Role of vagal neuropathy in the hyponatraemia of alcoholic cirrhosis.

Abstract

minimal bactericidal concentration of amoxycillin was 27-4 tmol/l (10-0 pg/ml) but the minimal inhibitory concentration was only 0 07 ,umol/l (0-025 [&g/ml); the failed prophylaxis against this relatively tolerant pathogen was ascribed to persistent exposure to largeinocula. Fromour dataeven ninehours after takingamoxycillin serum concentrations exceeding the minimal inhibitory-concentration (0-07 pmol/l) were likely but bactericidal concentrations pmol/l) would not have occurred. Clearly, even if amoxycillin concentrations exceed the minimal inhibitory concentration for prolonged periods failure to maintain bactericidal values may be critical.Our study suggests that nine hours after a 3 g dose of oral amoxycillin syrup (eight hours after dentistry) serum is not necessarily bactericidal against relatively resistant pathogenic strains of viridans streptococci in about half of all patients. Hence whenever the possibility of infection with viridans streptococci warrants a second dose of amoxycillin this should not be left till eight hours after the procedure as recommended hitherto.I By repeating the dose after about four hours, however, more effective prophylaxis may be obtained even against relatively resistant species.We thank the University of Hong Kong dental and medical faculties and Beecham Pharmaceuticals for financial support and facilitating this work. We are also indebted to Professor C E Renson for his helpful advice and encouragement. The hyponatraemia common in decompensated cirrhosis arises in part from secretion of antidiuretic hormone attributed to a decrease in effective blood volume. Baroreceptors send inhibitory impulses to the midbrain and hypothalamus through the vagus and glossopharyngeal nerves. Since vagal neuropathy often occurs in chronic alcoholism, this might theoretically contribute to the inappropriate secretion of antidiuretic hormone, which might in turn induce hyponatraemia. In a prospective study including 34 patients with cirrhosis a high incidence ofvagal neuropathy was found in the alcoholics (64%) and a clear cut increase in the incidence of hyponatraemia in patients with evidence of vagal damage and ascites (seven of eight patients (88%); p=002). Results of a retrospective study of 64 patients with cirrhosis and ascitic decompeusation showed hyponatraemia in 17 (50%) of 34 alcoholics but in only four (13%) of 30 patients with non-alcoholic disease (p=0.006).Vagal neuropathy in alcoholic cirrhosis may contribute to the low serum sodium concentrations commonly found in these patients. IntroductionThe hyponatraemia commonly found in cirrhosis-is generally attributed to an excessive secretion of antidiuretic hormone despite hypo-osmolality of the blood.' The classical theory suggests that patients with decompensated disease have a decrease in the "effective" central blood volume resulting in decreased vagal and glossopharyngeal afferent influx to the midbrain and hypothalamus. The decreased afferent neural input is associated with a non-osmotic release of antidiuretic hormone a...

The Relationship of Heart Rate Variability with Severity and Prognosis of Cirrhosis

“…Cirrhosis, both alcoholic and nonalcoholic, has been reported to be associated with autonomic neuropathy, as well as other hemodynamic and circulatory disturbances [1][2][3][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. It has also been reported that the prevalence of autonomic neuropathy is proportional to the severity of cirrhosis [3,8,9], and its presence is an indicator of poor prognosis in patients with both early and advanced liver cirrhosis [3,12,13].…”

Cirrhotic cardiomyopathy

“…Chronotropic incompetence is the failure of the heart rate to respond to physiological and pharmacological stimuli. Sympathetic activation by various means, such as Valsalva maneuver, ice-cold skin stimulation, mental stress, tilting, and isometric and isotonic physical exercise, does not evoke an adequate acceleration of heart rate despite a higher than normal increase in plasma norepinephrine concentrations [23,24]. Such a defect is exhibited by both alcoholic and nonalcoholic patients and is proportional to the severity of cirrhosis.…”

Autonomic dysfunction and hyperdynamic circulation in cirrhosis with ascites

“…First, the autonomic nervous system plays a central role in maintaining cardiovascular homeostasis, and an impaired autonomic function is expected to lead to hemodynamic abnormalities. Second, AD is commonly detected in patients with cirrhosis, [9][10][11][12][13]16,[18][19][20][21]35 and its prevalence increases in parallel with the severity of liver disease, 9,10 as does the hyperdynamic circulatory syndrome. 36 Moreover, the presence of both abnormalities heralds an adverse prognosis.…”

“…14,15 It has also been reported that the severity of AD is proportional to the severity of cirrhosis, 9,10 and its presence is an indicator of poor prognosis in patients with both early and advanced liver disease. [16][17][18] Finally, AD is associated with an impairment of free water generation and hyponatremia, 19,20 and is likely involved in the pathogenesis of prolonged electrocardiographic Q-T interval, 21 a common finding in advanced cirrhosis with an adverse prognostic significance. 22 Based on the previous discussion, we hypothesized that AD is involved in the pathophysiology of hyperdynamic circulation of advanced cirrhosis.…”