A randomized trial of automated intermittent ropivacaine administration vs. continuous infusion in an interscalene catheter.

BACKGROUND: Ultrasound-guided interscalene nerve block with ropivacaine as local anesthetic agent given as boluses or continuous infusion is the preferred pain management after major shoulder surgery. The use of automated intermittent boluses has been shown to be superior to continuous infusion in sciatic and epidural nerve block. HYPOTHESIS: Automated intermittent boluses reduce pain after major shoulder surgery. METHODS: Seventy patients aged 18-75 years, scheduled for major shoulder surgery under general anesthesia with interscalene nerve block were included in this randomized controlled trial. Patients were allocated to either automated intermittent boluses with 16 mg ropivacaine every 2 h combined with patient-controlled administration or to a conventional regimen of continuous infusion of 8 mg/h (4 ml/h) of ropivacaine combined with patient controlled administration (2 ml, lockout time 30 min). Pain (Visual Analog Scale, VAS) was assessed every 8 h postoperatively. RESULTS: Fifty-seven patients completed the study, 29 in the continuous infusion group and 28 in the automated intermittent bolus group. Shoulder arthroplasty was performed in 49 (86%) of the cases. There were no significant differences in VAS score from 8 to 48 h post-operatively. No significant difference in opioid usage was observed. The automated intermittent bolus group reported significantly less force on coughing and more hoarseness. A significantly lower volume of ropivacaine was used in the automated intermittent bolus group. CONCLUSION: Automated intermittent boluses did not reduce pain or rescue opioid consumption compared with continuous infusion of ropivacaine. The automated intermittent bolus group had significantly less force on coughing and more hoarseness.

Lack of effect of nifedipine on counterregulatory mechanisms in essential hypertension.

The influence of long-term nifedipine treatment on body fluid compartments, renal function, the renin-angiotensin system, and the adrenergic system was studied in 18 patients with essential hypertension. A placebo period of 4 weeks was followed by a 6-week dose-titration period. Thereafter, the dose was kept constant for an additional 6 weeks (mean dose, 51 mg/day). As compared with placebo values, diastolic blood pressure decreased approximately 12% during nifedipine treatment. Plasma volume, extracellular fluid volume, and the ratio of plasma to interstitial fluid volume did not change significantly, either in the group as a whole or in a subgroup in which pedal edema developed. Plasma concentrations of epinephrine and norepinephrine increased slightly after 2 weeks of treatment, but they returned to control values after 6 weeks of therapy. Plasma concentrations of renin, angiotensin II, and aldosterone did not change significantly. Glomerular filtration rate and renal clearances of sodium and potassium were unchanged as well. These results indicate that long-term nifedipine treatment does not lead to activation of counterregulatory mechanisms, such as fluid retention or the renin-angiotensin or adrenergic systems. This may well be of importance for the antihypertensive efficacy of nifedipine treatment.

Pseudohypoaldosteronism in eight families: different forms of inheritance are evidence for various genetic defects.

Pseudohypoaldosteronism is a rare hereditary disorder presenting in early infancy with renal salt loss leading to hyponatremia and hyperkalemia despite high levels of plasma aldosterone. The patients are insensitive to mineralocorticoids; however, sodium supplementation is able to correct electrolyte abnormalities. Absent or greatly diminished type I aldosterone receptors in peripheral mononuclear leucocytes have been recently demonstrated and explain the lack of response to mineralocorticoids. We have studied the mode of inheritance in eight families with a total of nine patients. There was evidence for an autosomal recessive form of inheritance in four families, while the other four families appeared to have an autosomal dominant mode of transmission. In three families the autosomal recessive form was characterized by normal receptor as well as hormone data in both parents, while in one family receptor levels in both parents were greatly reduced, but hormone levels were normal. In the four families with an autosomal dominant mode of transmission there was always one parent with reduced receptor binding in peripheral mononuclear leucocytes and elevated serum hormone levels. These parents were entirely asymptomatic. In an extended family we were able to study an aunt and her newborn daughter, who were both also biochemically affected but clinically asymptomatic. It, therefore, appears that this dual pattern of genetic transmission may indicate differing genetic defects which cause the same clinical picture of pseudohypoaldosteronism.

Effects of amiloride on plasma and total body potassium, blood pressure, and the renin-angiotensin-aldosterone system in thiazide-treated hypertensive patients.

Total body potassium content, plasma potassium concentration, blood pressure, and plasma concentrations of renin, angiotensin II, and aldosterone were measured in patients with essential hypertension after a run-in period of 8 wk on a regimen of hydrochlorothiazide (median dosage 75 mg/day). Patients were then randomly assigned to continued hydrochlorothiazide therapy (group I) or to receive adjunctive treatment with amiloride (group II, median dosage 15 mg/day or 5 mg per 25 mg hydrochlorothiazide) for the following 3 mo. There were no changes in group I patients during 3 mo on hydrochlorothiazide in plasma potassium, total body potassium content, or the renin-angiotensin-aldosterone system. Blood pressure was also unchanged. In group II patients addition of amiloride to hydrochlorothiazide induced a rise in plasma and total body potassium of approximately 15% and 4%. The potassium-retaining effect was maintained throughout the 12-wk period, although the maximal changes were observed after 8 wk of treatment. Supine blood pressure did not change, but there was a significant decrease in standing systolic blood pressure. There was a marked rise in plasma concentrations of renin, angiotensin II, and aldosterone.

Effects of natural oestrogen therapy on blood pressure and renin-angiotensin system in normotensive and hypertensive menopausal women.

The blood pressure level and the renin-angiotensin system were investigated in 24 menopausal women (12 normotensive and 12 hypertensive) before, during and after six months of treatment with either oestradiol or trisekvens (sequential preparation containing oestradiol, oestriol and norethisterone acetate). In the normotensive women no significant alterations in systolic or diastolic blood pressure were found during treatment for six months. In the hypertensive women systolic blood pressure fell significantly during treatment with oestradiol as well as with trisekvens, while diastolic pressure did not change. All individual variations of blood pressure were small. The plasma concentrations of renin, angiotensin II and aldosterone remained unchanged during the treatments. A statistically significant increase in plasma renin substrate concentration was observed in all groups with the exception of the normotensive women treated with oestradiol. Menopausal symptoms in hypertensive women may safely be treated with natural oestrogens on the same indications as used for normotensive women.

Changed cyclic guanosine monophosphate atrial natriuretic factor relationship in hypertensive man.

Plasma concentrations of atrial natriuretic factor (ANF) and cyclic guanosine monophosphate (cGMP) were measured in 10 patients with essential hypertension and 10 normotensive controls on the fifth day of a low (50 mmol/day), a medium (180 mmol/day) and a high (380 mmol/day) dietary sodium intake. Plasma ANF and cGMP concentrations were less on the low than on the high sodium intake. Values for ANF on the medium sodium intake were intermediate. In normotensive subjects cGMP concentrations did not differ significantly on the low and the medium sodium intake. As compared with the controls plasma concentrations of cGMP were significantly increased in hypertensive patients on all three levels of sodium intake, while ANF concentrations were identical in the two groups. Since cGMP is a second messenger to ANF the data suggest an increased cellular response to ANF in patients with essential hypertension.

Placental steroid sulfatase deficiency: biochemical diagnosis and clinical review.

Twenty-three cases of placental steroid sulfatase deficiency are reported. All children were boys who later acquired ichthyosis of the recessive X-linked type. The steroid sulfatase deficiency was present in placental tissue, umbilical cord leucocytes, and cultured skin fibroblasts of affected boys. An antepartum diagnosis can be obtained either by detecting the enzyme deficiency in cultured amniotic fluid cells or by finding an elevated total excretion of androstenetriol , 16 alpha-hydroxy-dehydroepiandrosterone, and 16 alpha-hydroxy-pregnenolone in maternal third-trimester urine. Vaginal delivery was accomplished in 16 patients (70%). No conspicuous pregnancy complications or neonatal problems were noted. However, birth weights tended to be relatively low. Intervention is unnecessary unless other obstetric indications require it. The incidence of this disorder appears to be approximately one per 2000 male births.

Measurement of angiotensin II in human plasma: technical modifications and practical experience.

This paper presents our experience in measurement of plasma angiotensin II concentration according to the method described by Düsterdieck, G. and McElwee, G. (1971) Eur. J. Clin. Invest. 2, 32-38. Certain technical modifications of the procedure have been worked out. For each individual plasma sample, the recovery across extraction and elution steps is determined by addition of radio-iodinated angiotensin II. A time-saving recycling elution procedure is described. Evidence for the clinical applicability of the modified method is presented.

Radioimmunoassay for saralasin by means of anti-angiotensin II sera.

A radioimmunoassay for the angiotensin II-inhibitor saralasin has been developed. The assay is based upon an exploitation of the cross-reactivity of antisera raised against angiotensin II, with radioiodinated saralasin as the tracer peptide. Performance data for the assay and results obtained in clinical infusion studies are presented.

Double-antibody solid-phase radioimmunoassay for blood bradykinin.

A solid phase radioimmunoassay for the determination of blood bradykinin has been developed. Highly specific antibodies against bradykinin were raised in rabbits after coupling the peptide to thyroglobulin. Iodination of [Tyr8]-bradykinin was carried out with a chloramine-T procedure resulting in a tracer with high specific activity. Bradykinin was isolated in the following way: blood was sampled directly into acetone, and lipids were removed by extraction with petroleum either (40-60 degrees C). The final purification was made on QAE-Sephadex A-25 at pH 7.4. The mean recovery of added [125I-Tyr8]-bradykinin was 28% with a sample volume of 6 ml whole blood. The sensitivity of the radioimmunoassay was 1.25 pg/tube or 3 pg/ml blood. The reproducibility of the method is satisfactory with a between-assay coefficient of variation below 16%. Levels found in venous blood were below 3 pg bradykinin/ml in normal persons.

[Unintended events in anesthesia due to reuse of disposable equipment]. / Utilsigtede haendelser i anaestesi ved gentagen brug af engangsudstyr.

Two cases concerning reuse of plastic-coated introducers (intended for single-use only) for intubation of children are described. If breaks in the coating occur, the airway can be compromised and removal of the broken piece of the plastic-coating can the treacherous. In this paper, the probable causes of the incidents are discussed and suggestions for avoiding breakage are outlined.

[Screening for prehypoxemia with oximetry--a study of two methods]. / Screening for praehypoksaemi med oximetri--en undersøgelse af to metoder.

The aim of the present study was to evaluate the validity of pulse oximetry screening for prehypoxaemia, to assess the agreement between pulse- and haem-oximetry and to elucidate any influence of peripheral temperature on pulse oximeter measurements. A consecutive prospective study was undertaken in 91 cardiac surgery patients still in treatment with controlled mechanical ventilation in the early postoperative period. We examined arterial oxygen tension (paO2), arterial oxygen saturation (SaO2) and pulse oximeter saturation (SpO2) from 657 arterial blood samples. The sensitivity of the pulse oximeter was 0.83, the specificity 0.73, and the diagnostic specificity was 0.10, at the chosen level of screening. The pulse oximeter showed a tendency to underestimate the oxygen saturation by 0.85%. The agreement between pulse- and haem-oxymetry was found to be good. The authors conclude that the pulse oximeter is acceptable for respiratory screening in postoperative cardiac surgery. The low specificity and the low diagnostic specificity results in frequent false alarms. Low peripheral temperature (down to 25%) do not influence the validity of either methods.

The influence of ACE-inhibition by captopril on renal formation and metabolism of angiotensins I and II in patients with renovascular hypertension.

Fourteen patients with hypertension of presumed renovascular etiology were studied by renal vein catheterization. Unilateral renin secretion was found in 8 patients. In 4 of these patients a positive veno-arterial difference of plasma angiotensin I concentration (PAI) across the affected kidney increased markedly after a single dose of captopril. Across the contralateral kidney the net veno-arterial PAI difference changed from about zero before captopril to clearly negative values after captopril. The PAI values in the remaining 4 patients, who were already on captopril before the catheterization, were similar to those observed after a single dose of captopril. In patients with bilateral renin secretion the renal veno-arterial PAI differences across the kidneys were positive or close to zero before captopril. After captopril both positive and negative veno-arterial differences of PAI were observed. The plasma angiotensin II concentrations decreased after captopril to low values. These low values together with extremely high PAI values demonstrate effective ACE-inhibition. A high generation rate of angiotensin I in the affected kidney in patients with unilateral renin secretion after captopril is probably explained by activation of the local renin secretion. The angiotensin I "consumption" in the contralateral kidney after captopril in spite of no angiotensin II formation suggests the presence of alternative degradation processes for angiotensin I in the human kidney.

Biochemical monitoring of vasoactive peptides during angiotensin converting enzyme inhibition.

We present a brief survey of changes in vasoactive peptide systems during therapy with angiotensin converting enzyme inhibitors. Particular attention is paid to several methodological problems which are relevant to the clinical biochemistry and physiology of patients treated with this new type of drug.

The influence of nifedipine treatment on counter-regulatory mechanisms in essential hypertension.

The influence of nifedipine treatment on plasma (PV) and extracellular fluid volume (ECV), the ratio of plasma volume to interstitial fluid volume (PV:IF), glomerular filtration rate (GFR), renal clearances of Na+ and K+, plasma concentrations of renin (PRC), angiotensin II (pANG II), aldosterone (pAldo), adrenaline (PA) and noradrenaline (PNA) were studied in 18 consecutive patients with essential hypertension. A 4-week placebo period was followed by a 6-week dose-titration period (period A). Thereafter the dose was kept constant for an additional 6 weeks (period B), the mean dose being 51 mg/day. As compared with placebo, diastolic blood pressure (DBP) decreased from 105 +/- 7 to 93 +/- 9 mmHg at the end of period B. Extracellular fluid volume, PV, and PV:IF were not significantly changed at the end of period A or B, neither in the group as a whole nor in a subgroup, who developed pedal oedema. After 2 weeks on nifedipine, PA as well as PNA increased slightly but returned to control values after 6 weeks of therapy. Plasma renin concentration, pANG II, pAldo and GFR did not change significantly. Renal sodium handling was also unchanged. It is concluded that long-term nifedipine therapy (exceeding 6 weeks) does not lead to activation of counter-regulatory mechanisms such as fluid retention, activation of the renin-angiotensin system and the adrenergic system. Renal function is unaffected by nifedipine.