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A technique is described for the intra-operative positioning of the burn patient, which allows circumferential access without the need for specialized equipment or extra personnel. The equipment is available in any standard operating room and table without the need for redesign or new construction. In addition, it allows full 360 degrees access and eliminates the need for extra personnel to hold proper positioning. This allows for more efficient operating and should minimize the unwanted sequelae of hypothermia and blood loss. Operating time may be decreased and the patient may require less operative procedures. The same or more work can be done by less personnel, in less time, with no added cost. [ABSTRACT FROM AUTHOR]

Background: The COVID-19 pandemic has disrupted clinician education. To address this challenge, our divisional difficult airway program (AirEquip) designed and implemented small-group educational workshops for experienced clinicians. Our primary aim was to test the feasibility and acceptability of a small-group, flexible-curriculum skills workshop conducted during the clinical workday. Secondary objectives were to evaluate whether our workshop increased confidence in performing relevant skills and to assess the work-effort required for the new program., Methods: We implemented a 1:1 and 2:1 (participant to facilitator ratio) airway skills workshop for experienced clinicians during the workday. A member of the AirEquip team temporarily relieved the attendee of clinical duties to facilitate participation. Attendance was encouraged but not required. Feasibility was assessed by clinician attendance, and acceptability was assessed using three Likert scale questions and derived from free-response feedback. Participants completed pre and postworkshop surveys to assess familiarity and comfort with various aspects of airway management. A work-effort analysis was conducted and compared to the effort to run a previously held larger-format difficult airway conference., Results: Fifteen workshops were conducted over 7 weeks; members of AirEquip were able to temporarily assume participants' clinical duties. Forty-seven attending anesthesiologists and 17 CRNAs attended the workshops, compared with six attending anesthesiologists and five CRNAs who attended the most recent larger-format conference. There was no change in confidence after workshop participation, but participants overwhelmingly expressed enthusiasm and satisfaction with the workshops. The number of facilitator person-hours required to operate the workshops (105 h) was similar to that required to run a single all-day larger-format conference (104.5 h)., Conclusion: It is feasible and acceptable to incorporate expert-led skills training into the clinical workday. Alongside conferences and large-format instruction, this modality enhances the way we are able to share knowledge with our colleagues. This concept can likely be applied to other skills in various clinical settings., (© 2022 John Wiley & Sons Ltd.)

Background: There are few data describing practice patterns related to the use of sedation/anesthesia for diagnostic imaging in pediatric radiology departments., Objective: To understand current practice patterns related to imaging with sedation/anesthesia in pediatric radiology departments based on a survey of the Society of Chiefs of Radiology at Children's Hospitals (SCORCH) in conjunction with the American College of Radiology's Pediatric Imaging Sedation and Anesthesia Committee., Materials and Methods: A multi-question survey related to imaging with sedation/anesthesia in pediatric radiology departments was distributed to SCORCH member institutions in January 2019. A single reminder email was sent. Descriptive statistical analyses were performed., Results: Of the 84 pediatric radiology departments, 23 (27%) completed the survey. Fifty-seven percent of the respondents self-identified as academic/university-affiliated and 13% as a division/section in an adult radiology department. Imaging sedation (excluding general anesthesia) is commonly performed by pediatric anesthesiologists (76%) and intensive care unit physicians (intensivists, 48%); only 14% of departments expect their pediatric radiologists to supervise imaging sedation. Ninety-six percent of departments use child life specialists for patient preparation. Seventy percent of departments have preparatory resources available on a website, including simulation videos (26%) and audio clips (17%). Nearly half (48%) of the departments have a mock scanner to aid in patient preparation. Imaging sedation/anesthesia is most often scheduled at the request of ordering clinicians (65%), while 57% of departments allow schedulers to place patients into imaging sedation/anesthesia slots based on specified criteria., Conclusion: Imaging sedation/anesthesia practice patterns vary among pediatric radiology departments, and understanding current approaches can help with standardization and practice improvement.

Biomedical research has been struck with the problem of study findings that are not reproducible. With the advent of large databases and powerful statistical software, it has become easier to find associations and form conclusions from data without forming an a-priori hypothesis. This approach may yield associations without clinical relevance, false positive findings, or biased results due to "fishing" for the desired results. To improve reproducibility, transparency, and validity among clinical trials, the National Institute of Health recently updated its grant application requirements, which mandates registration of clinical trials and submission of the original statistical analysis plan (SAP) along with the research protocol. Many leading journals also require the SAP as part of the submission package. The goal of this article and the companion article detailing the SAP of an actual research study is to provide a practical guide on writing an effective SAP. We describe the what, why, when, where, and who of a SAP, and highlight the key contents of the SAP., (© 2019 John Wiley & Sons Ltd.)

Background: General anesthesia during infancy is associated with neurocognitive abnormalities. Potential mechanisms include anesthetic neurotoxicity, surgical disease, and cerebral hypoxia-ischemia. This study aimed to determine the incidence of low cerebral oxygenation and associated factors during general anesthesia in infants., Methods: This multicenter study enrolled 453 infants aged less than 6 months having general anesthesia for 30 min or more. Regional cerebral oxygenation was measured by near-infrared spectroscopy. We defined events (more than 3 min) for low cerebral oxygenation as mild (60 to 69% or 11 to 20% below baseline), moderate (50 to 59% or 21 to 30% below baseline), or severe (less than 50% or more than 30% below baseline); for low mean arterial pressure as mild (36 to 45 mmHg), moderate (26 to 35 mmHg), or severe (less than 25 mmHg); and low pulse oximetry saturation as mild (80 to 89%), moderate (70 to 79%), or severe (less than 70%)., Results: The incidences of mild, moderate, and severe low cerebral oxygenation were 43%, 11%, and 2%, respectively; mild, moderate, and severe low mean arterial pressure were 62%, 36%, and 13%, respectively; and mild, moderate, and severe low arterial saturation were 15%, 4%, and 2%, respectively. Severe low oxygen saturation measured by pulse oximetry was associated with mild and moderate cerebral desaturation; American Society of Anesthesiology Physical Status III or IV versus I was associated with moderate cerebral desaturation. Severe low cerebral saturation events were too infrequent to analyze., Conclusions: Mild and moderate low cerebral saturation occurred frequently, whereas severe low cerebral saturation was uncommon. Low mean arterial pressure was common and not well associated with low cerebral saturation. Unrecognized severe desaturation lasting 3 min or longer in infants seems unlikely to explain the subsequent development of neurocognitive abnormalities.

Background: The use of isoflurane sedation for prolonged periods in the critical care environment is increasing. However, isoflurane-mediated neurotoxicity has been widely reported. The goal of the present study was to determine whether long-term exposure to low-dose isoflurane in mechanically ventilated rodents is associated with evidence of neurodegeneration or neuroinflammation., Methods: Adult female Sprague-Dawley rats were used in this study. Experimental animals (n=11) were induced with 1.5% isoflurane, intubated, and given a neuromuscular blockade with α-cobratoxin. EEG electrodes were surgically implanted, subcutaneous precordial EKG Ag wire electrodes, and bladder, femoral artery, and femoral vein cannulas permanently placed. After these procedures, the isoflurane concentration was reduced to 0.5% and, in conjunction with the neuromuscular blockade, continued for 7 days. Arterial blood gases and chemistry were measured at 3 time points and core body temperature servoregulated and maintenance IV fluids were given during the 7 days. Experimental animals and untreated controls (n=9) were euthanized on day 7., Results: Immunohistochemical and cytochemical assays did not detect evidence of microgliosis, astrocytosis, neuronal apoptosis or necrosis, amyloidosis, or phosphorylated-tau accumulation. Blood glucose levels were significantly reduced on days 3/4 and 6/7 and partial pressure of oxygen was significantly reduced, but still within the normal range, on day 6/7. All other blood measurements were unchanged., Conclusions: No neuropathologic changes consistent with neurotoxicity were detected in the brain after 1 week of continuous exposure to 0.5% isoflurane in healthy rats. These data suggest that even long exposures to low concentrations of isoflurane have no overt consequences on neuropathology.

The Pediatric Anesthesia Neuro Development Assessment (PANDA) team at the Anesthesiology Department at Columbia University Medical Center held its fifth biennial symposium to discuss issues regarding potential neurotoxicity of anesthetic agents in pediatric patients. Overall optimal surgical timing as well as a "critical window" for surgery on a specialty specific basis are areas of focus for the American Academy of Pediatrics Surgical Advisory Panel. An ad hoc panel of pediatric surgical experts representing general surgery, urology, neurosurgery, and ophthalmology was assembled for this meeting and provided a dialogue focused on the benefits of early intervention versus potential anesthetic risk, addressing parental concerns, and the need for continued interdisciplinary collaboration in this area.

Numerous preclinical and clinical studies investigating the neurodevelopmental and neurocognitive effects of exposure to anesthesia and the combination of anesthesia and surgery have demonstrated histopathological and both temporary and long-term cognitive and behavioral effects at the extremes of the human age spectrum. Increasing coverage in the lay press for both our youngest and oldest patient populations has led to heightened concerns regarding the potential harmful side effects of almost all commonly used anesthetic drug regimens. Although the majority of information regarding anesthetic risks in the developing brain derives from preclinical work in rodents, research involving the aged brain has identified a well-defined postoperative cognitive phenotype in humans. While preclinical and clinical data appear to support some association between anesthesia and surgery and the development of detrimental cognitive changes in both the developing and the aged brain, correlation between anesthesia and surgery and poor neurological outcomes does not imply causation. Given this information, no single anesthetic or group of anesthetics can be recommended over any other in terms of causing or preventing negative neurocognitive outcomes in either population. This review summarizes the growing body of preclinical and clinical literature dedicated to the detrimental effects of anesthesia on both the developing and the aging brain.

Background: Recent articles in both scholarly journals and the lay press about the topic of anesthetic related neurotoxicity have increased the awareness and discussion of this topic with parents and other pediatric medical specialties (i.e., surgeons, radiologists, and pediatricians)., Aim: The purpose of the present study was to survey how a subset of pediatric anesthesia departments in the US have responded to the issue of anesthetic related neurotoxicity in terms of clinical practice, training and communication with other medical specialties, and the frequency and timing of discussions with families., Methods: A survey consisting of 22 questions was sent to PALC (Pediatric Anesthesia Leadership Council) & PAPDA (Pediatric Anesthesia Program Directors Association) via SurveyMonkey. The survey was divided into sections on Anesthesia Faculty/Trainees, Parents and Non-Anesthesia Providers. Responses to the survey were solicited via email to PALC and PAPDA, and then followed up with reminders to individual emails using the mailing lists of both organizations., Results: The results of this survey demonstrate that pediatric anesthesia programs around the US do not have a consistent approach in managing the topic of anesthesia-related neurotoxicity with pediatric anesthesiologists, anesthesiology residents, pediatric anesthesiology fellows and their non-anesthesia medical and surgical colleagues, as well as the discussion of this topic with parents., Conclusion: A significant need exists to provide information to other pediatric professionals and parents. A consistent message from all providers that includes what is known, and indeed more importantly what is not known may be a useful approach., (© 2015 John Wiley & Sons Ltd.)

Objective: Anesthetics have been linked to widespread neuronal cell death in neonatal animals. Epidemiological human studies have associated early childhood anesthesia with long-term neurobehavioral abnormalities, raising substantial concerns that anesthetics may cause similar cell death in young children. However, key aspects of the phenomenon remain unclear, such as why certain neurons die, whereas immediately adjacent neurons are seemingly unaffected, and why the immature brain is exquisitely vulnerable, whereas the mature brain seems resistant. Elucidating these questions is critical for assessing the phenomenon's applicability to humans, defining the susceptible age, predicting vulnerable neuronal populations, and devising mitigating strategies., Methods: This study examines the effects of anesthetic exposure on late- and adult-generated neurons in newborn, juvenile, and adult mice, and characterizes vulnerable cells using birth-dating and immunohistochemical techniques., Results: We identify a critical period of cellular developmental during which neurons are susceptible to anesthesia-induced apoptosis. Importantly, we demonstrate that anesthetic neurotoxicity can extend into adulthood in brain regions with ongoing neurogenesis, such as dentate gyrus and olfactory bulb., Interpretation: Our findings suggest that anesthetic vulnerability reflects the age of the neuron, not the age of the organism, and therefore may potentially not only be relevant to children but also to adults undergoing anesthesia. This observation further predicts differential heightened regional vulnerability to anesthetic neuroapoptosis to closely follow the distinct regional peaks in neurogenesis. This knowledge may help guide neurocognitive testing of specific neurological domains in humans following exposure to anesthesia, dependent on the individual's age during exposure., (© 2013 American Neurological Association.)

Background: Accumulating evidence indicates that isoflurane and other, similarly acting anesthetics exert neurotoxic effects in neonatal animals. However, neither the identity of dying cortical cells nor the extent of cortical cell loss has been sufficiently characterized. We conducted the present study to immunohistochemically identify the dying cells and to quantify the fraction of cells undergoing apoptotic death in neonatal mouse cortex, a substantially affected brain region., Methods: Seven-day-old littermates (n = 36) were randomly assigned to a 6-hour exposure to either 1.5% isoflurane or fasting in room air. Animals were euthanized immediately after exposure and brain sections were double-stained for activated caspase 3 and one of the following cellular markers: Neuronal Nuclei (NeuN) for neurons, glutamic acid decarboxylase (GAD)65 and GAD67 for GABAergic cells, as well as GFAP (glial fibrillary acidic protein) and S100β for astrocytes., Results: In 7-day-old mice, isoflurane exposure led to widespread increases in apoptotic cell death relative to controls, as measured by activated caspase 3 immunolabeling. Confocal analyses of caspase 3-labeled cells in cortical layers II and III revealed that the overwhelming majority of cells were postmitotic neurons, but some were astrocytes. We then quantified isoflurane-induced neuronal apoptosis in visual cortex, an area of substantial injury. In unanesthetized control animals, 0.08% ± 0.001% of NeuN-positive layer II/III cortical neurons were immunoreactive for caspase 3. By contrast, the rate of apoptotic NeuN-positive neurons increased at least 11-fold (lower end of the 95% confidence interval [CI]) to 2.0% ± 0.004% of neurons immediately after isoflurane exposure (P = 0.0017 isoflurane versus control). In isoflurane-treated animals, 2.9% ± 0.02% of all caspase 3-positive neurons in superficial cortex also coexpressed GAD67, indicating that inhibitory neurons may also be affected. Analysis of GABAergic neurons, however, proved unexpectedly complex. In addition to inducing apoptosis among some GAD67-immunoreactive neurons, anesthesia also coincided with a dramatic decrease in both GAD67 (0.98 vs 1.84 ng/mg protein, P < 0.00001, anesthesia versus control) and GAD65 (2.25 ± 0.74 vs 23.03 ± 8.47 ng/mg protein, P = 0.0008, anesthesia versus control) protein levels., Conclusions: Prolonged exposure to isoflurane increased neuronal apoptotic cell death in 7-day-old mice, eliminating approximately 2% of cortical neurons, of which some were identified as GABAergic interneurons. Moreover, isoflurane exposure interfered with the inhibitory nervous system by downregulating the central enzymes GAD65 and GAD67. Conversely, at this age, only a minority of degenerating cells were identified as astrocytes. The clinical relevance of these findings in animals remains to be determined.

Despite our insufficient understanding of the exact molecular mechanisms of general anesthetics and sedatives, every year millions of children are treated with these drugs in a seemingly safe manner. However, increasing evidence particularly from animal studies has suggested the possibility for deleterious effects in pediatric patients. All currently clinically utilized anesthetic drugs have been found to induce neuronal cell death in the developing brain and to potentially cause long-term neurological impairment. Conversely, painful stimuli without analgesia and anesthesia have also been shown to initiate a harmful stress response in young children and to trigger neurotoxic effects in the developing brain, which can be blunted by anesthetics. Moreover, anesthetic drugs may also confer neurological protection during hypoxic and ischemic insults. The mechanisms and human applicability of anesthetic neurotoxicity and neuroprotection remain under intense investigation and this Perspectives article summarizes the current state of research., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Mounting evidence from animal studies has implicated that all commonly used anaesthetics and sedatives may induce widespread neuronal cell death and result in long-term neurological abnormalities. These findings have led to serious questions regarding the safe use of these drugs in young children. In humans, recent findings from retrospective, epidemiological studies do not exclude the possibility of an association between surgery with anaesthesia early in life and subsequent learning abnormalities. These results have sparked discussions regarding the appropriate timing of paediatric surgery and the safe management of paediatric anaesthesia. However, important questions need to be addressed before findings from laboratory studies and retrospective clinical surveys can be used to guide clinical practice. This article summarises the currently available preclinical and clinical information regarding the impact of anaesthetics, sedatives, opioids, pain and stress, inflammation, hypoxia-ischaemia, co-morbidities and genetic predisposition on brain structure and long-term neurological function. Moreover, this article outlines the putative mechanisms of anaesthetic neurotoxicity, and the phenomenon's implications for clinical practice in this rapidly emerging field.

Background: Burn cellulitis is an infection of the unburned skin at the margin of a burn wound or graft donor site, typically caused by group A beta-hemolytic streptococci and Staphylococcus aureus. beta-Lactam antibiotics exhibit time-dependent killing and, because of their narrow spectrum, minimize bacterial resistance. We therefore use continuous-infusion oxacillin in the treatment of burn cellulitis., Methods: Patients at a regional burn center who were treated for burn cellulitis from January 2003 to December 2005 were included. Charts were reviewed for all pertinent data regarding the antibiotic treatment methods and outcomes. Successful treatment was defined as resolution of physical findings, fever, and leukocytosis and intravenous antibiotic cessation., Results: Thirty-seven patients were treated for burn cellulitis, 26 (70%) of whom were treated initially with continuous-infusion oxacillin. Other initial antibiotics were chosen because of concomitant infections, penicillin allergy, or development of cellulitis during treatment with a beta-lactam antibiotic. Oxacillin treatment was successful in 19 patients (73%). Success required an average of 5.16 days, with 1.53 days required for fever resolution and 0.89 days for resolution of leukocytosis. Seven patients who did not respond rapidly were switched to intravenous vancomycin an average of 2.4 days after starting oxacillin, leading to a 100% success rate. There were no deaths, and only one suspected case of allergic reaction to oxacillin. In eleven patients treated with other antibiotics, the success rate was 75%. Success with these drugs required a longer treatment course of 6.45 days. Leukocytosis resolved significantly more slowly at 4.45 days (p = 0.02), and fever resolution was also slower at 3.18 days., Conclusions: Continuous-infusion oxacillin was successful in the treatment of 73% of patients, a success rate that might have been higher with clinical patience, and leukocytosis resolved faster than with other antibiotics. Failure of continuous-infusion oxacillin can be managed without clinical consequence by conversion to intravenous vancomycin.

Natural resistance to infection, which does not depend on antibiotics, is a powerful protective mechanism common to all mankind that has been responsible for the survival of our species during countless millennia in the past. The normal functioning of this complex system of phagocytic cells and tissue fluids is entirely dependent on an extremely low level of free ionic iron (10(-18) M) in tissue fluids. This low-iron environment is maintained by the unsaturated iron-binding proteins transferrin and lactoferrin, which depend on well-oxygenated tissues, where a relatively high oxidation-reduction potential (Eh) and pH are essential for the binding of ferric iron. Freely available iron is derived from iron overload, free haem compounds, or hypoxia in injured tissue leading to a fall in Eh and pH. This can severely damage or abolish normal bactericidal mechanisms in tissue fluids leading to overwhelming growth of bacteria or fungi. The challenge for clinical medicine is to reduce or eliminate the presence of freely available iron in clinical disease. In injured or hypoxic tissue, treatment with hyperbaric oxygen might prove very useful by increasing tissue oxygenation and restoring normal bactericidal mechanisms in tissue fluids, which would be of huge benefit to the patient.

The purpose of this study was to review our experience with a mass casualty incident resulting from a boiler room steam explosion aboard a cruise ship. Experience with major, moderate, and minor burns, steam inhalation, mass casualty response systems, and psychological sequelae will be discussed. Fifteen cruise ship employees were brought to the burn center after a boiler room explosion on a cruise ship. Eleven were triaged to the trauma resuscitation area and four to the surgical emergency room. Seven patients were intubated for respiratory distress or airway protection. Six patients had >80 per cent burns with steam inhalation, and all of these died. One of the 6 patients had 99 per cent burns with steam inhalation and died after withdrawal of support within the first several hours. All patients with major burns required escharotomy on arrival to trauma resuscitation. One patient died in the operating room, despite decompression by laparotomy for abdominal compartment syndrome and pericardiotomy via thoracotomy for cardiac tamponade. Four patients required crystalloid, 20,000 mls/m2-27,000 ml/m2 body surface area (BSA) in the first 48 hours to maintain blood pressure and urine output. Three of these four patients subsequently developed abdominal compartment syndrome and died in the first few days. The fourth patient of this group died after 26 days due to sepsis. Five patients had 13-20 per cent bums and four patients had less than 10 per cent burns. Two of the patients with 20 per cent burns developed edema of the vocal cords with mild hoarseness. They improved and recovered without intubation. The facility was prepared for the mass casualty event; having just completed a mass casualty drill several days earlier. Twenty-six beds were made available in 50 minutes for anticipated casualties. Fifteen physicians reported immediately to the trauma resuscitation area to assist in initial stabilization. The event occurred at shift change; thus, adequate support personnel were instantaneously to hand. Our mass casualty preparation proved useful in managing this event. Most of the patients who survived showed signs of post-traumatic stress syndrome, which was diagnosed and treated by the burn center psychology team. Despite our efforts at treating large burns (>80%) with steam inhalation, mortality was 100 per cent. Fluid requirements far exceeded those predicted by the Parkland (Baxter) formula. Abdominal compartment syndrome proved to be a significant complication of this fluid resuscitation. A coordinated effort by the facility and preparation for mass casualty events are needed to respond to such events.

Bacterial resistance to antibiotics is a major threat to clinical medicine. However, natural resistance to bacterial infection, which does not depend on antibiotics, is a powerful protective mechanism common to all mankind. The availability of iron is the heart of the matter and the successful functioning of these antibacterial systems depends entirely upon an extremely low level of free ionic iron (10(-18) M) in normal tissue fluids. This in turn depends on well-oxygenated tissues where the oxidation-reduction potential (Eh) and pH control the binding of iron by unsaturated transferrin and lactoferrin. Bacterial virulence is greatly enhanced by freely available iron, such as that in fully-saturated transferrin or free haemoglobin. Following trauma a fall in tissue Eh and pH due to ischaemia, plus the reducing powers of bacteria, can make iron in transferrin freely available and abolish the bactericidal properties of tissue fluids with disastrous results for the host. Hyperbaric oxygen is a possible therapeutic measure that could restore normal bactericidal systems in infected tissues by raising the Eh and pH.

The wound healing and antimicrobial properties of maggots are well known. Maggot debridement therapy has been used for the treatment of various conditions. For maggot debridement therapy, the larvae of the blowfly are applied over necrotic or nonhealing wounds. We used maggot debridement therapy with the larvae of Phaenicia sericata for limb salvage after bilateral lower extremity fourth-degree burns.

Adequate penetration of antibiotics into burn tissue and maintenance of effective serum levels are essential for the treatment of patients sustaining major thermal injuries. The pharmacokinetics and burn eschar penetration of intravenous ciprofloxacin were determined in 12 critically ill patients with burn injuries. Mean age for the 12 patients was 45 +/- 17 (range 25-82 years), total body surface area burned (TBSAB) = 38 +/- 15% and Acute Physiology and Chronic Health Evaluation (APACHE) II score = 8 +/- 6. Patients received recommended doses of ciprofloxacin, 400 mg q12h iv, for three doses beginning 72 h post-burn. Serum concentrations were measured at t = 0, 0.25, 0.5, 0.75, 1.0, 1.25, 1.5, 2.0, 4.0 and 12.0 h after the first and third doses. Burn eschar biopsies were obtained after the third ciprofloxacin dose. Three of these 12 patients (25%) manifested later signs of clinical sepsis (TBSAB = 61 +/- 6% and APACHE II score = 11 +/- 3) and underwent a second infusion of three doses of intravenous ciprofloxacin, blood sampling and eschar biopsy. Serum and eschar concentrations were determined by high performance liquid chromatography. Serum ciprofloxacin concentrations were comparable to those of normal volunteers (C(max) = 4.0 +/- 1 mg/L and AUC = 11.4 +/- 2 mg.h/L) during the immediate post-burn period after dose 1 (C(max1) = 4.8 +/- 3 mg/L and AUC(0-12) = 12.5 +/- 7 mg. h/L) and dose 3 (C(max3) = 4.9 +/- 2 mg/L and AUC(24-36) = 17.5 +/- 11 mg.h/L). Mean burn eschar concentration during the 72 h post-burn was significantly lower than that found during clinical sepsis (18 +/- 17 compared with 41.3 +/- 54 microg/g; P < 0.05 by t test). Similar serum concentrations were achieved in patients with clinical sepsis (C(max1) = 4.2 +/- 0.2 mg/L and AUC(0-12) = 15.0 +/- 3 mg. h/L; C(max3) = 5.0 +/- 1 mg/L and AUC(24-36) = 22.8 +/- 9 mg.h/L). A positive correlation between burn eschar concentrations and C(max) (r = 0.71, r(2) = 0.51, P = 0.01) was found by linear regression analysis. A C(max)/MIC ratio > 10 (MIC = 0.5 mg/L) and an AUC/MIC ratio > 100 SIT(-1).h (serum inhibitory titre) (MIC = 0.125 mg/L) were achieved. High burn eschar concentrations and serum levels, similar to those found in normal volunteers, can be achieved after intravenous ciprofloxacin infusion in critically ill burns patients.

The rapid movement of information technologies into health care organizations has raised managerial concern regarding the capability of today's institutions to satisfactorily manage their introduction. Indeed, several health care institutions have consumed huge amounts of money and frustrated countless people in wasted information systems implementation efforts. Unfortunately, there are no easy answers as to why so many health informatics projects are not more successful. In this light, the aim of this study is to provide a deeper understanding of how clinical information systems are being implemented by emphasizing research efforts on the dynamic nature of the process, that is, the "how" and "why" of what happened. Using a case study methodology, we examined the implementation of a patient charting system in the Burn Center of a large, not-for-profit, teaching hospital. Based on an in-depth examination of this implementation, several insights are offered to those who have responsibility for managing complex and risky clinical information system implementation projects.

Unsaturated transferrin in plasma ensures that the amount of free ferric iron available to bacteria is about 10(-18) mol/L. This low iron environment is essential for the bacteriostatic and bactericidal systems in blood, lymph, and exudates. Antibacterial systems are abolished when iron becomes freely available. This results in rapid extracellular bacterial growth and greatly increased bacterial virulence. In human plasma, a fall in Eh (oxidation-reduction potential) or pH results in the abolition or marked reduction of its bactericidal properties. This is highly relevant to infection after trauma, where a fall in Eh and pH frequently accompanies tissue damage. Bacterial resistance to antibiotics has put the treatment of serious infections in jeopardy. Reinforcement of natural means of resistance needs to be explored, as well as examining new antibacterials that interfere with bacterial iron metabolism.

The surface thermal burn associated with high voltage (HV) electrical injuries represents only the tip of the iceberg. Occult muscle damage may not become apparent for 5 to 10 days. In this study, the efficacy of Technetium-99m (Tc) pyrophosphate scanning was investigated. Early scanning (within 3 days of injury) of 19 limbs in 15 patients demonstrated a sensitivity of 75 per cent, with a specificity of 100 per cent. The predictive value of a positive test, however, was 100 per cent. Compared to a control group of 17 patients treated without Tc scan, the scan was not associated with reduced hospital length of stay or with decrease in the number of surgical procedures.

The bactericidal power of fresh human plasma against Klebsiella pneumoniae and Escherichia coli was extremely sensitive to changes in Eh and pH. At a high Eh (approx. +200 mV) the bacteria were destroyed, but rapid regrowth occurred when the Eh was lowered to approx. -400 mV. Abolition of the bactericidal effect was also produced by adding ferric iron at a high Eh (approx. +200 mV). Lowering the pH to 6.50 reduced or prevented the bactericidal effect. These results are probably related to the availability of iron for bacterial growth, and could be important for understanding the development of infection in injured or diseased tissue.

The decision not to resuscitate a patient with burns is an issue of concern, with advocates both for and against. Most patients have not had previous experience with major burn injuries. It is therefore unreasonable to expect them or their families to act from a position of knowledge. There is a subset of patients considered for "do not resuscitate" orders who are nonsurvivors. If the outcome is predictable, the responsibility of the burn team is to inform patients and their families. Such discussion should come within the first few hours of admission, when the patient is fully awake and able to understand, to respond, and to make plans.

Trauma is the fifth leading cause of death for the elderly. Approximately 7.4 million (3% of the population) are more than 80 years old (the so-called "old" old). More than 40% of Americans will reach the age of 80 years, and those who do can expect to live an average of 8 years more. The advanced elderly burn victim creates special demands because of a greater morbidity and mortality associated with a smaller body surface area burn. From September 1982 through August 1990, there were 29 patients 80 years old or older treated at our burn center. The mean age was 83 years, and 72% of the patients were women. The most common preexisting medical problems were hypertension and diabetes. Seventeen (59%) survived. The mean percentage of body surface area (BSA) burned was 6% among the survivors, with a mean length of hospital stay of 24 days. The mean BSA burned was 32% among those who died, with a mean stay of 17 days. Five of the 12 deaths were due to burns of less than 20% BSA, below the standard commonly used to define a "major" burn. The abbreviated burn severity index (ABSI) was a good indicator of survival. Eleven of 12 with an ABSI of 7 or less survived, and nine of 11 with an ABSI of 9 or more died. Twelve patients had operation; seven survived. Of the 15 survivors living independently before the injury, 11 were discharged home and four were transferred to nursing facilities. In this age group, even small burns can be problems, and indications for hospital admission should be broadened. The advanced elderly also cause financial burdens to burn centers because of inadequate diagnosis-related group (DRG) reimbursement. For those surviving, there is a good chance for maintaining independent function and for being discharged home.

The role of iron in certain clinical infections is revealed. In normal persons the antibacterial and antifungal properties of blood and other tissue fluids cannot be maintained unless there are exceptionally low levels of available iron. This is controlled by the presence of the unsaturated iron-binding proteins, transferrin and lactoferrin. In several clinical conditions an abnormal availability of iron is responsible for fatal septicaemia. This is because the phagocytic system is overwhelmed by rapidly growing organisms when iron is freely available.

Vibrio vulnificus is killed by normal human blood but grows rapidly in blood from patients with hemochromatosis. It also grows in normal blood if the saturation of the transferrin is increased or if hematin, which contains iron, is added. It is suggested that the increased availability of iron in the blood of patients with chronic iron overload is responsible for their enhanced susceptibility to infection with V vulnificus.

Clinical information systems can extend the scope of computerization beyond laboratory data collection and storage. An automated and computerized intensive care unit flowsheet and patient chart can reduce nonnursing work and improve the quality, quantity, and recall of clinical information.

A clinically lethal strain of Pseudomonas aeruginosa was tested and its growth patterns in normal plasma and in normal whole blood clotted with thrombin were compared. Two stock cultures were used; one was maintained in liquid nitrogen and one was passed from plate to plate 24 times on blood agar plates at room temperature. The results showed that plasma alone and whole blood controlled the growth of a clinically pathogenic strain of P. aeruginosa consistently and uniquely for each donor, dependent on size of inoculum, length of incubation, and means by which the culture was maintained. The changing virulence of an organism and its unique growth patterns in different individuals' plasma and whole blood may explain why patients exposed to the same organisms within the same environment vary in susceptibility to clinical infection.