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B Sonnenberg

Publications and source records attributed to B Sonnenberg.

5 recordsLinked to original sources
PubMed2000

Dilation of the pulmonary autograft after the Ross procedure.

OBJECTIVE: Dilation of pulmonary autograft after the Ross procedure is being recognized with increasing frequency. This study was undertaken to examine the extent of this problem and factors that may be associated with it. METHODS: The clinical, operative, and echocardiographic data of 118 patients who underwent the Ross procedure were reviewed. The mean age of 79 men and 39 women was 34 +/- 9 years, range 17 to 57 years. Bicuspid or other congenital aortic valve disease was present in 81% of patients. The pulmonary autograft was sutured as a valve in the subcoronary position in 2 patients, as a root inside of the aortic root in 45, and was used for complete aortic root replacement in 71. Teflon felt was not used to buttress the proximal or the distal anastomosis of the pulmonary autograft. The diameters of the sinuses of Valsalva, aortic anulus, and sinotubular junction were measured early and late after the operation with echocardiography. The mean follow-up was 44 months. RESULTS: The diameter of the sinuses of Valsalva increased from 31.4 +/- 0.4 mm to 33.7 +/- 0.5 mm (P =.01). Analysis of covariance revealed a significant change over time in this diameter, as well as a difference between operative techniques, with replacement of the aortic root being associated with a higher risk of dilation (P =. 0006). In 13 patients the diameter ranged from 40 to 51 mm. The diameter of the aortic anulus decreased in most patients and increased in 15, but there was no interaction between these changes and the operative technique. The diameter of the sinotubular junction increased in patients who had aortic root replacement and decreased in patients who had aortic root inclusion (P =.007). Moderate aortic insufficiency developed in 7 patients, and 3 required replacement of the pulmonary autograft. All patients with moderate aortic insufficiency had dilation of the aortic anulus and/or sinotubular junction. CONCLUSIONS: Dilation of the pulmonary autograft after the Ross procedure may occur because of an intrinsic abnormality of the pulmonary root in patients with congenital aortic valve disease. The technique of aortic root replacement is associated with a higher risk of dilation of the sinuses of Valsalva and sinotubular junction than the technique of aortic root inclusion.

Adolescent↗
PubMed1996

Coexistence of central diabetes insipidus and salt wasting: the difficulties in diagnosis, changes in natremia, and treatment.

Both central diabetes insipidus (DI) and a high rate of excretion of sodium (Na) and chloride (Cl) contributed to the development of polyuria and dysnatremia in two patients during the acute postoperative period after neurosurgery. To minimize difficulties in diagnosis and projections for therapy, two available (but not often used) clinical tools were helpful. First, the osmole excretion rate early on revealed the co-existence of central DI and an osmotic diuresis. The osmoles excreted were largely Na salts; after antidiuretic hormone acted, this electrolyte diuresis caused the urine flow rate to be much higher than otherwise anticipated. Interestingly, part of this saline diuresis occurred when the extracellular fluid volume was contracted. The tool to explain the basis for the dysnatremias was a tonicity balance. Hypernatremia, which developed before treatment of central DI, was primarily a result of a positive balance for Na rather than a large negative balance for water. Moreover, hyponatremia that developed once antidiuretic hormone acted was primarily a result of a negative balance for Na; the urine volume was large and its Na concentration was hypertonic. To prevent a further decline in the plasma Na concentration, either the Na concentration in the urine should be decreased by provision of urea or a loop diuretic while replacing all unwanted water and electrolyte losses; alternatively, the fluid infused should have a similar Na concentration and volume as the urine (infuse hypertonic saline).

Adult↗
PubMed1994

Metabolic alkalosis mimicking the acute sequestration of HCl in rats: bucking the alkaline tide.

Loss or sequestration of HCl induces an acute metabolic alkalosis. The purpose of these experiments was to examine the renal handling of bicarbonate (HCO3-) in awake, euvolemic rats to determine if a significant degree of bicarbonaturia would develop because, if present, it could lead to large negative balances for sodium (Na+) and/or potassium (K+). Metabolic alkalosis was induced acutely by creating the equivalent of an acute and large loss of HCl; the net effect was to lose Cl- and gain equimolar HCO3- in rats that were in Na+ and K+ balance. A loop diuretic induced the loss of 1,860 mumol Na+, 842 mumol K+ and 2,444 mumol Cl- over a 4-h period; the loss of Cl- was replaced as its Na+ or K+ salt by infusing equivalent amounts of NaHCO3 and KHCO3 (ultimately, a "simple exchange" of 2,444 mumol of HCO3- for Cl-). Metabolic alkalosis was sustained for 4 h (mean plasma [HCO3-] = 43 mmol/L); there was a parallel fall in the plasma [Cl-]. From a renal perspective, the fractional excretion of HCO3- was only 0.4%. This adaptation could be viewed as potentially life-saving, because excretion of NaHCO3 would result quickly in a severe reduction in ECF volume and metabolic acidosis and, in addition, in a severe degree of K(+)-depletion.

Alkalosis↗
PubMed1991

Can oxygen consumption in blood in vitro be detected by a change in PCO2?

The PO2 measured in a sample of blood can be misleadingly low, owing to consumption of oxygen in vitro in patients with leukemia. The purpose of this study was to determine whether a rise in PCO2 in such blood could be a useful indication of consumption of oxygen in vitro. Because of the non-bocarbonate buffer capacity of blood and the carriage of CO2, mainly as bicarbonate, we reasoned that the rise in PCO2 would be too small to be helpful. Hence the quantitative relationship between the consumption of oxygen and the production of CO2 in blood was determined. Other reactions yielding CO2 (the titration of lactic acid) were monitored. Consumption of oxygen was stimulated in blood of normals in vitro by adding methylene blue (100 mumol/L); in addition, blood from four patients with leukemia was studied without additions. The rate of consumption of oxygen at 22 degrees C was linear over 60 min; the respiratory quotient was close to unity. The rise in PCO2 was small even when the fall in PO2 was 60 mmHg. We conclude that a rise in PCO2 is not a reliable way to diagnose consumption of oxygen in blood in vitro as patients may hyperventilate, making it very difficult to recognize a small rise in PCO2.

Adult↗