivariate clinico-physiologic-therapeutic aspects are presented and discussed, and a proposition is made for ventilatory optimization under circumstances of predominantly diffuse acute brain insults. A novel technique is introduced for practical, bedside quantification of ventilatory adjustments. This technique allows simultaneous optimization of intracranial pressure and global cerebral extraction of oxygen. The latter represents therapeutic coupling between global cerebral blood flow and oxygen metabolism.
In a total of 309 frequent serial studies, arteriojugular differences in glucose and oxygen levels were concurrently evaluated in 33 adult patients who were experiencing the most acute phase of severe brain trauma. Hyperventilation therapy was optimized to maintain both normalized intracranial pressure and cerebral extraction of oxygen. Under these circumstances, global cerebral glucose extraction was found to be closest to normal during profound optimized hyperventilation, with PaCO2 levels below 25 mm Hg. In contrast, during normocapnia global cerebral glucose extraction dropped below normal range, indicating impairment of cerebral glucose uptake. Findings from this study show that in severe acute brain injury, optimized hyperventilation exerts an additional metabolic effect with respect to cerebral glucose uptake.
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STUDY OBJECTIVE: to characterize the high mortality rate by ischemic heart disease in Azores, by evaluating the main coronary heart disease risk factors prevalence in the population. DESIGN: sample study referring the population of 5 islands: 37 counties. Aleatory choose in the electoral lists. SETTING: the selected individuals were convocated by mail to show up at the Hospital for evaluation. PATIENTS: 1089 individuals selected by aleatory choose from the electoral lists. INTERVENTIONS: the sample was stratified regarding rural (R) and urban (U), by sex feminine (F) and masculine (M), age 20-40 and 40 to 60 years old. All of them were determined three values of blood pressure, and was taken for exact value the medium of the three, inquired the smoking habits and serum lipids were determined. We considered risk factors (RF); blood pressure > 140/90 mmHg, total cholesterol > 200 mg/dl, HDL cholesterol < 35 mg/dl, triglycerides > 180 mg/dl and smoking habits were stratified in three scores: 1: 1-10, 2: 11-20, and 3: more than 20 cigarettes a day. MAIN RESULTS: total prevalences; HBP 20.4%, smoking habits 33%, total hypercholesterolemia 47.3%, low HDL cholesterol 17.4% and triglycerides 30.5%. CONCLUSIONS: the values found for total cholesterol, triglycerides and smoking habits were high and superior to the national medium and to those found in reference studies. Preventive strategies are pointed out.
Diaphragmatic Pacing was used to treat ventilatory failure in a young boy with bilateral diaphragmatic palsy secondary to cervical cord injury, on chronic mechanical ventilation for 6 months. The indications for diaphragmatic pacing in ventilatory failure were discussed, as well as the assessment of phrenic nerve integrity and the pacing schedules utilized to slowly improve the diaphragm endurance and achieve a full-time weaning from mechanical ventilation.
OBJECTIVE: To evaluate the occurrence of global cerebral ischemia in acute brain trauma with acute anemia by combined measurements of cerebral hemodynamics, oxygenation, and lactate production. DESIGN: Prospective, intervention study. SETTING: Neuroscience intensive care unit of a university hospital. PATIENTS: Adults (n = 22) with severe acute brain trauma (Glasgow Coma Scores ranging from 4 to 8), undergoing frequent serial measurements of total hemoglobin content, jugular oxyhemoglobin saturation, arteriojugular oxygen content difference, arteriojugular lactate concentration difference, lactate-oxygen index, and cerebral blood flow, along with other routine procedures. MEASUREMENTS AND MAIN RESULTS: Acute anemia (disclosed by a total hemoglobin content of < 11 g/dL in at least three measurements) was found in 19 (86%) of 22 patients. In 211 serial multivariate physiologic observations, only one (0.4%) disclosed abnormally negative arteriojugular lactate difference consistent with global cerebral ischemia. However, in 18 (8.5%) studies in seven (31.8%) patients, acute anemia resulted in markedly decreased values of arteriojugular oxygen content difference. The latter, in turn, yielded abnormally high values of lactate-oxygen index despite normal cerebral lactate production (arteriojugular lactate difference) and oxygenation (jugular oxyhemoglobin saturation). CONCLUSIONS: In acute brain injury with acute anemia, global cerebral ischemia is a rare finding. However, false cerebral ischemia may be frequently found, if assessed by the lactate-oxygen index, because the denominator of the index (the arteriojugular oxygen content difference) frequently decreases as a function of decreasing hemoglobin, thus yielding false calculated ischemic high values for lactate-oxygen index despite normal cerebral oxygenation and lactate production.
A case of severe acute brain trauma is presented in which the patient made a satisfactory recovery after suffering a marked reduction in cerebral blood flow, to a level previously reported in association with impending brain death (10 ml/100 gm/min). This is believed to be the first report of a patient with severe acute brain injury in whom serial clinical and physiological assessments allowed documentation of the reversibility of such a critical level of cerebral hypoperfusion.
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Serum lipid profiles were evaluated in 143 white (31 men, 112 women, aged 58.4 +/- 0.9 years) and in 75 black-individuals (16 men, 59 women, aged 52.6 +/- 1.0 years) with treated essential hypertension. Hypertension onset was earlier in the blacks than the whites (39.7 +/- 1.0 vs. 46.6 +/- 1.1 years). Duration of hypertension was similar in both races (11.8 +/- 1.0 and 12.9 +/- 1.0 years) and did not correlate with serum lipid values. Mean serum lipids, excluding HDL-C, were significantly higher in white than in black hypertensives (LDL-C 4.19 +/- 0.08 vs. 3.82 +/- 0.13; TG 1.80 +/- 0.10 vs. 1.40 +/- 0.09 mmol/l; LDL-C/HDL-C 4.0 +/- 0.1 vs. 3.6 +/- 0.2). The prevalence of dyslipidaemia was significantly higher in white than in black patients (64% vs. 52%). Types IIa, IIb and IV were more prevalent in whites and isolated low HDL-C in blacks. Obesity was found in 27% of the whites and 31% of the blacks. Hypertriglyceridaemia was more frequent in obese hypertensives of both races, but mostly among the white obese patients. Among lipid values within the normal range, the mean levels of serum lipids were similar in both races, with the exception of triglyceridaemia, which was significantly lower in black than in white hypertensives. These findings may be attributed to racial differences rather than to nutritional trends.
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PURPOSE: To analyse bacterial infections in the period immediately following bone-marrow transplantation. PATIENTS AND METHODS: A retrospective study of 174 febrile episodes appearing on 103 patients treated with bone-marrow transplantation in 1990 and 1991 was carried out, special attention being paid to the bacterial infections. RESULTS: Virtually all patients (100/103) had at least one febrile episode, and its infectious character was documented in 54% of the instances. Gram-positive germs were most commonly present, 85% of the bacteria isolated, and coagulase-negative staphylococci, especially St epidermidis, predominated (60%). Different species of streptococci, mostly of the viridans group, were isolated in 22% of the blood cultures attained in the first febrile episodes. The mortality due to infection in the series as a whole was 4.8%. CONCLUSIONS: Infections by gram-positive germs, especially coagulase-negative staphylococci, are commonly found among the patients subjected to bone-marrow transplantation. Increased streptococci infections, mostly of the viridans group, are also appreciated. These facts, along with decreased number of gram-negative infections, must be born in mind when designing initial antimicrobial coverage for these patients.
Recently [Roepe, P.D. (1992) Biochemistry 31, 12555-12564], increased steady-state levels of chemotherapeutic drug efflux from multidrug-resistant (MDR) myeloma cells were correlated with intracellular alkalinization. To better understand elevated pHi in MDR cells, Na(+)- and Cl-dependent recovery of pHi upon intracellular acid or alkaline shock has been examined for this same series of MDR cell lines. In agreement with another recent report [Boscoboinik, D., Gupta, R.S., & Epand, R.M. (1990) Br. J. Cancer 61, 568-572], we find that the rate of Na(+)-induced alkalinization after an intracellular acid shock is increased in the MDR cells, relative to the drug-sensitive parent. Interestingly, we also now find that mRNA encoding the human Na+/H+ exchanger (NHE) is overexpressed in these MDR cells, but the level of overexpression does not correlate with the relative drug resistance or steady-state pHi. It is also found that the efficiency of Cl(-)dependent reacidification of pHi, after an intracellular alkaline shock is reduced in the MDR cells. This effect appears to correlate with the relative expression of MDR protein, but not the relative expression of Cl-/HCO3- exchanger (AE), which we now find is also altered in the series of cells. Since elevated pHi will increase delta pH across the plasma membrane, we have also measured the electrical potential for these cells using three different methods. Most interestingly, the magnitude of the plasma membrane electrical potential (delta psi) decreases concomitant with increased expression of the MDR protein. Energy provided by increased delta pH compensates for the lowered delta psi, such that the total electrochemical membrane potential (delta mu H+) remains similar among the cells in this series (delta mu H+ = delta psi - Z delta pH). These data, along with other recent experiments that associated an increased Cl- conductance with the expression of MDR protein [Valverde, M., Diaz, M., Sepúlveda, F.V., Gill, D.R., Hyde, S.C., & Higgins, C.F. (1992) Nature 355, 830-833], are consistent with a model for MDR protein-mediated multidrug resistance that does not entail direct active transport of lipophilic drugs by the MDR protein.
PURPOSE: To evaluate the effect of Brain Tomour (BT) and Neurosurgery (NS) on the renal handling of H2O and Na, and the clinical importance of SIADH in this setting. METHODS: Fourteen patients with BT pre-op for NS and 6 controls (C) pre-op for general surgery, were assessed in a controlled prospective trial. All patients were normovolaemic, with normal renal function. They received 400 mg of lithium carbonate (Li) 8 hours before each of two test periods (I and II) and a standard water load only before period II. Clearances studies were performed pre-op (period I) and 24 hours post-op (period II). RESULTS: Serum Na was normal at all times. Despite normovolaemia, a 1% decrement in serum osmolality and the water load, ADH dramaticaly increased from time I to II mainly in the BT group (36.2 +/- 9.4 vs 7.1 +/- 0.6 pmol/L, p = 0.02). FENa, FELi and FEUricA were significantly more elevated in the BT group pre and post-op (at time II respectively 4.6 +/- 1.6 vs 1.1 +/- 0.3%; 29.3 +/- 4.9 vs 22.6 +/- 5.5; 26.0 +/- 8.1 vs 11.3 +/- 2.2, p = 0.03). Proximal and distal H2O re-absorption and distal fractional Na re-absorption were identical in both groups pre and post-operatively. CONCLUSIONS: 1-BT and NS always induce a SIADH. 2-There was a primary Na loss at the proximal tubule level not explained by ADH increment, that did not significantly changed H2O handling. 3-To prevent hyponatraemia, hypotonic I.V. fluids should be avoided, but more importantly saline must be provided to this potentially salt-wasting condition.
OBJECTIVE: To comparatively evaluate cerebral metabolic rate of oxygen consumption and a modification of it, cerebral consumption of oxygen, in patients with acute brain injury with acute anemia. DESIGN: Prospective, observational study. SETTING: Neuroscience intensive care unit (ICU) of a university hospital. PATIENTS: Adults (n = 62) with acute brain trauma, undergoing serial 133xenon studies of regional cerebral blood flow and global cerebral oxygen metabolism, along with other routine monitoring techniques. MEASUREMENTS AND MAIN RESULTS: In 173 combined studies of blood flow and oxygen metabolism, in the presence of spontaneous decreases in hemoglobin, cerebral metabolic rate of oxygen consumption and cerebral consumption of oxygen were comparatively evaluated in three groups with different hemoglobin levels. Cerebral metabolic rate of oxygen consumption was calculated as the product of averaged regional cerebral blood flow and arterio-jugular oxygen content difference, while cerebral consumption of oxygen was calculated as the product of averaged regional cerebral blood flow and the arterio-jugular oxyhemoglobin saturation difference, i.e., cerebral extraction of oxygen. Results indicated that a decrease of hemoglobin content is paralleled by a decrease in cerebral metabolic rate of oxygen consumption, even though the level of consciousness (coma score) is essentially unchanged across three hemoglobin groups. On the other hand, cerebral consumption of oxygen does not follow the decrease in hemoglobin and cerebral metabolic rate of oxygen consumption, thus demonstrating better stability to changing hemoglobin content. The low cerebral metabolic rate of oxygen consumption is due to a decrease in arterio-jugular oxygen content difference in anemia, while the cerebral extraction of oxygen does not follow the trend of the arterio-jugular oxygen content difference. CONCLUSIONS: In acute brain trauma with acute anemia, calculated arterio-jugular oxygen content difference and cerebral metabolic rate of oxygen consumption tend to be progressively lower, depending on the extent of anemia, which is in disagreement with coma scores. These changes in hemoglobin tend to have an inverse influence on cerebral consumption of oxygen, which, therefore, constitutes an alternative and independent measure of cerebral oxygen and independent measure of cerebral oxygen consumption under these limiting circumstances.
OBJECTIVE: To continuously evaluate the relationship between global systemic and cerebral oxygenation during temporary profound hypocapnia, which was attempted for prompt management of posttraumatic intracranial hypertension. DESIGN: Prospective, intervention study. SETTING: Neuroscience intensive care unit of a university hospital. PATIENTS: Young adults (n = 21) with acute brain trauma, undergoing routine monitoring of jugular bulb and pulmonary artery oxyhemoglobin saturations, along with other monitoring. MEASUREMENTS AND MAIN RESULTS: In 102 multivariate observations carried out on days 2 and 3 post-trauma, two new physiologic variables were assessed. These variables, systemic-cerebral oxygenation index and the systemic-cerebral ventilatory index, were evaluated in terms of baseline and post-hyperventilation changes. Overall, when intracranial pressure was largely increased, this increase was associated with decreased cerebral oxygen extraction ("luxury perfusion"), and high values of systemic-cerebral oxygenation index. In response to transient profound hypocapnia, the cerebral oxygen extraction normalized (increased), as did the systemic-cerebral oxygenation index (decreased), under most circumstances. The systemic-cerebral ventilatory index showed adequate systemic-cerebral response to hypocapnia in 92 (90.2%) observations. In the remaining ten (9.8%) observations, this response was considered inadequate, but it did not result in abnormal systemic or cerebral oxygenation parameters. CONCLUSIONS: In young adults with severe acute brain trauma who require prompt management of intracranial hypertension, transient profound hypocapnia is effective in lowering the intracranial pressure, as well as in offsetting the cerebral luxury perfusion, while improving or maintaining adequate systemic oxygenation. The systemic-cerebral oxygenation index and the systemic-cerebral ventilatory index are potentially useful, physiologically monitorable variables for the combined assessment of global systemic and cerebral oxygenation in a variety of areas involving physiologic and/or therapeutic approaches.
OBJECTIVES: To discuss theoretical and practical aspects of cerebral oxygenation, from isolated observational measurements to continuous interventional monitoring. DATA SOURCES: Relevant articles from the pertinent literature, as well as a multivariate physiologic diagram developed in this article. STUDY SELECTION: Theoretical, experimental, and clinical information that further clarifies the physiologic relevance of cerebral oxygenation. DATA EXTRACTION: All basic concepts of cerebral hemometabolism were used, up to cerebral hemodynamic reserve, and were interrelated accordingly. DATA SYNTHESIS: Cerebral perfusion pressure alone does not allow global cerebral hemometabolic optimization. The same situation is true for cerebral blood flow. The reason for this limitation is because these variables lack metabolic information. Cerebral arteriovenous differences do allow global cerebral hemometabolic optimization, because they reflect the exchange between the capillary and the tissue. In addition, cerebral hemodynamic reserve allows quantification of the cerebral microcirculatory tolerance to increases in intracranial "tightness" (decreases in intracranial compliance). CONCLUSIONS: Multivariate optimization of global cerebral oxygenation, primarily based on global cerebral oxygen delivery and extraction, may strongly affect outcome in a variety of predominantly diffuse, acute intracranial disorders. Cerebral hemodynamic reserve may be further explored in experimental and clinical areas, involving not just acute brain trauma.
A case of acute closed brain trauma is presented in which the patient developed a right middle cerebral artery infarction, while frequent measurements of the arteriojugular lactate difference (AVDL) remained normal, failing to disclose ischemia. To our knowledge, this is the first report on sequential AVDL measurements during evolving cerebral infarction.