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Tonsilloadenoidectomy is performed over 340,000 times per year in the United States, usually as a same day admission procedure with a postoperative overnight stay. Because of the current emphasis on reducing health care costs, many insurers are requiring the procedure of tonsilloadenoidectomy be performed on an outpatient basis, even though there is a lack of data supporting the safety of such a requirement. The charts of 2,944 pediatric patients who underwent tonsillectomy and/or adenoidectomy from January 1, 1983 to December 31, 1984 were reviewed. Analyses revealed predictive variables that could be used to identify patients with a low risk of complications. Nineteen percent of the patients could be released 4 hours postoperatively with an 8.1% chance of subsequent complications. No patients who underwent the combined procedure of tonsillectomy and adenoidectomy were in this group. Of the remaining patients, 0.4% could be released 6 hours after surgery, or 85.9% could be released 8 hours after surgery, or 98.2% could be released 10 hours after surgery, all with a less than 10% chance of subsequent complications. This study supports keeping tonsilloadenoidectomy patients at least 8 hours and possible 10 hours after surgery to minimize the risk of complications after discharge. [ABSTRACT FROM AUTHOR]

Facial fractures may portend intracranial and skullbase injury and may lead to rapid compromise of the airway. Primary care physicians may provide emergency care for patients who have sustained facial trauma. After immediate resuscitation and stabilization, management of facial fractures requires knowledge of the anatomy, rapid treatment methods and identification of potential associated injuries for each type of facial fracture. Differentiation between the life-threatening aspects of these injuries and the less urgent, but more apparent, facial injuries will lessen the risk of complications such as bleeding, meningitis and asphyxia. Knowledge of the anatomy of the facial skeleton and of the potential injuries associated with each of the various types of facial fractures will facilitate effective management decisions. Consultation should be sought when functional features are involved or when the injury threatens to produce future cosmetic anomalies.

Background: Perichondrial cutaneous grafts (PCCGs) are composite grafts comprised of skin and subjacent perichondrium. Animal models and preliminary clinical reports have shown that PCCGs are thicker, survive better and contract less than full-thickness skin grafts, and are simpler to perform that alternative reconstructive methods such as two-stage flaps., Objective: The applicability of PCCGs to surgical defects following Mohs surgery was investigated., Methods: PCCGs were used to reconstruct patients with surgical defects following Mohs excision of skin cancers from facial sites near free anatomic margins and in defects with exposed cartilage., Results: A series of cases is described, all with good to excellent cosmesis and function., Conclusion: PCCGs are useful in reconstruction of defects following Mohs excision of skin cancers.

Fifteen days after transection of the hypothalamo-neurohypophysial tract at the lateral retrochiasmatic hypothalamic area, neurosecretory axons had vigorously regenerated into transplants of explanted hypophysial neural lobe, to a lesser extent into sciatic nerve transplants, and least into optic nerve transplants. Regenerating axons were always closely associated with the specific glial cells of these grafts. When these glial cells were killed by cryotreatment prior to transplantation, neurosecretory axons did not regenerate into the abundant extracellular matrix of the transplants, including persisting basal lamina tubes in neural lobe and sciatic nerve grafts. The presence of viable glial cells is a prerequisite for neurosecretory axon regeneration.

Neural lobes that had been explanted 30 days earlier were transplanted into retrochiasmatic lesions of the hypothalamo-neurohypophysial tract 15 days before being observed by electron microscopy and neurophysin immunohistochemistry. Neurovascular contact regions consisting of microvascular networks surrounded by neurophysin-immunoreactive terminals developed in 86% of the grafted explants. The fine structure of such regions resembled that of the neural lobe, with palisades of neurosecretory axon terminals abutting the basal laminae associated with the microvessels and plexuses of neurosecretory axons occupying the spaces within the vascular network. Both continuous and fenestrated blood vessels were present. Lamellopodia from glial cells partially ensheathed both axons and terminals, and sometimes separated the terminals from the perivascular basal lamina. Profiles in which neurosecretory granulated vesicles were depleted and many microvesicles were present were interpreted as terminals from which hormones had been released. No regeneration occurred into explants that had been cryotreated to kill their pituicytes and other cells before transplantation. These observations demonstrate that neurosecretory axons served in the hypothalamus can regenerate to form a new neural lobe-like structure when an appropriate microenvironment is available, and that neural lobes explanted 21 days earlier retain the elements required to supply that microenvironment. They also provide evidence that viable pituicytes are essential for regeneration of neurosecretory axons and terminals into transplanted explants.

Fifteen days after bilateral transection of the hypothalamo-neurohypophysial tract at the level of the lateral retrochiasmatic area, neurovascular contact regions had developed proximal to 66% of the lesions. Contact regions developed in every case when neural lobe explants were placed into the lesions, and near approximately half of the lesions into which small pieces of sciatic or optic nerve were transplanted. Neurovascular contact regions were characterized by microvascular networks surrounded by dense neurophysin-immunoreactive plexuses. At the fine structural level, the organization of such regions resembled that of the neural lobe, with the single exception that capillaries were not fenestrated. Numerous neurosecretory axons were present, and palisades of neurosecretory axon terminals abutted perivascular basal laminae. Lamellopodia from glial cells partially ensheathed regenerating neurosecretory axons and often lay between terminals and the perivascular basal lamina. Terminals with many microvesicles and few neurosecretory granulated vesicles provided morphological evidence of hormone release.

Lesions of the tissue surrounding the preoptic recess (AV3V region) have severe effects on body fluid homeostasis; these include acute adipsia and failure of the antidiuretic response. Because neurosecretory cells in supraoptic nuclei comprise the major source of antidiuretic hormone (ADH) in this species, we have previously observed the fine structure of supraoptic nuclei in rats with AV3V lesions. Paraventricular nuclei are the other major source of ADH in rats. Therefore, in this investigation we compared the fine structure of paraventricular nuclei in rats which had received AV3V lesions 3 days earlier with that of control rats which had received sham lesions and either had drinking water available or had water withheld for 3 days. Degenerating axons and axon terminals were present in paraventricular nuclei of lesioned rats. The degenerating terminals were in axodendritic and less often in axosomatic synapses. Morphometric evaluation revealed that neurosecretory cells did respond to the dehydrated state of the adipsic-lesioned animals, but the response was significantly attenuated compared to that which occurred in sham-lesioned rats deprived of water for 3 days. It appears that AV3V lesions damage afferent connections and impair the response of neurosecretory cells to dehydration in paraventricular as well as supraoptic nuclei. However, in paraventricular nuclei the response is not completely prevented by AV3V lesions during the adipsic period as was observed in supraoptic nuclei. The presence of a response in paraventricular nuclei may be at least partially stimulated by reduced body fluid volume. Information from volume receptors would be carried from the medulla to paraventricular nuclei by ascending pathways which are not affected by AV3V lesions.

Accidental ingestion and impaction of disc batteries in the esophagus has been a constant predictor of severe morbidity presumably due to leakage of highly caustic potassium or sodium hydroxide contained in these electric cells. Fewer than ten reports of esophageal burns from disc battery ingestion have appeared in the medical literature; an additional case involving ingestion of a mercury disc battery was recently encountered at the James Whitcomb Riley Hospital for Children, Indiana University School of Medicine. Two children died as a direct result of the impaction and resultant esophageal burn; six children experienced perforation of the esophagus, with four children developing tracheoesophageal fistulae. We report the ingestion of a 1.35-V mercury camera disc battery by a 10-month-old girl in whom a severe burn of the anterior midesophagus was noted 18 to 22 hours after impaction. The child subsequently developed a tracheoesophageal fistula and esophageal stricture at the site of the burn and required tracheotomy, closure of the fistula, partial esophagectomy and gastrostomy for eventual successful management. Stimulated by this experience, we have conducted an in vivo study of the time course and severity of esophageal burns resulting from alkaline and mercury battery ingestion in 15 cats. Mucosal damage can be seen as early as one hour after ingestion, rapidly progressing to involvement of all muscular layers by four hours. Removal of this foreign body should be assigned highest priority to prevent rapid development of these burns and the long-term sequelae mentioned above.(ABSTRACT TRUNCATED AT 250 WORDS)

In this investigation we have observed the effects of withholding water for 5 days, the effects of long-term (5 weeks) lesions of the tissue surrounding the preoptic recess in the anteroventral third ventricle (AV3V region), and the interaction of the effects of long-term AV3V lesions and water deprivation on paraventricular nuclei. The purpose of these observations was to see if recovery of the antidiuretic response after AV3V lesions is associated with recovery of fine structural responses in these neurosecretory cells. Paraventricular neurosecretory cells of rats deprived of water for 5 days were hypertrophied in controls and in rats with AV3V lesions. Areas of cell bodies and their nuclei were increased, as were the number of Golgi stacks and electron dense (immature) neurosecretory granules. A greater percentage of nucleoli were adjacent to the nuclear envelope. Paraventricular neurons of rats with AV3V lesions also had fine structural changes characteristic of increased secretory activity, even in animals with free access to drinking water. The areas of cells and their nucleoli in coronal sections, and the number of Golgi stacks and electron-dense neurosecretory granules per cell were significantly increased in both treatment groups with AV3V lesions. There was a greater increase in the numbers of Golgi stacks and immature neurosecretory granules tended to be more numerous in water-deprived lesioned rats than in water-deprived controls. We suggest that recovery of body fluid balance in rats with chronic AV3V lesions involves enhanced secretory activity of neurosecretory cells in paraventricular nuclei, possibly stimulated via undamaged descending connections from the subfornical organ and by ascending pathways activated by cardiovascular volume receptors.

Small lesions of the tissue surrounding the anterior ventral third ventricle (AV3V) cause adipsia, but there is no compensatory antidiuretic response. Therefore, the fine structure of the supraoptic nucleus and neural lobe, the major sites of synthesis and release of antidiuretic hormone (ADH), were compared in rats rendered adipsic by AV3V lesions 3 days earlier, rats deprived of water for 3 days and rats drinking normally. In sham-lesioned rats which were deprived of water, neuronal somas in the supraoptic nucleus show signs of stimulated secretory activity. However, the neuronal somas of supraoptic nuclei of rats which did not drink because they were made adipsic by AV3V lesions resemble those of normally hydrated controls. Neural lobes of water deprived animals contain a sharply reduced number of neurosecretory granulated vesicles and reduced apposition of glial processes with the perivascular connective tissue compared to those of normally hydrated rats. In contrast, neural lobes of rats with AV3V lesions contain large accumulations of densely packed neurosecretory vesicles, as well as abundant dense bodies and multilamellar bodies which may be evidence of increased crinophagy, and they have increased interposition of glial processes between axon endings and the perivascular connective tissue. In rats with AV3V lesions the severe dehydration due to adipsia was unable to stimulate release of ADH. The accumulation of neurosecretory vesicles in the neural lobe indicates that transport of ADH to the neural lobe was not impaired in this time period, but that exocytosis of ADH-containing neurosecretory vesicles in the neural lobe was blocked.

Lesions of the tissue surrounding the preoptic recess (anteroventral third ventricle (AV3V) region) have been shown to severely impair normal mechanisms of body fluid homeostasis, including the antidiuretic response. In an earlier investigation of the pathways affected by these lesions, coronal cuts were placed between the level of the organum vasculosum lamina terminalis in the AV3V region and the level of the supraoptic nuclei. Rats with such cuts exhibited hyperdipsia and polyuria, but their plasma levels of antidiuretic hormone (ADH) were elevated. The fine structure of the supraoptic nucleus, a major site of ADH production, and of the neural lobe of the hypophysis, where ADH is released, were observed in rats with similar cuts. Although neural lobes showed evidence of hormone depletion and degenerating axons and terminals were present in supraoptic nuclei, there was no morphological evidence that neurosecretory cell bodies in supraoptic nuclei were affected by these cuts. Therefore, in this investigation we observed the ultrastructural effects of such cuts on paraventricular nuclei, which are the other major source of ADH. Degenerating axons and terminals were common in paraventricular nuclei of lesioned rats, both in the major magnocellular subnucleus and in the periventricular region. Cell bodies and nuclei of neurosecretory cells were not significantly larger in lesioned animals, but morphometric evaluations revealed dispersion of the Golgi complex and alterations in the rough endoplasmic reticulum of the cells. In addition, more multiple nucleoli were present, and nucleoli tended to lie adjacent to the nuclear envelope more frequently. We conclude that the neurosecretory cells in the paraventricular nuclei become more active in rats with these knife cuts.

Electrolytic ablation of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) alters fluid and electrolyte regulation. In addition, these lesions produce neural degeneration in the supraoptic nucleus (SON) and neural lobe, which suggests a neural pathway from the AV3V region to the SON. To determine if pathways in this brain area may mediate some of the effects which follow AV3V periventricular ablation, food and water ingestion, urine volume, and body weight, as well as drinking responses to a number of dipsogenic challenges were determined following placement of small knife cuts between the level of the organum vasculosum lamina terminalis (OVLT) and the SON. Metabolism measurements were taken daily for 7 days following either knife cuts or control operations, and again 4 weeks after surgery. Drinking responses following subcutaneous injections of angiotensin II, water deprivation, and cellular dehydration were determined at least 2 weeks after surgery. Rats with knife cuts exhibited an increase in water ingestion and urine volume, an enhanced water consumption following water deprivation and acute cellular dehydration, and did not gain weight at the same rate as control operated rats. The hyperdipsia following cellular dehydration was abolished by bilateral nephrectomy. These data indicate that a neural pathway coursing through this brain region is critical for fluid regulation and maintenance of body weight.

In previous investigations, lesions of the AV3V region surrounding the preoptic recess in the rat caused acute loss of the antidiuretic response to severe dehydration. Ultrastructural study of the supraoptic nuclei and neural lobes following several days of adipsia revealed a lack of response in neurosecretory cell bodies, which would normally show hypertrophy, and engorgement of axon terminals in the neural lobe with unreleased hormone, which would normally be depleted. When rats with such lesions were sustained through the acute phase, they regained their ability to concentrate their urine maximally in response to water deprivation, but their antidiuretic responses to angiotensin II or centrally injected hypertonic saline were still impaired. In this study we compared the fine structure of supraoptic nuclei and neural lobes of rats with AV3V lesions and rats with sham lesions after a recovery period of 5 weeks. We also compared responses to 5 days of water deprivation in lesioned and sham lesioned rats. Neurosecretory cell bodies in lesioned rats were smaller and contained fewer neurosecretory granulated vesicles, and axon terminals in the neural lobe contained more neurosecretory granulated vesicles compared to controls. In addition, the basal lamina surrounding fenestrated capillaries was covered to a greater degree by pituicyte processes in neural lobes of lesioned rats. Lesioned rats deprived of water for 5 days had changes in supraoptic nuclei and neural lobes which in general were qualitatively similar to those of controls. However, AV3V lesions blocked the increase in neurosecretory granulated vesicles in cell bodies in supraoptic nuclei and significantly inhibited depletion of neurosecretory granulated vesicles from axon terminals in the neural lobe of water deprived rats. We conclude that after 5 weeks of recovery the neurosecretory system had regained its ability to respond to dehydration, but the response was chronically affected by AV3V lesions.

Lesions of the tissue surrounding the anteroventral third ventricle (AV3V) alter mechanisms controlling body fluid homeostasis and hemodynamics. A period of adipsia and impaired antidiuresis follows AV3V destruction, which causes lesioned animals to become severely dehydrated. In lesioned rats, mechanisms maintaining water balance appear to be refractory to angiotensin and osmotic stimuli. To further investigate the neural basis for the observed alterations in body fluid balance, the supraoptic nucleus (SON) and subfornical organ (SFO) of rats with adipsia-producing lesions in the AV3V were examined by electron microscopy. In SONs of lesioned rats, degenerating fibers and terminals were present. Degenerating axonal terminals were seen in both axodendritic and axoaxonal synapses on magnocellular neurosecretory cells. These affected terminals in the SONs of lesioned rats may arise from osmoreceptors and angiotensin receptors which have somas or fibers in the lesioned area. Some fibers containing neurosecretory granulated vesicles also underwent degeneration. Neuronal somas displaying retrograde degenerative changes were present in SFOs after AV3V lesions. Degenerating fibers, some of which may be fibers of passage through the SFO, were common. However, little evidence of degenerative changes was seen in axon terminals in the SFOs. The evidence that lesions in the AV3V damaged an efferent projection field of the SFO is discussed in light of reports that AV3V lesions destroy responses in which the SFO is believed to participate.

Electrolytic lesions of tissue surrounding the preoptic recess (AV3V region) appear to cause loss of stimulatory input to the supraoptic nuclei from angiotensin receptors and osmoreceptors. To investigate the pathways affected by AV3V lesions, we observed the ultrastructural effects of coronal cuts in a plane caudal to the organum vasculosum lamina terminalis upon supraoptic nuclei and neural lobes of rats. Like AV3V lesions, these cuts caused degeneration of axons and terminals in the supraoptic nuclei. Degenerating terminals lay in axodendritic synapses and in axosomatic synapses on neurosecretory cells. Unlike AV3V lesions, the cuts did not result in an appearance of decreased secretory activity in the supraoptic nuclei or decreased release of hormone from the neural lobe. On the contrary, terminals in the neural lobe tended to be depleted of neurosecretory material, and glial cell processes tended to be withdrawn from the secretory interface at the basal lamina surrounding fenestrated capillaries; both are changes which have been associated with enhanced hormone release. We suggest that inhibitory input to the supraoptic nuclei is lost as a result of these cuts.