Tuberculosis as primary cause of death among AIDS cases in Rio de Janeiro, Brazil.

SETTING: Data from the mortality database, Rio de Janeiro City (RJC) Health Department, Rio de Janeiro, Brazil. OBJECTIVES: To determine the role played by tuberculosis (TB) in Brazil's human immunodeficiency virus (HIV) positive population, we investigated the frequency of TB as the primary cause of death among HIV-positive subjects in RJC. DESIGN: Information about acquired immune-deficiency syndrome (AIDS) deaths from 1996 to 2005 in individuals aged >12 years was obtained from the Mortality Information System (SIM), and the cause of death was classified according to the International Classification of Diseases (ICD-10), through primary causes coded in Chapter I--B20 to B24 (HIV disease). RESULTS: There were 8601 AIDS-related deaths in RJC between 1996 and 2005. TB was the primary cause of death in 9.0% of all AIDS-related deaths, while Pneumocystis carinii pneumonia (PCP) accounted for 4.7%. TB cases erroneously classified under other infectious diseases may have contributed to an underestimation of the number of TB deaths among HIV-positive patients. CONCLUSION: Our study showed that TB is the leading cause of AIDS-related deaths and is responsible for twice as many deaths as PCP, in a scenario of free access to antiretrovirals. The potential benefits of TB preventive treatment and of the availability of highly active antiretroviral treatment could not be established by this analysis.

Treatment of pain in acutely burned children.

The child with burns suffers severe pain at the time of the burn and during subsequent treatment and rehabilitation. Pain has adverse physiological and emotional effects, and research suggests that pain management is an important factor in better outcomes. There is increasing understanding of the private experience of pain, and how children benefit from honest preparation for procedures. Developmentally appropriate and culturally sensitive pain assessment, pain relief, and reevaluation have improved, becoming essential in treatment. Pharmacological treatment is primary, strengthened by new concepts from neurobiology, clinical science, and the introduction of more effective drugs with fewer adverse side effects and less toxicity. Empirical evaluation of various hypnotic, cognitive, behavioral, and sensory treatment methods is advancing. Multidisciplinary assessment helps to integrate psychological and pharmacological pain-relieving interventions to reduce emotional and mental stress, and family stress as well. Optimal care encourages burn teams to integrate pain guidelines into protocols and critical pathways for improved care.

The early assessment and intensive care unit management of patients with severe traumatic brain and spinal cord injuries.

The assessment and management of neurotrauma have progressed significantly over the past several years. Improved understanding of the physiology of injured neural tissue and advances in technology have refined the approach to the care of patients suffering neurologic injury. Evidence-based clinical management guidelines, such as those developed by the Brain Trauma Foundation and the American Association of Neurological Surgeons, for the management of traumatic brain injury have been introduced to standardize certain aspects of care. The ongoing evolution of critical care also has had a significant impact on the care of patients suffering from neurotrauma. This article reviews some current issues related to the diagnosis and management of traumatic brain injury and spinal cord injury as we head into the next millennium.

Volatile anesthetics depress spinal motor neurons.

BACKGROUND: Depression of spinal alpha-motor neurons apparently plays a role in the surgical immobility induced by isoflurane. Using the noninvasive technique of F-wave analysis, the authors tested the hypothesis that depressed motor neuron excitability is an effect common to other clinically relevant inhaled anesthetics. METHODS: The authors measured F-wave amplitude in rats anesthetized with desflurane, enflurane, halothane, or sevoflurane. Each animal received one anesthetic at five equipotent anesthetic concentrations (0.6, 0.8, 1.2, and 1.6 minimum alveolar concentration [MAC] and 0.8 MAC with 65% N2O). F waves were detected as late potentials in electromyographic responses evoked in the intrinsic muscles of the hind paw after monopolar stimulation of the ipsilateral posterior tibial nerve. RESULTS: All tested inhaled anesthetics depressed F-wave amplitude but not M-wave (orthodromic, early muscle activation) amplitude, and increased M-F latency in a dose-dependent manner. At 1.0 MAC, the estimated F/M ratio was 70 +/- 13% SD of that at baseline (0.6 MAC). Nitrous oxide added to 0.8 MAC of the potent vapors depressed F/M ratio by 63 +/- 17%. CONCLUSIONS: All anesthetics tested appeared to depress the excitability of spinal motor neurons. This effect may contribute to surgical immobility, and its magnitude is comparable at equipotent concentrations of agents. The authors hypothesize that this effect is due to hyperpolarization, although, currently, there is insufficient information to discriminate between pre- and postsynaptic mechanisms.

Nitrous oxide depresses spinal F waves in rats.

BACKGROUND: Evoked, recurrent electromyographic activity (F waves) reflect alpha-motor neuron excitability. Based on observations that other inhaled anesthetics do so, we hypothesized that nitrous oxide, alone or in combination with isoflurane, would depress F-wave activity and correlate with depression of movement response to tail clamp or electric stimulation. METHODS: In study 1, the authors examined the effect of nitrous oxide in combination with isoflurane in 13 normocapnic Sprague-Dawley rats anesthetized with 1.0% isoflurane (0.7 minimum alveolar concentration) in oxygen. The tibial nerve was stimulated at the popliteal fossa, and evoked electromyographic activity [M (direct neuromuscular junctional response) and F waves] were recorded from ipsilateral foot muscles. The effect of the addition of 30% or 70% nitrous oxide was measured. F-wave amplitude/M-wave amplitude ratio (F/M) was determined from each stimulus-electromyographic response pair. F/M vs. movement response to 60-s tail clamp was assessed after each recording session. F-wave amplitude/M-wave amplitude ratio at adjacent doses that permitted and prevented movement were compared. In study 2, the authors examined the effect of (hyperbaric) nitrous oxide as the sole anesthetic agent on F waves. In 11 rats anesthetized with isoflurane, stimulation and recording electrodes were placed as described above, with additional electrodes for stimulation placed in the tail. Rats were placed in a pressure chamber pressurized with nitrous oxide/oxygen to 3.4 atm. Thirty m were allowed for isoflurane washout. Electromyographic activity was evoked and recorded at 1.0, 1.6, 2.2 and 2.7 atm N2O (random order). Movement in response to 60 s of 15 V, 50-Hz tail stimulation was evaluated after each recording session. RESULTS: Nitrous oxide with or without isoflurane produced a dose-dependent decrease in F/M. By interpolation of this data, the authors found that 2 atm N2O alone, or 44% N2O added to 1.0% isoflurane at 1.0 atm, produced 1.0 minimum alveolar concentration anesthesia. At the deepest level of isoflurane/ nitrous oxide that permitted movement, mean F/M was 20.6 +/- 17.5%; at the lowest concentration that blocked movement, rats had a mean F/M of 13.7 +/- 13.9% (P = 0.01). At the minimal hyperbaric nitrous oxide blocking movement, rats had a mean F/M of 3.7 +/- 2.9%, whereas the F/M at the highest nitrous oxide dose that permitted movement was 4.4 +/- 2.7% (P < 0.04). CONCLUSIONS: Because nitrous oxide depressed F-wave but not M-wave activity, the data suggest a central (spinal) rather than neuromuscular junctional site of action of this agent. The direct correlation between nitrous oxide dose, F-wave amplitude depression, and surgical immobility suggests the possibility of using F-wave activity to predict the likelihood of anesthetic-induced immobility. However, the mechanism of action of nitrous oxide may differ from that of the potent inhaled agents.

Halothane selectively inhibits bradykinin-induced synovial plasma extravasation.

BACKGROUND: In vitro studies demonstrate that halothane, but not isoflurane, inhibits bradykinin-induced calcium currents and prostacyclin release in cultured endothelial cells. Because bradykinin is an important endogenous mediator of inflammation, we assessed the effects of halothane, isoflurane, and pentobarbital on plasma extravasation, a component of tissue inflammation induced by bradykinin, in rats. METHODS: We anesthetized 23 rats with halothane (0.8 or 1.3 minimum alveolar concentration [MAC]), isoflurane (1.3 MAC), or pentobarbital (total of 85 mg/kg intraperitoneally). Their tracheas were intubated and their lungs mechanically ventilated. After intravenous administration of Evans blue dye, we perfused normal saline followed by bradykinin or platelet-activating factor, another inflammatory mediator, intraarticularly via needles placed in the knee joint. We collected perfusate and estimated extravasation by measuring dye in the perfusate using spectrophotometry. RESULTS: Bradykinin increased plasma extravasation eight- to ninefold above baseline in both pentobarbital- and isoflurane-anesthetized rats. In contrast, bradykinin-induced plasma extravasation at 0.8 MAC and 1.3 MAC of halothane was approximately 40% (P < 0.01) and 15% (P < 0.001), respectively, of that in pentobarbital- and isoflurane-anesthetized rats. Baseline plasma extravasation was lower in rats anesthetized with either concentration of halothane compared with pentobarbital or isoflurane (all P < 0.001). Platelet-activating factor-induced plasma extravasation was similar for all anesthetics. CONCLUSION: Halothane, but not isoflurane or pentobarbital, inhibits both baseline and bradykinin-induced peripheral plasma extravasation, demonstrating that volatile anesthetics differentially modulate this important component of inflammation.

Anesthetic depression of spinal motor neurons may contribute to lack of movement in response to noxious stimuli.

BACKGROUND: Previous studies suggest that anesthetics produce immobility by an action on the spinal cord. We postulated that immobility results from a depression of alpha-motor neuron excitability in vivo, and that this depression would be reflected in a depression of recurrent, (F)-wave activity. METHODS: The lungs of 15 normocapnic, normothermic, normotensive rats were mechanically ventilated with 0.5, 0.8, 1.2, and 1.6 MAC isoflurane, in random sequence, with at least 30 min of equilibration at each step. In addition, at 1.2 MAC, inspired carbon dioxide was altered to create hypercapnia and hypocapnia. The sizes of the orthodromic (M) wave and F wave were measured in ten sequential trials as the activity in the intrinsic muscles of the ipsilateral foot evoked by stimulation of the tibial nerve. RESULTS: M-wave amplitude did not change. F-wave amplitude did not decrease between 0.5 and 0.8 MAC but decreased 50% between 0.8 and 1.2 MAC (P < 0.001) and 60% between 1.2 and 1.6 MAC (P < 0.05). Hypocapnia (17 mmHg) increased F-wave amplitude by 15%, and hypercapnia (73 mmHg) reduced it by 60% compared with normocapnia at 1.2 MAC (31 mmHg) (P < 0.0001). CONCLUSIONS: Anesthetics may cause and moderate hypercapnia may contribute to surgical immobility by depressing excitability of alpha-motor neurons. Monitoring F waves may indicate the adequacy of this aspect of anesthesia and may detect states in which spontaneous or nocifensive movements might occur.

Immunological studies of poisonous anacardiaceae: effect of vehicle on absorption of 3-n-pentadecylcatechol and its diacetate ester derivative after oral feeding in rats.

Tritium-labeled 3-n-pentadecylcatechol and its diacetate ester were fed to Sprague-Dawley rats. Both compounds were dissolved in ethanol and in corn oil vehicles and administered by gavage. The rats were placed in metabolic cages, and the urine and feces was determined by liquid scintillation counting, and the percentage of the administered dose was utilized as a measure of absorption. While there was no difference between the absorption of either compound, absorption was affected by the vehicle. Approximately 30% of the administered radioactivity appeared in the urine when ethanol was the vehicle, but about half that amount (14%) was excreted in the urine when the compounds were dissolved in corn oil. A subsequent bile cannulation study showed that the balance of the radioactivity found in the feces was not a result of biliary excretion. The majority of the activity recovered from urine and feces was eliminated within 48 hr after dosing. These data indicate that oil is a poor vehicle for GI absorption of urushiol components.