Early medical abortion by telemedicine in the United Kingdom: a costing analysis.

OBJECTIVE: To determine the potential cost savings resulting from the introduction of routine early medical abortion (EMA) at home by telemedicine in the UK. DESIGN: A costing study. SETTING: The UK. POPULATION: Women in 2020 undergoing EMA provided by three independent abortion providers and two National Health Service (NHS) abortion clinics. METHODS: Computation of the costs of each abortion procedure and of managing failed or incomplete abortion and haemorrhage requiring blood transfusion. MAIN OUTCOME MEASURES: Cost savings. RESULTS: Overall estimated cost savings are £15.80 per abortion undertaken by independent abortion providers, representing a saving to the NHS of over £3 million per year. Limited data from NHS services resulted in an estimated average saving of £188.84 per abortion. CONCLUSIONS: Were telemedicine EMA to become routine, an increase in the number of women eligible for medical rather than surgical abortion, and a reduction in adverse events resulting from earlier abortion, could result in significant cost savings. TWEETABLE ABSTRACT: Early medical abortion at home using telemedicine could save the NHS £3 million per year.

Otolithic membranes of the saccule and utricle in man.

The otolithic membranes of the human saccule and utricle can be prepared as whole mounts or surface specimens for microscopic examination. They are not simple, homogeneous, gelatinous structures as heretofore described. Instead, each shows a definite and characteristic fibrillar design, which appears to be correlated with the known cytoarchitectural pattern of the underlying neuroepithelium.

Auditory intensity discrimination after selective loss of cochlear outer hair cells.

The contributions of the inner and outer hair cells of the mammalian cochlea to auditory intensity discrimination were evaluated in a combined behavioral-anatomical study of the guinea pig. Intensity difference thresholds were unchanged from baseline values after selective destruction of outer hair cells, suggesting that those cells are unnecessary for normal intensity discrimination.

The species-specific nature of the ototoxicity of dihydrostreptomycin in the patas monkey.

The remarkable susceptibility of the inner ear of the patas monkey (Erythrocebus patas) to the ototoxic action of dihydrostreptomycin (DHSM) (and streptomycin (SM)) is well established in this paper and affords a rare example of a species-specific reaction to a restricted class of compounds within the aminoglycoside group of antibiotics. In a series of experiments, behavioral and morphological observations together provided the following profile of DHSM ototoxicity in the patas monkey: Sudden onset of hearing loss beginning after 7-9 weeks of treatment; Substantial, though often partial, hearing impairment beginning at the high frequencies and progressing with or without continued treatment to the low frequencies; In the inner ear, a corresponding and selective loss of nerve fibers and of outer hair cells, relative to inner hair cells, beginning in the base of the cochlea and proceeding toward the apex; Continued and progressive loss of hearing for several months after cessation of drug treatment; and Non-auditory effects in some animals on the kidney and vestibular system. Results from control experiments confirmed this special relationship between the patas monkey and DHSM: Other nonhuman primates (macaques and vervet monkeys) were essentially unaffected by DHSM; The patas showed no equivalent sensitivity to other aminoglycosides such as kanamycin or to other forms of ototraumatic insult such as intense noise.

Threshold elevation at high frequencies of the auditory nerve action potentials in acute versus chronic recordings in guinea pigs.

Thresholds of the auditory nerve compound action potential (CAP) responses to filtered clicks from 0.5 to 40 kHz, defining a CAP frequency threshold curve, have been determined in the same guinea pigs: (1) in acute conditions, the animal still anesthetized at the end of the operation for permanent implantation of a round-window electrode, and (2) several days later in the implanted awake and unrestrained animal. The results show higher CAP thresholds for high frequencies in acute conditions as compared to chronic recordings. This difference appears above about 12.5 kHz and increases progressively to around 40 dB at 40 kHz. Similar effects, although somewhat less pronounced, were observed during anesthesia alone in already implanted guinea pigs. Thes observations could explain the discrepancies which appear between electrophysiological thresholds, acutely recorded either from single fibers or whole-nerve responses, and behavioral audiograms. Moreover, in the accurate evaluation of the cochlea, slight impairments may be masked by this phenomenon as illustrated in guinea pigs treated with low doses of ototoxic antibiotic.

Apical hair cells and hearing.

This study assessed the contribution of the apical hair cells to hearing. Guinea pigs, chinchillas and monkeys were behaviorally trained using positive reinforcement to respond to pure-tone stimuli. When a stable audiogram had been determined, each subject received one of three experimental treatments: ototoxic drug administration, low-frequency noise exposure, or the application of a cryoprobe to the bony wall of the cochlear apex. After post-treatment audiograms stabilized, subjects were euthanized and the percentage of hair cells remaining was assessed by light microscopy. Results indicate that a redundancy of encoding mechanisms exist in the mammalian cochlea for low-frequency stimuli. They also suggest that a very small percentage of apical hair cells are sufficient for some low-frequency hearing. Finally, data from this and other studies suggest that the low-frequency threshold shift caused by the loss of a certain percentage of apical hair cells is less pronounced than the high-frequency threshold shift caused by the loss of a comparable percentage of basal hair cells. These data agree with anatomical and electrophysiological evidence that functional as well as anatomical differences may exist between the apex and base of the cochlea.

Ototoxic and nephrotoxic effects of combined treatment with cis-diamminedichloroplatinum and kanamycin in the guinea pig.

Ototoxic and nephrotoxic potentiation with concomitant cis-diamminedichloroplatinum, or cis-platinum II (CSP), and aminoglycoside therapy was investigated in the guinea pig. We evaluated possible potentiation of the toxic effects of CSP and kanamycin compared with CSP alone in the inner ear and kidney and quantitatively localized CSP in the cochlea with gamma emission analysis of 195mPt. Kanamycin-treated animals demonstrated cytocochleograms and ABR waveforms, absolute latencies, and interwave latencies for waves I, II, and III similar to control animals at our maximum level of acoustic stimulation. CSP treatment produced 60% to 70% mean outer hair cell (OHC) loss in the basal turn of the cochlea, a reduction in ABR waveform and amplitude, and an increase in latencies of ABR waves I, II, and III. Combined CSP and kanamycin treatment produced 90% to 100% mean OHC loss in all rows of the basal turn of the cochlea, with no discernible ABR waveform corresponding to the region stimulated by a 4500 to 7000 Hz acoustic click. Combined treatment produced the most significant cortical medullary tubular necrosis and interstitial nephritis. Furthermore, this study reports for the first time localization of platinum in the inner ear.

Degeneration patterns in human ears exposed to noise.

Various forms of sensorineural degeneration patterns related to noise exposure are illustrated in six pairs of temporal bones selected from a group of 33 male patients with histories of noise exposure. For the entire group the commonest form of lesion, associated with a 4-kHz dip in the audiogram, was a relatively diffuse degeneration in the second quadrant of the basal turn, in the 9-13 mm area. An advanced form of this lesion had a wide gap of more or less complete sensorineural degeneration affecting the entire second quadrant and displaying various degrees of extension toward the apex and base. The pattern associated with an "abrupt high-tone loss," with more or less complete hair cell and nerve degeneration in both the second and first quadrants and extending to the basal end of the cochlea, was rare. In one case this pattern appeared to have evolved from the first type of lesion as the remaining nerve fibers in the first quadrant had degenerated. The protective effect of the acoustic shadow of the head for the right ear, in shooting from the right shoulder, is demonstrated for the higher frequencies. Two almost identical cases of sharply-circumscribed single areas of degeneration in the first quadrant and one case with two such areas represent the third type of lesion. In one of these cases there was a history of firearm usage. It is postulated that this type of lesion is caused by impulse noise. In most of the material the degeneration pattern differed markedly from the diffuse degeneration seen with presbycusis. Degeneration patterns with knife-sharp transitions between completely degenerated and apparently undamaged areas appear to be characteristic of noise-induced injuries.

Inner ear pathology associated with Reye's syndrome.

Severe pathological changes were observed in the inner ear tissues of a 2-month-old patient who died of Reye's syndrome after 5 days of hospitalization. In the organ of Corti, the inner hair cells appeared to be more severely damaged than the outer hair cells. Various degrees of degeneration were observed in all non-sensory epithelial cells lining the cochlear duct. In most turns of the cochlear duct, Reissner's membrane was ruptured and/or collapsed onto the organ of Corti. Likewise, both sensory and non-sensory cells of the vestibular end organs were markedly degenerated. These observations suggest that the inner ear tissues are acutely affected in patients with Reye's syndrome, and that the changes may cause impairment of hearing and/or equilibrium in patients who recover.

Functional and morphological changes in experimental endolymphatic hydrops.

Electrocochleograms (ECochG) in response to tone bursts and electronystagmograms (ENG) during sinusoidal rotational stimulation were monitored in guinea pigs equipped with chronically implanted round-window and periocular electrodes before and for as long as 90 days after uni- or bilateral surgical obliteration of the endolymphatic duct. The presence of cochlear and saccular endolymphatic hydrops was verified during microdissection of the inner ear, and cochlear hair cell counts were performed in some of the animals. The results indicate that in surgically-induced endolymphatic hydrops, cochlear and vestibular changes occur similar to those observed clinically in Menière's disease: fluctuant threshold shifts, threshold elevation at low frequencies, sensorineural loss at all frequencies with recruitment, increase in the ratio of summating potential to compound action potential (SP/CAP), asymmetry and recruitment in the ENG, and increased vestibular excitability, with occasional post-rotational and spontaneous nystagmus. Functional changes could not be clearly correlated with those seen by light microscopy, since hair cell loss was confined mainly to the apical coil. The observations indicate that the guinea pig with surgically-induced endolymphatic hydrops can be a useful model of Menière's disease, not only on morphological grounds, but also on the basis of functional changes, which over the relatively short term of observation represent a dysfunction rather than a loss of sensorineural structures.

The patas monkey as a model for dihydrostreptomycin ototoxicity.

Although the cochlear toxicity of dihydrostreptomycin (DHSM) is well-recognized in man, it has always proved difficult to demonstrate in animals. Hearing thresholds in M. nemestrina monkeys remained essentially unchanged after DHSM 100 mg/kg im daily for 8 months, but E. patas monkeys were severely deafened by DHSM 20 mg/kg for 90 days, a regimen formerly used in treating human tuberculosis. The patas monkey may prove to be the animal model of choice for evaluating aminoglycoside ototoxicity.

Hearing loss and cochlear pathology in monkeys after noise exposure.

Old World monkeys were exposed to octaveband noise from 0.5 to 8 kHz at 120 dB SPL, 8 hours daily for 20 days. Restricted permanent threshold shifts and localized loss of outer hair cells were produced, which were reasonably well correlated with the exposure frequencies. There was also a loss of both inner and outer hair cells at the extreme basal end of Corti's organ, regardless of the exposure frequency. Implications for human inner ear pathology are discussed.

Abnormal otoconia and calcification in the labyrinths of deaf Dalmatian dogs.

Abnormal mineral deposits from the membranous labyrinths of deaf Dalmatian puppies were examined microscopically. Most such deposits were located on the saccular otoconial membrane and were associated with collapse of the saccule and of Reissner's membrane. In both ears of one pup, crystals resembling otoconia were found on the surface of the stria vascularis. In two others, grossly abnormal crystals were seen on the utricular otoconial membrane, and in one of these crystals were also attached to the cupula of the left horizontal canal. In four animals the tectorial membrane was calcified. Most deposits consisted of apatite spherulites, but large multiple crystals (probably of calcite) were occasionally present. Some of the abnormal mineral deposits in the Dalmatian closely resemble those found in man, and they may originate in the same way.

Cochlear and vestibular lesions in capsular otosclerosis as seen in microdissection.

In 24 temporal bones from patients with otosclerosis prepared by the method of microdissection and surface preparations, otosclerotic foci could be clearly seen during removal of the otic capsule. The state of activity of each focus was estimated on the basis of its consistency and vascularity. Small anterior foci constituted the most common form of involvement of the otic capsule. All were judged to be inactive, and none of them appeared to have caused obvious sensorineural degeneration. No cases of "pure cochlear otosclerosis" were seen. Sensorineural degeneration was associated with large anterior foci which reached the upper basal turn. One specimen displayed a circumscribed sensorineural degeneration in the upper basal turn, with an almost exact correspondence between the location and extent of the cochlear lesion and the site of invasion by the otosclerotic process in the bone and endosteum bordering on scala media and scala tympani. It is postulated that a toxic factor had diffused from the focus and acted directly on the organ of Corti. When multiple foci were present they were usually poorly defined. The otosclerotic process involved the round window, with new lamellar bone formation in the scala tympant of the lower half of the basal turn. The most extensive sensorineural degeneration in the entire material was seen in this group. One specimen also had severe cochlear hydrops. In three specimens large shunts were observed to connect the otosclerotic foci with the cochlear vasculature, which was severely dilated. Where otosclerosis involved the endosteum of the scala tympani, loss of vessels was observed. One specimum with extensive active capsular otosclerosis had severe sensorineural degeneration of the vestibular system. Vestibular pathology in fenestrated ears is also described. In a specimen from a patient with no caloric reaction, numerous hair cells were present in the macular organs.

Cochlear and otoconial abnormalities in capsular otosclerosis with hydrops.

Temporal bones from four patients with capsular otosclerosis were examined by microdissection. Otoconia and abnormal crystalline deposits were studied by scanning electron microscopy and x-ray analytical methods. One patient showed more or less symmetrical invasion of the basilar membrane and osseous lamina by connective tissue from thickened endosteum adjacent to the larger anterior foci. In one ear sensorineural degeneration was circumscribed; in the other it was extensive and associated with cochleosaccular hydrops. Two other patients were deaf, with severe sensorineural degeneration; one had multiple active foci and evidence of cochleosaccular hydrops. In the fourth patient, who had small anterior foci, no specific inner ear pathology was found related to otosclerosis. In the hydropic labyrinths, apatite was present as abnormal deposits in the cochlear duct and as rigid crusts replacing the otoconia. Apparently these changes had been associated with abnormal labyrinthine fluid dynamics rather than with the otospongiotic process per se.

The effectiveness of pressure-reducing table pads as an intervention to reduce the risk of intraoperatively acquired pressure sores.

The purpose of this study was to determine the effectiveness of specialty pads as an intervention to reduce the incidence of intraoperatively acquired pressure sores. A convenience sample (N = 361) was drawn from all inpatients who underwent cardiothoracic or major vascular surgery on the standard operating room table (group 1), the air-filled pad (group 2), or the specialty foam pad (group 3). This sample was inclusive of 100% of patients during the study period who met the criteria. The incidence of pressure sore development was seven in group 1, zero in group 2, and one in group 3. There was at statistically significant difference (p = 0.0003) between group 1 and group 2. Additionally, a statistically significant difference (p = 0.0003) was found between group 1 and group 3. The foam pad and the air-filled pad were effective interventions for reducing the risk of intraoperatively acquired pressure sores.

Structure of the reticular lamina and repair after noise injury.

Laser Scanning Confocal Microscopy (LSCM) and specific labeling techniques were employed to examine the distributing of F-actin and microtubules in the reticular lamina of the guinea pig and monkey organ of Corti. Actin specific label was found in the circumferential belt of adherens junction at the borders between cells in the reticular lamina, and in the cuticular plate of hair cells. The distribution of actin in the adherens junction belt was asymmetric. Actin label was not found in the fonticulus, where the microtubule organizing center resides. Actin free areas were also found between the junctional actin and the cuticular plate. Microtubule specific label was very intense in supporting cells. In normal hair cells, the spatial distribution of tubulin at the reticular lamina is mutually exclusive with that of actin. After noise exposure, a belt of actin was found in the central portion of degenerating outer hair cells, possibly representing a constricted circumferential junction. Expanded supporting cells replaced degenerating hair cells and maintained the confluence of the reticular lamina during the dynamic process of scar formation. A complex network of actin-rich cables appeared at sites of degenerating inner hair cells, suggesting that more than two supporting cells are involved in scar formation for inner hair cells. LSCM proved an attractive method for analysis of the organ of Corti since preparation of the tissue is relatively rapid, preparation artefacts are minimized, different markers in the same specimen may be co-localized and out-of focus fluorescence blurring is eliminated.