Patient satisfaction following emergency admission via a surgical assessment unit and an emergency department.

AIM: Acute surgical patients are admitted to our regional hospital through the emergency department (ED) and through a new surgical assessment unit (SAU). The aim of this study was to compare the efficiency of the two units in seeing and assessing acute surgical patients, as well as patients' satisfaction with their experiences in both units. METHODS: A patient satisfaction scoring questionnaire was distributed to 115 consecutive surgical patients attending the SAU and ED over an 8-week period. Patients' impressions of waiting times, pain management and interactions with staff were detailed. The actual times taken for assessment, admission and discharge were recorded and compared with those perceived by the patients. RESULTS: Patients' perceptions of care were very high within both the ED and the SAU, with 95 % of SAU patients reporting their care as excellent or very good compared with 86 % of ED patients (p = 0.014). Patients were assessed considerably faster in the SAU compared with the ED, with an average wait from registration to admission or discharge totalling 5 h in the SAU compared with 12 h in the ED. CONCLUSION: The SAU provides an effective and efficient mode of assessment of acute surgical patients. While patients were discharged faster from the SAU than the ED, patients rated both units highly in terms of satisfaction with the service provided.

Proximal tibiofibular dislocation.

Proximal tibiofibular joint dislocation is an uncommon injury, which may be easily missed on plain radiography. If recognised, it can be treated in the emergency department, avoiding surgery and long term problems. The case is presented of a 22 year old male rugby player who was tackled from the left hand side while turning to the left. He heard a "pop" from his knee as he fell to the ground. Clinical examination revealed a prominence in the area of the fibular head. There was no evidence of peroneal nerve injury. Plain x rays confirmed a clinical suspicion for anterior dislocation of the proximal tibiofibular joint. Proximal tibiofibular joint dislocation typically occurs when the knee is slightly flexed and the foot is rotated and plantar flexed. Antero lateral dislocation is the most common pattern. Diagnosis is largely clinical, but the findings may be subtle. Plain films may not show any abnormality and computed tomography is the investigation of choice if there is clinical suspicion for the injury. The dislocation should be reduced in the emergency department, but controversy exists whether early mobilisation or casting is the most appropriate course of action.

Accident and emergency department access to the child protection register: a questionnaire survey.

OBJECTIVES: To ascertain how UK accident and emergency (A&E) departments access the child protection register, their levels of satisfaction with that access and their criteria for checking the register. METHODS: A postal questionnaire was sent to 254 "major" A&E departments listed in the 1996 British Association for Accident and Emergency Medicine directory. RESULTS: 190 questionnaires were returned (response rate 75%). Ninety (48%) responding departments access the register through the duty social worker, 33 (17%) use a computerised copy, 32 (17%) a hard copy and 27 (14%) a combination. Twenty seven of 33 respondents (82%) using a computerised copy were satisfied with their mode of access. This compares with figures of 21 (66%) for hard copy, 45 (50%) for duty social worker and 14 (50%) for a combination. No departments using the duty social worker checked all patients routinely compared with 23 (72%) for hard copy, 22 (67%) for computer copy and 12 (44%) for departments using a combination of modes of access. CONCLUSION: There is no uniformity of the way in which UK A&E departments access the child protection register and there is also substantial variation in the criteria used to check the register. This survey suggests that the most common form of access (via the duty social worker) often fails to meet the needs of A&E departments, principally because it takes so long.

Screening for carbon-bound phosphorus in marine animals by high-resolution 31P-NMR spectroscopy: coastal and hydrothermal vent invertebrates.

Animals of hydrothermal vents live in a unique environment that conceivably could lead to modifications of the usual phosphorus functional groups of importance in living systems. To explore this possibility, specimens of a sea anemone (unidentified) from the TAG hydrothermal field, Mid-Atlantic Ridge, the mussel Bathymodiolus N. sp. from the Mid-Atlantic Ridge, and the tubeworm Riftia pachyptila from the East Pacific Rise were analyzed for compounds containing the carbon&z.sbnd;phosphorus bond. The analysis was based on the use of 31P-nuclear magnetic resonance, which gives signals for C-P compounds that are well separated from those of biological phosphoric acid derivatives. The animals were extracted to provide a lipid- and a water-soluble fraction, leaving an insoluble, largely proteinaceous solid residue. The lipid and residue fractions were subjected to hydrolysis to release bound forms of phosphonic acids. All fractions were analyzed by 31P-NMR. Aminophosphonic acids [primarily NH2CH2CH2PO(OH)2 (1) and CH3NHCH2CH2PO(OH)2 (2)] represented the only type of C-P compound detected. These are well-known constituents of coastal invertebrates. For the mussel and sea anemone, these compounds were present in bound form in both the lipid and insoluble residue. The tube worm contained C-P material only in the insoluble residue, but in quite small amounts. The 31P-NMR method is especially valuable in being able to discriminate between compounds 1 and 2. By this technique, two coastal sea anemones (Tealia felina and Bunadosoma cavernata), previously thought to have 1 as the dominant aminophosphonic acid, were in fact found to be much richer in originally undetected 2. This compound was also detected for the first time in a mussel (Genkensia demissa).

Technetium-99m-MDP uptake in hilar lymph nodes in sarcoidosis.

We describe a patient with unexplained hypercalcemia who under went bone scintigraphy, which demonstrated marked tracer uptake within the hilar lymph nodes. The pattern strongly suggested sarcoidosis, which was subsequently confirmed by bronchoscopy-directed biopsy.

Simultaneous scintigraphic depiction of aldosteronoma and adrenal infarction.

Primary aldosteronism is a potentially curable cause of hypertension, especially when caused by an adrenal adenoma. Aldosteronomas because of their small size often elude techniques to locate them. This case illustrates the advantages, disadvantages and complications of noninvasive techniques used for their diagnosis. A patient with hypertension and hypokalemia underwent an adrenal venous effluent sampling for measurement of aldosterone concentrations. This procedure was complicated by an injury to the right adrenal gland. Subsequently, it was difficult to control the patient's hypertension and hypokalemia with medical therapy alone. A re-assessment years after his initial diagnosis included a CT scan, which now visualized a left adrenal tumor. The functional status of this tumor and lack of function of the previously injured right adrenal gland were demonstrated by NP-59 scintigraphy. This information modified the surgical intervention (adenectomy rather than total adrenalectomy) and the residual left sided adrenal tissue prevented adrenocortical insufficiency. A year later the patient remains euadrenal.

Evidence that pyrrole formation is a pathogenetic step in gamma-diketone neuropathy.

Previous studies from this laboratory have demonstrated that the addition of methyl groups at the 3 and 4 positions of the 2,5-hexanedione (2,5-HD) molecule results both in more rapid pyrrole formation and in enhanced neurotoxicity. In order to define more clearly the relationship between rates of pyrrole formation and neurotoxicity, the dl and meso diastereomers of 3,4-dimethyl-2,5-hexanedione (DMHD), 3,4-diethyl-2,5-hexanedione (DEHD), and 3,4-diisopropyl-2,5-hexanedione (DiPHD) were synthesized and purified. The rates of pyrrole formation were compared with that of unsubstituted 2,5-HD, and rates of in vitro crosslinking were determined. Each of the compounds was administered to rats to determine relative neurotoxicity. Hindlimb paralysis was reached after a total administered dose of 1.6 mmol/kg of dl-DMHD, while 5.9 mmol/kg of meso-DMHD was required. Paralysis was not achieved with either diastereomer of DEHD or DiPHD, although both produced systemic toxicity. Histologic sections of spinal cords and anterior roots from rats treated with DMHD revealed large neurofilament-filled axonal swellings, while more distal sections contained axons undergoing Wallerian-type degeneration. Neither axonal swellings nor Wallerian-type degeneration were seen in sections from spinal cord or peripheral nerve of rats treated with DEHD or DiPHD. The rates of pyrrole formation were in the order dl-DMHD greater than meso-DMHD greater than 2,5-HD greater than dl-DEHD greater than meso-DEHD greater than dl-DiPHD greater than meso-DiPHD, while in vitro crosslinking rates were in the order dl-DMHD greater than meso-DMHD greater than dl-DEHD greater than meso-DEHD greater than 2,5-HD greater than dl-DiPHD greater than meso-DiPHD. Cyclic voltammetry showed that the autoxidation of pyrroles derived from DMHD, DEHD, and DiPHD occurred more readily than that derived from 2,5-HD. In addition, we report for the first time the segregation of axoplasmic organelles in animals treated with DMHD, providing further evidence that the neurofilamentous axonopathies caused by such compounds as beta,beta'-iminodipropionitrile (IDPN), 2,5-HD and CS2 share a common underlying mechanism. The strong correlations between rates of pyrrole formation, rates of in vitro crosslinking and relative neurotoxicity are seen as evidence that pyrrole formation is a step in the pathogenetic sequence of gamma-diketone neuropathy.

dl- versus meso-3,4-dimethyl-2,5-hexanedione: a morphometric study of the proximo-distal distribution of axonal swellings in the anterior root of the rat.

The neurotoxicity of the dl and meso diastereomers of the gamma-diketone 3,4-dimethyl-2,5-hexanedione (DMHD) was studied to determine if the difference in rates of pyrrole derivatization would influence the clinical and morphological appearance of the neuropathy associated with these gamma-diketones. Two groups of rats received 0.2 mmol/kg/day intraperitoneal injections of their respective diastereomer, and two groups of control rats received comparable volumes of water. The dl-DMHD treated group reached the clinical end-point of hindlimb paralysis in a period of time threefold shorter than the meso-DMHD treated group, paralleling the in vitro kinetics of pyrrole formation with a model amine. A computerized morphometric analysis of cross-sectional axonal areas along the lengths of L4 and L5 anterior roots revealed that the dl-DMHD treated rats had axonal swellings more proximal and of smaller caliber than the meso-DMHD treated rats. 14C-labeled dl and meso diastereomers were synthesized and used to determine relative ability of the diastereomers to gain access to the nervous system. There was approximately 25% more dl-DMHD in the brain after 2 hr. The brain:serum ratios of the diastereomers, however, were equivalent. The more distal location of the neurofilament-filled swellings after meso-DMHD intoxication corroborates previous findings regarding toxicant potency and location of axonal swellings and suggests that the rate of neurofilament crosslinking determines the location of swellings along the length of the axon in the neurofilamentous axonopathies.

Hyperbaric oxygen accelerates the neurotoxicity of 2,5-hexanedione.

The molecular pathogenesis of n-hexane neurotoxicity has been postulated to proceed as follows: The gamma-diketone metabolite, 2,5-hexanedione (HD), reacts with lysyl-amino groups on neurofilaments to form imines. The imines cyclize to form pyrroles. The pyrroles autoxidize, resulting in covalent protein-protein crosslinking within or between neurofilaments. A resultant impairment of neurofilament transport is proposed to lead to neurofilament-filled axonal swellings. This experiment was designed to test whether oxidation is a necessary pathogenetic step in vivo by comparing time of onset of paralysis of an HD treated group of rats to that of a group receiving HD plus oxygen under high pressure (OHP). The group of rats receiving the hyperbaric oxygen treatment reached the endpoint of hindlimb paralysis significantly sooner than the group receiving none. The fact that OHP does accelerate HD neuropathy points towards an oxidative step in the molecular pathogenesis of gamma-diketone neuropathy.

Covalent crosslinking of neurofilaments in the pathogenesis of n-hexane neuropathy.

These studies test the hypothesis that in n-hexane neuropathy the gamma-diketone metabolite 2,5-hexanedione (2,5-HD) results in covalent crosslinking of neurofilaments via nucleophilic attack on oxidized pyrrole rings formed from the reaction of 2,5-HD with epsilon-amino groups of lysyl residues. The 2,5-HD analogue and gamma-diketone,3,4-dimethyl-2,5-hexanedione (DMHD), was found to result in more rapid pyrrole formation, pyrrole autoxidation, and protein crosslinking when compared with 2,5-HD. DMHD was 20-30 times more potent than 2,5-HD in producing hindlimb paralysis. Following 2,5-HD intoxication the neurofilament filled axonal swellings were found in the distal, subterminal axon. After treatment with DMHD, swellings were present in the proximal axon, similar to those seen after intoxication with beta,beta'-iminodipropionitrile (IDPN). DMHD was proposed as a connecting link between the proximal neurofilamentous axonopathy caused by IDPN and the distal neurofilamentous axonopathies from n-hexane, acrylamide, and carbon disulfide intoxication. [14C]DMHD was found to alkylate nerve protein and to result in polymers of radiolabeled protein too large to pass through nitrocellulose filters with pore sizes as large as 12 nm. An even greater proportion of radiolabeled protein was retained by nitrocellulose filters when DMHD was reacted with nerve in which SCa (slow component a of axonal transport) had been pulse-labeled with [35S] methionine. Radiolabeled nerve proteins acylated with [125I]Bolton-Hunter reagent were minimally retained by nitrocellulose filters, suggesting that filter retention reflects polymerization rather than non-specific adsorption.

In vitro evidence that covalent crosslinking of neurofilaments occurs in gamma-diketone neuropathy.

We have postulated that the toxic neuropathies associated with neurofilament-filled axonal swellings have a common pathogenesis, the covalent crosslinking of neurofilaments during anterograde transport. The newly described gamma-diketone, 3,4-dimethyl-2,5-hexanedione (DMHD), is a more potent analogue of the toxic metabolite of n-hexane, 2,5-hexanedione. The axonal swellings observed in DMHD toxicity are in the proximal axon, as seen in intoxication with beta, beta'-iminodipropionitrile, rather than in the distal axon, where neurofilamentous swellings are observed in n-hexane, carbon disulfide, and acrylamide neurotoxicity. In these studies, 14C-labeled DMHD and 2-butanone were synthesized and allowed to react with peripheral nerve. Only 14C-labeled DMHD resulted in stable radiolabeled protein polymers, which were retained by nitrocellulose filters with pore sizes as large as 12 microns. More specific evidence for covalent crosslinking of neurofilaments was obtained when DMHD was allowed to react with peripheral nerve in which the neurofilaments had been pulse-labeled with L-[35S]methionine.

Phencyclidine and phenylcyclohexene disposition after smoking phencyclidine.

Five men who smoked parsley cigarettes containing 100 micrograms of [3H]-phencyclidine hydrochloride (PCP.HCl) inhaled 69 +/- 5(SEM) % of the total radioactivity in the cigarette. Both PCP and its pyrolysis product, 1-phenylcyclohexene (PC), were found and measured in plasma. Calculations based on the assumption that the ratio of these two products was the same as in simulated smoking studies and based on either area under the curve or urinary excretion of PCP indicated that most of the PCP in smoke was absorbed. Mean half-life (t1/2) of PCP (24 +/- 7 hr, harmonic mean 18 hr) and ratios of metabolites in plasma and urine were close to those previously reported after intravenous and oral doses. A second peak in PCP plasma concentrations was observed, possible due to show efflux from the lungs. PC plasma concentrations (maximum 0.35 +/- 0.06 pmol/ml) were lower than those of PCP (maximum 0.62 +/- 0.09 pmol/ml) and its mean t1/2 (14 +/- 3 hr, harmonic mean 12 h) was shorter than that of PCP. Only traces of PC were found in urine. Only small amounts of metabolites from PC were found nonconjugated in plasma (to about 0.1 pmol/ml) or urine (less than 2% of radioactivity), but larger quantities were found as enzyme-hydrolyzable conjugates in urine (6% of radioactivity). Conjugates were also found in plasma (to about 0.12 pmol/ml).