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Biomedical subjects

L K Weaver

Publications and source records attributed to L K Weaver.

At least 19 recordsLinked to original sources

De novo cryptogenic hepatitis after sustained eradication of hepatitis C following liver transplantation.

Patients with recurrent hepatitis C (HCV) after liver transplantation (OLT) are often treated with interferon and ribavirin in an attempt to eradicate HCV and prevent cirrhosis. We report four patients who developed de novo cryptogenic hepatitis following sustained eradication of recurrent HCV, which led to decompensated liver disease in two patients, both of whom required listing for retransplantation. Between September 2000 and October 2001, 38 consecutive patients with recurrent HCV were treated with interferon alpha 2b and ribavirin, of whom eight patients (21%) developed a sustained response to HCV eradication. Four of these patients developed cryptogenic hepatitis, which led to decompensated cirrhosis in two patients. Both patients were listed for retransplantation but died on the waiting list. No etiology for liver disease was identified despite extensive investigations in all four patients including postmortem analysis in the two patients. We hypothesize that these individuals developed an aberrant immune response leading to allograft injury whose severity may be determined by underlying haplotype, degree of immunosuppression, presence/absence of HCV, and duration of treatment. We have not found any similar reports in the literature but anticipate more cases to be reported given the universal use of antiviral therapy for recurrent HCV.

Female↗

White matter hyperintensities and neuropsychological outcome following carbon monoxide poisoning.

BACKGROUND: Carbon monoxide (CO) poisoning may result in white matter hyperintensities (WMH) and neurocognitive impairments. OBJECTIVE: To assess in a prospective study WMH in CO-poisoned patients and their relationship to cognitive functioning. METHODS: Seventy-three consecutive CO-poisoned patients were studied. MR scans and neurocognitive tests were administered on day 1 (within 36 hours after CO poisoning), 2 weeks, and 6 months. Age- and sex-matched control subjects for white matter analyses only were obtained from the authors' normative imaging database. MR scans were rated for WMH in the periventricular and centrum semiovale regions, using a 4-point rating scale. Two independent raters rated the scans, and a consensus was reached. RESULTS: Thirty percent of CO-poisoned patients had cognitive sequelae. Twelve percent of the CO-poisoned patients had WMH, with significantly more periventricular, but not centrum semiovale, WMH than control subjects. The WMH in CO-poisoned patients did not change from day 1 to 6 months. Centrum semiovale hyperintensities were related to worse cognitive performance. Duration of loss of consciousness correlated with cognitive impairment at all three times. Initial carboxyhemoglobin levels correlated with loss of consciousness but not with WMH or cognitive sequelae. CONCLUSIONS: CO poisoning can result in brain injury manifested by WMH and cognitive sequelae. The WMH were not related to CO poisoning severity. The WMH occurred in both the periventricular and the centrum semiovale regions; however, only those in the centrum semiovale were significantly associated with cognitive impairments.

Adolescent↗

Verbal memory deficits associated with fornix atrophy in carbon monoxide poisoning.

Magnetic resonance (MR) images and neuropsychological testing data of 69 carbon monoxide (CO) poisoned patients were prospectively obtained within 1 day of CO poisoning, two weeks and six months. CO patients' Day 1 cross-sectional fornix surface area measurements, corrected for head size by using a fornix-to-brain ratio (FBR), were compared to normal age and gender-matched controls. Additionally, a within-subjects analysis was performed comparing the mean areas between CO patients' Day 1, 2 weeks and 6-month FBR. The FBR was correlated with patients' neuropsychological data. There were no significant differences between CO patients' Day 1 fornix measurements compared to normal control subjects. However, significant atrophic changes in the fornix of CO poisoned patients occurred at two weeks with no progressive atrophy at 6 months. By 6 months, CO patients showed significant decline on tests of verbal memory (when practice effects were taken into account), whereas visual memory, processing speed and attention/concentration did not decline. This study indicates that CO results in brain damage and cognitive impairments in the absence of lesions and other neuroanatomic markers.

Adolescent↗

Pulmonary edema associated with hyperbaric oxygen therapy.

We report three cases of pulmonary edema associated with hyperbaric oxygen therapy, including one fatality. All three patients had cardiac disease and reduced left ventricular (LV) ejection fractions (EFs). Two patients had diabetes, and one patient had severe aortic stenosis. Hyperbaric oxygen therapy may contribute to pulmonary edema by increasing LV afterload, increasing LV filling pressures, increasing oxidative myocardial stress, decreasing LV compliance by oxygen radical-mediated reduction in nitric oxide, altering cardiac output between the right and left hearts, inducing bradycardia with concomitant LV dysfunction, increasing pulmonary capillary permeability, or by causing pulmonary oxygen toxicity. We advise caution in the use of hyperbaric oxygen therapy in patients with heart failure or in patients with reduced cardiac EFs.

Aged↗

Acute psychosis associated with diving.

There are only a few reported cases of psychiatric disorders presenting a s decompression sickness (DCS). Previous reports indicate that DCS can result in personality change, depression, Munchausen's syndrome, and pseudo stroke. We report two cases of acute psychoses that occurred following diving as suspected DCS and were treated with hyperbaric oxygen, which did not improve the psychotic features. One patient had symptoms of DCS including myalgias, weakness, and fatigue; however the symptoms were inconsistent. The symptom onset and nitrogen loading from his dive profiles made the diagnosis of DCS unlikely. The second patient exhibited mild joint pain, fatigue, and psychosis that was temporally associated with diving but no other symptoms of DCS. Following a detailed medical evaluation we determined that these two patients did not have DCS or arterial gas embolism (AGE). Although it is highly unlikely that a pure psychotic episode will arise as a result of DCS, physicians caring for divers with symptoms of DCS or AGE and acute psychosis may consider a trial of recompression therapy while completing the medical evaluation. Divers with acute psychosis without signs and symptoms and benign dive profiles are unlikely to have DCS or AGE.

Acute Disease↗

Carbon monoxide poisoning: interpretation of randomized clinical trials and unresolved treatment issues.

Since hyperbaric oxygen therapy (HBO2) appeared as a treatment for CO poisoning in 1960, whether and when to use it for CO poisoning have often been debated. HBO2 has been advocated to treat severe CO poisoning to limit delayed and permanent neurologic sequelae. Initially, inferences about efficacy were based on clinical experience and uncontrolled studies, but since1989, six prospective clinical trials have been reported comparing HBO2 and normobaric O2 administration to treat patients with acute CO poisoning. Of the six trials, four found better clinical outcomes among patients receiving HBO2 while two have shown no treatment effect. The most recent and best-designed randomized controlled clinical trial, performed in Salt Lake City, supports the efficacy of HBO2 in severe acute CO poisoning in accordance with scientific rationale and clinical experience. However, a number of important issues remain for future investigation, which could be addressed in a large multi-center trial. Such a trial should attempt to determine the optimal number of HBO2 treatments and the maximum treatment delay from CO poisoning for HBO2 to provide efficacy in patients with specific risk factors for a poor outcome.

Carbon Monoxide Poisoning↗

Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure.

STUDY OBJECTIVES: There are large reported differences for the carboxyhemoglobin (COHb) half-life (COHb t(1/2)) in humans breathing 100% atmospheric O(2) following CO inhalation in tightly controlled experiments compared to the COHb t(1/2) observed in clinical CO poisoning (range, 36 to 131 min, respectively). Other reports have suggested that the COHb t(1/2) may be affected by gender differences, age, and lung function. We wished to test the hypothesis that the COHb t(1/2) might also be influenced by CO poisoning vs experimental CO exposure, by a history of loss of consciousness (LOC), concurrent tobacco smoking, and by PaO(2). The purpose of the present study was to measure the COHb t(1/2) in a cohort of CO-poisoned patients and to determine if those listed factors influenced the COHb t(1/2). DESIGN: Retrospective chart review from 1985 to 1995. We calculated the COHb t(1/2) of CO-poisoned patients who were treated with high-flow supplemental atmospheric pressure O(2) delivered by nonrebreather face mask or endotracheal tube. SETTING: Hyperbaric medicine department of a tertiary-care teaching hospital. PATIENTS: Of 240 CO-poisoned patients, 93 had at least two COHb measurements > 2% (upper limit of normal) with recorded times of the measurements, permitting calculation of the COHb t(1/2). RESULTS: The COHb t(1/2) was 74 +/- 25 min (mean +/- 1 SD) with a range from 26 to 148 min. By stepwise multiple linear regression analysis, the PaO(2) influenced the COHb t(1/2) (R(2) = 0.19; p < 0.001), whereas the COHb t(1/2) was not influenced by gender, age, smoke inhalation, history of LOC, concurrent tobacco smoking, degree of initial metabolic acidosis (base excess), or initial COHb level. CONCLUSIONS: The COHb t(1/2) of 93 CO-poisoned patients treated with 100% O(2) at atmospheric pressure was 74 +/- 25 min, considerably shorter than the COHb t(1/2) reported in prior clinical reports (approximately 130 +/- 130 min) and was influenced only by the patient's PaO(2).

Adolescent↗

Performance of the Baxter Flo-Gard 6201 volumetric infusion pump for monoplace chamber applications.

For non-hyperbaric purposes, the Baxter Flo-Gard 6201 volumetric pump is capable of infusing multiple types of fluids at rates of 1-1,999 ml x h(-1). We designed a study to determine flow accuracy of this pump at variable rates, fluid viscosities, and volumes over a range of chamber pressures. For hyperbaric use, the pump pressure sensor was adjusted. Sodium chloride solution 0.9% (NS), enteral formula, and packed red blood cells (PRBC) were infused at varying rates from 86.1 to 304 kPa (0.85 to 3.0 atm abs). For NS, measured compared to set flow rates ranged from 12.5% to -7.5% at settings of 1 and 5 ml x h(-1) from 86.1 to 304 kPa (0.85 to 3.0 atm abs) pressures, respectively. For NS infusions at a set rate of 100 ml x h(-1), the measured flow was identical to the set rate at all pressures. At flow settings of 1,999 ml x h(-1), the measured flow varied from the set flow by +/-4.9% Enteral infusion at 100 ml x h(-1) showed approximately a 3% increase in the measured vs. set flow rate. PRBC measured flow rates ranged from -0.4 to 6% of the set rate. During chamber compression and decompression, with set flow rates from 1 to 10 ml x h(-1), the measured flow was considerably less than expected during compression and more than expected during decompression. In conclusion, the Baxter Flo-Gard 6201 infusion pump demonstrated acceptable performance for infusing saline, enteral formula, and PRBC at low and high infusion rates into the pressurized monoplace hyperbaric chamber up to 304 kPa (3 atm abs), with the exception of low rates during compression and decompression.

Atmosphere Exposure Chambers↗

Carbon monoxide poisoning.

Carbon monoxide (CO) poisoning is common and frequently unrecognized since the signs and symptoms are relatively nonspecific. CO poisoning causes tissue hypoxia. Additionally, various animal studies have demonstrated that CO interferes with myoglobin, P450, and other enzyme function; causes lipid peroxidation through neutrophil activation; produces oxidative stress manifested by peroxynitrate deposition in endothelium; binds to cytochrome aa3, disrupting intracellular oxygen utilization; can cause neuroexcitotoxicity; and contributes to hippocampal cellular death through apoptosis. Emergency treatment for CO poisoning is 100% oxygen. Hyperbaric oxygen therapy (HBO2) is accepted in CO poisoning, although data from randomized clinical trials regarding the efficacy of HBO2 in CO poisoning is conflicting. CO poisoning, even when treated with supplemental oxygen can leave the patient with permanent neurocognitive or affective problems. Unfortunately, there appears to be no marker or constellation of signs or symptoms at presentation that predicts long-term outcome following CO poisoning. Given the neurocognitive sequelae following CO poisoning, increased awareness and prevention of CO poisoning is imperative.

Apoptosis↗

MRI, quantitative MRI, SPECT, and neuropsychological findings following carbon monoxide poisoning.

Carbon monoxide (CO) poisoning has been shown to result in neuropathologic changes and cognitive impairments due to anoxia and other related biochemical mechanisms. The present study investigated brain-behaviour relationships between neuropsychological outcome and SPECT, MRI, and Quantitative magnetic resonance imaging (QMRI) in 21 patients with CO poisoning. Ninety-three per cent of the patients exhibited a variety of cognitive impairments, including impaired attention, memory, executive function, and mental processing speed. Ninety-five per cent of the patients experienced affective changes including depression and anxiety. The results from the imaging studies revealed that 38% of the patients had abnormal clinical MRI scans, 67% had abnormal SPECT scans, and 67% had QMRI findings including hippocampal atrophy and/or diffuse cortical atrophy evidenced by an enlarged ventricle-to-brain ratio (VBR). Hippocampal atrophy was also found on QMRI. SPECT and QMRI appear to be sensitive tools which can be used to identify the neuropathological changes and cerebral perfusion defects which occur following CO poisoning. Cerebral perfusion defects include frontal and temporal lobe hypoperfusion. Significant relationships existed between the various imaging techniques and neuropsychological impairments. The data from this study indicate that a multi-faceted approach to clinical evaluation of the neuropathological and neurobehavioural changes following CO poisoning may provide comprehensive information regarding the neuroanatomical and neurobehavioural effects of CO poisoning.

Adult↗

Neuropsychological sequelae and impaired health status in survivors of severe acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is a disease of acute respiratory failure manifested by severe hypoxemia with a high mortality rate. Previous outcome studies of ARDS have assessed survival and/or pulmonary function as the primary outcome variables. Cognitive or psychological outcomes following ARDS have not been described, despite the possibility that ARDS patients are at risk for brain injury through hypoxemia or other mechanisms. In the current study 55 consecutive ARDS survivors completed a battery of neuropsychological tests and questionnaires regarding health status, cognitive and psychological outcomes at the time of hospital discharge and 1 yr after onset of ARDS. At hospital discharge, 100% (55 of 55) of survivors exhibited cognitive and affective impairments, as well as problems with health status which affected their quality of life. At 1 yr after ARDS, 17 of 55 (30%) patients still exhibited generalized cognitive decline. Forty-three of 55 (78%) patients had all or at least one of the following: impaired memory, attention, concentration and/or decreased mental processing speed. One year after ARDS a substantial portion of ARDS survivors exhibit impaired health status and cognitive sequelae which may be due to hypoxemia, emboli, inflammation, drug toxicity, and/or other etiologies.

Adolescent↗

Operational use and patient care in the monoplace hyperbaric chamber.

The author has made an attempt to describe presently available monoplace chambers, provide codes for their appropriate use in hospitals, and emphasize chamber safety. If appropriate safety precautions are not strictly adhered to, catastrophic accidents may occur, and have occurred. Critically ill patients may have indications for HBO and, indeed, can be treated with HBO in the monoplace chamber. This requires strict attention to detail and an understanding of critical care medicine as well as hyperbaric medicine. To facilitate care of these patients within the monoplace chamber several modifications have been implemented. Complete pulmonary and arterial hemodynamic monitoring, transcutaneous and laser Doppler monitoring, as well as vasopressors, sedation, paralysis, and mechanical ventilation can be supplied to patients treated with HBO within a monoplace chamber (Fig. 19). Suction within the monoplace chamber can be accomplished by adapting existing hospital equipment. Likewise, air breaks can be provided to all patients in the monoplace chamber, including those who are intubated and mechanically ventilated. These modifications have been presented here. Hemodynamic and intravenous access to the critically ill patient is important. Physiologic pressures, ECG, and typical intravenous setups have been described. Several techniques that the author has have personally found helpful have also been provided. The final section of this article presents clinical observations in a few critically ill patients. These anecdotes were only included to try to stimulate thought and hopefully an interchange of ideas that may help us deal more effectively with the management of these patients. This article also raises the question of what is the optimal arterial partial pressure of oxygen as opposed to merely treating the HBO patient with a standard protocol, particularly if the patient has a significant right-to-left shunt (anatomic or physiologic). It is hoped that further discussion, thought, and research can help elucidate answers to these questions.

Blood Gas Analysis↗

A computer-assisted management program for antibiotics and other antiinfective agents.

BACKGROUND AND METHODS: Optimal decisions about the use of antibiotics and other antiinfective agents in critically ill patients require access to a large amount of complex information. We have developed a computerized decision-support program linked to computer-based patient records that can assist physicians in the use of antiinfective agents and improve the quality of care. This program presents epidemiologic information, along with detailed recommendations and warnings. The program recommends antiinfective regimens and courses of therapy for particular patients and provides immediate feedback. We prospectively studied the use of the computerized antiinfectives-management program for one year in a 12-bed intensive care unit. RESULTS: During the intervention period, all 545 patients admitted were cared for with the aid of the antiinfectives-management program. Measures of processes and outcomes were compared with those for the 1136 patients admitted to the same unit during the two years before the intervention period. The use of the program led to significant reductions in orders for drugs to which the patients had reported allergies (35, vs. 146 during the preintervention period; P<0.01), excess drug dosages (87 vs. 405, P<0.01), and antibiotic-susceptibility mismatches (12 vs. 206, P<0.01). There were also marked reductions in the mean number of days of excessive drug dosage (2.7 vs. 5.9, P<0.002) and in adverse events caused by antiinfective agents (4 vs. 28, P<0.02). In analyses of patients who received antiinfective agents, those treated during the intervention period who always received the regimens recommended by the computer program (n=203) had significant reductions, as compared with those who did not always receive the recommended regimens (n= 195) and those in the preintervention cohort (n = 766), in the cost of antiinfective agents (adjusted mean, $102 vs. $427 and $340, respectively; P<0.001), in total hospital costs (adjusted mean, $26,315 vs. $44,865 and $35,283; P<0.001), and in the length of the hospital stay days (adjusted mean, 10.0 vs. 16.7 and 12.9; P<0.001). CONCLUSIONS; A computerized antiinfectives-management program can improve the quality of patient care and reduce costs.

Anti-Bacterial Agents↗

Neuropsychological impairments following hantavirus pulmonary syndrome.

Recently an outbreak of acute respiratory infection associated with the hantavirus occurred in the southwestern United States. Hantavirus pulmonary syndrome (HPS) is a life threatening illness that carries with it a high mortality rate. Patients with HPS experience prolonged periods of hypoxemia requiring mechanical ventilation and treatment in intensive care units. We have recently seen 2 survivors of HPS. A neuropsychological test battery was administered immediately following their acute hospitalization and at 1 year postrecovery from HPS. Both patients exhibited cognitive impairments immediately following HPS as well as persistent cognitive impairments at 1 year. The cognitive impairments seen in these two HPS survivors are similar to those seen in other patients who have experienced brain anoxia, including memory impairments. It is also possible that hantavirus may directly cause brain injury with concomitant cognitive impairments. Additional research needs to be carried out in order to determine the extent and severity of the cognitive impairments in survivors of HPS.

Female↗

Venous and arterial gas embolism associated with positive pressure ventilation.

We report a 53-year-old woman with ARDS who required positive pressure ventilation with positive end-expiratory pressure. She sustained an acute right ventricular myocardial infarction associated with cardiovascular instability. The next day she sustained a fatal cerebral arterial gas embolism. Intravascular gas was documented within the cerebral, coronary, and pulmonary arterial circulations. Clinicians need to be aware of venous and arterial gas embolism as a complication of mechanical ventilation.

Embolism, Air↗

Three dimensional image reconstruction of neuroanatomical structures: methods for isolation of the cortex, ventricular system, hippocampus, and fornix.

Magnetic Resonance (MR) imaging allows volumetric quantification of a variety of neuroanatomical structures using two dimensional (2D) images as well as three-dimensional (3D) reconstruction of the brain and any of its constituent parts. Three-dimensional analysis permits integration of the neuroanatomical changes which occur in pathologic states, with the cognitive and behavioral changes elucidated through neuropsychological assessment. This paper describes uniform methods for 3D neuroanatomical isolation of the neocortex, ventricular system, and hippocampus in both normal and pathologic states. The 3D methods are described in detail using two different software programs, ANALYZE and IMAGE. Three-dimensional neuroanatomical reconstructions were carried out on a patient who sustained a very severe traumatic brain injury. The 3D image analysis in the patient with traumatic brain injury, revealed structural changes in frontal and temporal cortex, ventricular dilation, and hippocampal atropy. The neuropsychological impairments in this patient, were consistent with the observed neuroanatomical changes revealed on 3D image reconstruction. This technology permits precise determinations of the extent and severity of the neuroanatomical changes which follow neurological injury disease.

Adult↗