PubMed Health⌕ Search

Biomedical subjects

A Hendrich

Publications and source records attributed to A Hendrich.

8 recordsLinked to original sources
PubMed1995

Hospital falls: development of a predictive model for clinical practice.

A retrospective case-control study related to falls was conducted at an 1,120-bed acute care tertiary hospital. The case (fall) sample consisted of 102 falls and 236 control (nonfall) charts during a 1-month period. An instrument developed by Hendrich (1988) was modified for use in the study. Demographic data and risk factors were recorded. Descriptive statistics included risk factor percentages for each sample and the corresponding univariate relative risks. Logistic regression was used to develop a multivariate risk factor model with seven risk factors. The significant risk factors were recent history of falls, depression, altered elimination patterns, dizziness or vertigo, primary cancer diagnosis, confusion, and altered mobility. The adjusted relative risks were converted to risk points to be used to assess a patient's level of fall risk. Within the data set, a sensitivity of 77% (79 of 102) and specificity of 72% (169 of 236) were calculated. The model was cross-validated in a 1987 data set with a sensitivity of 83% (59 of 71) and specificity of 66% (106 of 161).

Accidental Falls↗
PubMed1990

Hormonal changes in brain dead patients.

Thirty neurologically impaired (Glasgow Coma Score less than 7) patients were evaluated to determine if changes in serum levels of thyroid hormone, cortisol, insulin, or lactate suggest that replacement therapy is needed before removal of organs for donation. Serum levels of free thyroxine (fT4), thyroid-stimulating hormone (TSH), reverse T3 (rT3), cortisol, insulin, and lactate were monitored in 16 patients before and after brain death and in 14 additional patients who were similarly compromised but did not become brain dead. Low fT3, normal fT4, and normal or high rT3 as found in most patients were consistent with a variant of the euthyroid sick syndrome although TSH was elevated in some patients. Cortisol, insulin, and lactate levels were also normal or high. No correlation was found between low thyroid hormones and elevated lactate or the amount of vasopressor needed to sustain BP. No significant changes occurred in hormone or lactate levels after brain death. The explanation for an elevated lactate remains unclear but we do not believe this single finding justifies the diagnosis of a hypothyroid state in these patients or the administration of thyroid hormone to brain dead organ donors.

Adult↗
PubMed1987

The role of group structure in the action of some morpholinium chloride derivatives on model systems.

Effects of morpholinium chlorides, which exhibit fungicidal activity, on model lipid systems is discussed. It was shown by means of DSC and BLM techniques that for different salts possessing alkyl chains of identical length, the interaction with lipids depends strongly on the polar head charge and the structure of the salt. The results obtained and conclusions drawn can be useful in explaining the possible mechanism of the biological effectiveness of the compounds tested; this is suggested by the observation that salts tested showed the same sequence of activity in both biological tests and model experiments.

Antifungal Agents↗
PubMedDate not supplied

Changes in serum catecholamine levels in patients who are brain dead.

Prospective blood samplings from 15 patients admitted with a Glasgow Coma Score of less than 7 were obtained to observe and compare epinephrine, norepinephrine, and dopamine serum levels in patients with brain injury before, after, and in the absence of brain death. Nine of the patients developed or were admitted after brain death. Wide variations in catecholamine blood levels over time were documented, and subgroup analysis precluded useful statistical comparison or inference of the data. The data are presented therefore as descriptive observations only. No apparent differences were noted between similarly injured patients in whom brain death did not develop and patients before brain death or between patients with penetrating versus nonpenetrating brain injury. Brain death was preceded by hypertension and corresponding elevations in serum catecholamine levels in one patient with complete data. Catecholamine levels appeared to fall after brain death in most patients. Only minimal changes in myocardial histology were present in three donor hearts, and the two transplanted hearts functioned satisfactorily. Serum catecholamine measurement or monitoring does not provide a precise method of determining potential injury to the donor heart before or after brain death. Other experimental data and clinical observation indicate that some hearts may be injured in the donor during the evolution of brain death. Pharmacologic intervention may prevent such injury in experimental animals but must be used before brain death is induced. Such interventions should be studied in selected human donors before brain death to determine whether cardiac function is improved in the donor or recipient.

Adult↗