Prevalence and characteristics of diagnostic groups amongst 1034 patients seen in ENT practices for dizziness.

OBJECTIVE: To determine the prevalence and characteristics of various diagnostic groups amongst patients referred to ENT practices with the primary complaint of dizziness. STUDY DESIGN: A prospective, observational, multicentre study. METHODS: Consecutive patients presenting with dizziness to the participating ENT practices were enrolled. Seven ENT specialists at three clinics participated. RESULTS: Benign paroxysmal positional vertigo was diagnosed in 53.3 per cent of the 1034 study patients. Fifty-nine per cent of these experienced night-time awakening with dizziness, which was a significant proportion in comparison to the other diagnostic groups. Benign paroxysmal positional vertigo was the most frequent diagnosis in all age groups, including those over 70 years. CONCLUSION: In this study of patients referred to ENT for dizziness, benign paroxysmal positional vertigo was the dominant diagnostic entity, in all age groups and overall. All clinicians in contact with dizzy patients must consider benign paroxysmal positional vertigo, especially in the elderly.

Juvenile nasopharyngeal angiofibromas in Denmark 1981-2003: diagnosis, incidence, and treatment.

CONCLUSIONS: Juvenile nasopharyngeal angiofibroma (JNA) is a rare tumor in young males, with a non-negligible potential for recurrence. Preoperative embolization is a safe procedure that diminishes the peroperative blood loss and the need for blood transfusion. The endoscopic approach was used with good results in JNA stage I and II (Chandler). OBJECTIVES: To estimate the incidence rate of JNA in the Danish population and to describe symptoms and treatment. PATIENTS AND METHODS: This was a national retrospective cohort study. All cases of JNA diagnosed in Denmark from 1981 to 2003 were identified. Data were extracted from medical records. RESULTS: Forty-five male (no female) JNA cases were identified. In 43 cases, clinical data were recovered. Median age was 15 years. The incidence rate in Denmark was 0.4 cases per million inhabitants per year and 3.7 cases per million males (aged 10-24) per year. All patients underwent surgery, and the endoscopic approach was increasingly being used. The embolization procedure proved to be safe and decreased the intraoperative blood loss statistically to 650 ml in the embolized group from an average of 1200 ml in the non-embolized group (p<0.05). Similarly, the need for peroperative blood transfusion was reduced (p<0.005). The primary recurrence rate was 23% and no patients died.

[Risk of hemorrhage after outpatient versus inpatient tonsillectomy]. / Risiko for efterblødning ved tonsillektomi i dagkirurgisk versus stationaert regi.

INTRODUCTION: This study evaluates the risk of post-tonsillectomy haemorrhage in outpatient surgery compared to conventional inpatient management. MATERIAL AND METHODS: We reviewed 528 tonsillectomies performed at the ENT Department, Rigshospitalet, University of Copenhagen, in the period 1.6.1997 to 31.5.1998. The 264 outpatient tonsillectomies were compared with 264 inpatient procedures. The number of post-operative haemorrhages and the time interval from operation to post-operative bleeding were registered, along with the need for re-operation. Outpatients were discharged 8 hours after surgery, inpatients after 24 hours. RESULTS: Forty-five (8.5%) of 528 tonsillectomies had post-operative haemorrhage complications, 15 (2.8%) patients needed a re-operation. Twenty-five (55%) cases of reactionary haemorrhage occurred < 8 hours after surgery and nine needed a re-operation. Two of three cases of post-operative haemorrhage 8-24 hours after primary surgery were re-operated, whereas four of 17 patients with haemorrhage > 24 hours post-operatively needed another surgery. There were no differences between inpatient and outpatient management. Eighty-nine per cent of all early (0-24 h) post-operative haemorrhages occurred < 8 hours post-operatively. In the time period from 8-24 hours post-operatively there were only three cases of reactionary haemorrhage. The risk of post-operative haemorrhage after discharge was 4.2% and 3.4% after outpatient and inpatient management respectively, a difference of only 0.8%. This makes outpatient tonsillectomy an acceptable alternative to inpatient management.

Vascular smooth muscle contraction is an independent regulator of endothelial nitric oxide production.

This investigation was conducted to determine whether endothelial nitric oxide (NO) production is regulated by vascular smooth muscle contraction. Unperfused ring segments of rat aorta and mesenteric artery were studied using isometric tension recording (n = 6-8 in all experiments). Following a reference contraction to K+ 80 mM (100%), arteries were left either unstimulated or stimulated by different concentrations of K+ or prostaglandin F2alpha (PGF2alpha) to induce different levels of vascular precontraction. N(G)-nitro-L-arginine methyl ester (L-NAME 0.1-300 microM) or NS 2028 (0.03-3 microM), which is a new specific inhibitor of the NO-sensitive guanylate cyclase, was then added at increasing concentrations to evaluate endothelial NO production. L-NAME and NS 2028 produced a concentration-dependent vasoconstrictor response which was progressively enhanced with increasing levels of precontraction. For L-NAME, this amounted in aorta to (% of reference contraction): 35+/-1% and 105 +/- 4% (precontraction by K(+) 20 and 30 mM) and 22+/-1%, 89+/-1%, 138+/-1% and 146+/-2% (precontraction by PGF2alpha 0.5, 1, 2 and 3 microM). A similar coupling was found in the mesenteric artery. A precontraction as little as 2% was enough to trigger a vasoconstrictor response to L-NAME. In contrast, L-NAME and NS 2028 had no effect in non-contracted arteries, not even when passive mechanical stretch was increased by 100%. The results suggest (i) that endothelial NO formation is progressively increased with increasing vascular tone, and (ii) that vascular isometric contraction per se stimulates endothelial NO formation. It is concluded, that active vascular smooth muscle contraction is an independent regulator of endothelial NO production.

Hydralazine-induced vasodilation involves opening of high conductance Ca2+-activated K+ channels.

The purpose of this study was to investigate whether high conductance Ca2+-activated K+ channels (BK(Ca)) are mediating the vasodilator action of hydralazine. In isolated porcine coronary arteries, hydralazine (1-300 microM), like the K+ channel opener levcromakalim, preferentially relaxed contractions induced by K+ (20 mM) compared with K+ (80 mM). In addition, concentration-relaxation curves for hydralazine (pD2 = 5.38 +/- 0.06; Emax = 85.9 +/- 3.6%) were shifted 10-fold to the right by the BK(Ca) blockers tetraethylammonium (1 mM) and iberiotoxin (0.1 microM). In contrast, nimodipine (a Ca2+-entry blocker), relaxed contractions induced by K+ (20 mM) and K+ (80 mM) equally and nimodipine-induced relaxations were neither antagonized by tetraethylammonium nor by iberiotoxin. In isolated perfused rat hearts, hydralazine (1 microM) increased coronary flow by 28.8 +/- 2.7%. Iberiotoxin (0.1 microM) suppressed this response by 82% (P < 0.05). In conscious, chronically catheterized rats the hypotensive response to hydralazine (0.6 mg kg(-1) min(-1)) was significantly reduced by 41% during infusion of iberiotoxin (0.1 mg kg(-1)). It is concluded, that opening of BK(Ca) takes part in the mechanism whereby hydralazine produces vasodilation.

Coronary vasorelaxant effect of levosimendan, a new inodilator with calcium-sensitizing properties.

We examined the action of levosimendan, a new Ca2+-sensitizing inodilator, on isolated porcine coronary arteries. Vessel rings were studied in isometric myographs. Arterial cyclic adenosine monophosphate (cAMP) levels were determined by radioimmunoassay. Levosimendan (10(-7)-10(-3) M) completely relaxed arteries preconstricted by prostaglandin F2alpha (PGF2alpha) with a pD2 (-logEC50) value of 3.99 +/- 0.05 (n = 6-9 in all experiments). Pretreatment with levosimendan also prevented contraction induced by PGF2alpha. The vasorelaxation produced by levosimendan (10(-7)-10(-3) M) was not attenuated by removal of the endothelium. Levosimendan (10(-7)-10(-3) M) relaxed contractions induced by 30 mM K+ as well as 80 mM K+, whereas the K+ channel opener levcromakalim selectively relaxed contraction induced by 30 mM K+. Neither the cyclooxygenase inhibitor indomethacin nor the beta-adrenoceptor blocker propranolol influenced levosimendan-induced vasorelaxation. The Ca2+-entry blocker isradipine failed to relax arteries precontracted by endothelin-1 in Ca2+-free/EGTA medium. However, levosimendan (10(-7)-3 x 10(-3) M) completely relaxed endothelin-1-induced contractions in this medium. Levosimendan potentiated the relaxant effect of a cAMP-stimulating drug, isoprenaline, but also that of nitroglycerin and isradipine. At a maximal effective concentration, it increased arterial tissue contents of cAMP twofold. In conclusion, levosimendan produces coronary vasorelaxation by a mechanism that seems to be endothelium independent and not mediated by K+ channel opening, Ca2+-entry blockade, release of cyclooxygenase products, or beta-adrenoceptor stimulation. Accumulation of cAMP may possibly participate in vasorelaxation at high concentrations of levosimendan, but a cAMP-independent mechanism seems to be involved at lower concentrations.