Late-phase allergy and eustachian tube dysfunction.

OBJECTIVE: This study investigated the role of late-phase allergy in the development of otitis media with effusion. METHODS: Brown Norway rats were sensitized to ovalbumin and later challenged transtympanically. Eustachian tube ventilatory function was assessed 2, 4, 8, 24, 28, and 32 hours postchallenge by measuring passive opening and closing pressures, active clearance of positive and negative middle ear pressure, and mucociliary clearance. RESULTS: The results demonstrate that exposure to transtympanic allergen induces eustachian tube dysfunction and subsequent formation of effusion. Allergic animals showed significant increases in passive and active opening pressures, as well as a decreased ability to actively clear middle ear pressure. Finally, the mucociliary was significantly impaired in all sensitized rats exposed to transtympanic allergen. CONCLUSION: These findings demonstrate that late-phase allergy leads to significant eustachian tube dysfunction and subsequent formation of effusion by impairing the ventilatory and clearance functions of the eustachian tube.

Function of the eustachian tube after weekly exposure to pepsin/hydrochloric acid.

OBJECTIVE: To determine the effects of repeated pepsin/hydrochloric acid (HCl) exposure on the eustachian tube (ET). STUDY DESIGN AND SETTING: ET function was studied in 22 rats. Group I (control) rats received transtympanic phosphate buffered saline solution; groups II (0.5 mg/ml) and III (2.0 mg/ml) received transtympanic pepsin/HCl. Test solutions were applied on day 0 with ET function evaluated on days 1, 2, 3, and 7 after exposure. Each 7-day period represents 1 cycle; all groups underwent 4 cycles. ET function was evaluated using passive opening and closing pressure, and active clearance of positive and negative pressure tests. RESULTS: Rats exposed to pepsin/HCl had elevated passive opening pressures and a decreased ability to clear positive and negative pressure. A temporal relationship exists. CONCLUSION: The results suggest middle ear exposure to pepsin/HCl leads to ET dysfunction in rats, and that this dysfunction is enhanced with repeated exposures. SIGNIFICANCE: Gastroesophageal reflux may induce ET dysfunction.

Non-insulin-dependent diabetic microangiopathy in the inner ear.

UNLABELLED: Hearing loss has long been associated with diabetes mellitus. Microangiopathy, associated with thickening of the basement membranes of small vessels, has been implicated as a major source of multiple system organ disease. OBJECTIVE: This study was designed to evaluate changes in basement membrane thickness in the inner ear of laboratory animals suffering from non-insulin-dependent diabetes mellitus (NIDDM) with, and without, exposure to moderate intensity noise exposure in an attempt to extrapolate the same disease process in humans. DESIGN: Spontaneously hypertensive-corpulent non-insulin-dependent rats (SHR/N-cp) were selected as a genetic model for the above study. Both lean and obese rats were used in this study. A genetically similar control group of animals (LA/N-cp) were used as controls. These animals express both the lean and obese phenotypes, but they lack the NIDDM gene. Forty-eight animals in each group were sacrificed at the end of the study. The cochleas were dissected and fixed. The basement membrane of the stria vascularis was examined using transmission electron microscopy. SETTING: This study was a laboratory-based, standard animal study. MAIN OUTCOME: This study was designed to show microangiography of the inner ear as related to NIDDM with, and without, obesity and noise exposure. RESULTS/CONCLUSIONS: NIDDM alone does not cause statistically significant basement membrane thickening; however, NIDDM in combination with obesity and/or noise exposure did show significant thickening and the combination of all three showed the greatest thickening. NIDDM appeared to be the greatest contributing factor.

Single-stage laryngotracheal reconstruction: the Great Ormond Street experience and guidelines for patient selection.

OBJECTIVES: To review all patients undergoing single-stage laryngotracheal reconstruction and to determine guidelines to predict successful outcomes and prevent the necessity of tracheotomy following laryngotracheal reconstruction. DESIGN: Chart review. SETTING: Tertiary care children's hospital. PATIENTS: A retrospective chart review was performed at our institution involving all patients who underwent single-stage laryngotracheal reconstruction from 1993 through 1996. A total of 28 patients were reviewed. RESULTS: Based on this chart review, a statistically higher incidence of extubation complications (P = .045), ie, bleeding, reintubation, or subcutaneous emphysema, occurred in children who weighed less than 4 kg. Although not statistically significant (P>.99), the relative risks of failure, defined as tracheotomy dependent or significant airway compromise following single-stage laryngotracheal reconstruction, were 3.43 if the child's weight was less than 4 kg at the time of surgery and 2.31 if the gestational age was less than 30 weeks at the time of surgery. Length of time for intubation did not appear to have any effect on outcome. CONCLUSIONS: Patients' gestational age and weight at the time of surgery appear to have the most impact on successful outcome. Children weighing more than 4 kg and those with gestational age of greater than 30 weeks appear to have a greater chance at successful extubation and eventual patent airway. Duration of intubation following single-stage laryngotracheal reconstruction does not appear to affect outcome.

Orbital osteology: a study of the surgical landmarks.

This study was conducted to re-examine the osteological anatomy of the orbit. Previous studies examined dried human skulls; this study looks at cadaveric specimens in a population that more closely resembles the population in the United States. Measurements were made of the bony orbit to define safe distances for surgical intervention and to identify distances to intraorbital fissures, canals, and foramina. Safe distances to the optic nerve were identified by subtracting 5 mm from the shortest measured specimen. The safe distances were as follows: medial quadrant, 29 mm; inferior quadrant, 39 mm; superior quadrant, 38 mm; and lateral quadrant, 36 mm. Staying close to the bony wall, not exceeding these parameters, and careful identification of anatomical structures should keep the surgeon from inadvertent damage to the intraorbital structures.

Unilateral supraglottitis in adults: fact or fiction.

Supraglottitis and epiglottitis have been described for many years by various authors. Haemophilus influenzae type b is the primary cause of childhood epiglottitis, which classically appears between the ages of 2 and 4 years. Onset is usually acute and the presentation can be dramatic with drooling, high temperatures, and stridor. Compared to childhood supraglottitis, adult supraglottitis usually pursues a more indolent course with no significant airway compromise and no identifiable pathogen. Rarely, adult supraglottitis can resemble its childhood counterpart with acute respiratory compromise secondary to H. influenzae infection. Although most incidences of adult supraglottitis are infectious in origin and involve the entire supraglottitis and epiglottis, we present two cases of unilateral supraglottitis caused by inhalation of a hot wire screen used as a filter for smoking crack cocaine.

Regeneration of the neurohemal terminals for identified cerebral neurosecretory cells in an insect.

The axons of specific neurosecretory cells, L-NSC III, in the brain of the tobacco hornworm, Manduca sexta, were transected during larval-pupal development to study the effects of this type of lesion on these peptidergic neurons and to begin to identify factors that may regulate their regeneration and growth. The two somata of these bilaterally paired neurons produce the prothoracicotropic hormone and are located in the pars intercerebralis. Their axons exit from the contralateral brain lobe via a retrocerebral nerve and pass through the corpus cardiacum before terminating at the glandular corpus allatum. At the corpus allatum, the L-NSC III axons arborize to form the terminal neurohemal organ for prothoracicotropic hormone release. The retrocerebral nerve was severed either in vitro followed by brain transplantation or in situ; in either protocol, the distal axon segments and corpus allatum were removed. The ability of the injured L-NSC III axons to regenerate was assessed immunocytologically by using a monoclonal antibody against the prothoracicotropic hormone. In both treatments, the proximal axon stumps exhibited regenerative growth as early as 1 day after axotomy, and, by the third day, neurites had extended. By the fifth day, the regenerating axons had branched to form terminal varicosities similar to those of a normal neurohemal organ. The regenerated neurohemal structure appeared to be functional, because larvae that had been bilaterally axotomized were able to metamorphose to pupae, a process requiring temporally precise periods of prothoracicotropic hormone release. In addition to the regeneration of the terminal axon structures, several other responses to axotomy and retrocerebral organ excision occurred. These included an apparent accumulation of prothoracicotropic hormone in the axons and regenerating neurohemal-like structure, sprouting of ectopic neurites from the axotomized somata, and a change in shape of the cell bodies from spherical to avoid.