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BACKGROUND: The extent of involvement of the subcutaneous Tenckhoff catheter tract in CAPD peritonitis and catheter-related infections is of major therapeutic importance. By definition, both peritonitis and exit-site infections do not involve the catheter tract. However, diagnosis of these infections as well as the more sinister tunnel infection is based mainly on clinical signs. METHODS: We examined the usefulness of ultrasound examination (US) of the catheter tract in delineating catheter-related (exit-site and tunnel) infections, and their relationship to each other and to peritonitis. CAPD patients with no evidence of peritonitis or catheter-related infections for 6 months prior to examination served as controls. US were performed by one of two experienced radiologists using the Acuson 128XP/10 scanner with a 7-MHz linear transducer. A positive US was defined as an area of hypoechogenicity (indicative of fluid collection) >2 mm in width along any portion of the catheter tract. Findings were localized into segments(S) as follows: S1, limited to external cuff; S2, intercuff segment adjacent to the external cuff; S3, intercuff segment adjacent to the internal cuff; S4, limited to the internal cuff; and S5, involvement extending throughout the catheter tract. RESULTS: Between March 1993 and January 1995, 39 CAPD patients, all with a double-cuff straight Tenckhoff catheter with the exit site situated above the point of entry into the peritoneum were studied. A total of 56 US were performed divided among 26 episodes of peritonitis, four tunnel infections, 13 exit-site infections,and 13 controls. There were 30 positive US distributed among 16 peritonitis, four tunnel, eight exit site infections and two control patients. The two positive controls went on to develop peritonitis within 1 month of the US. The majority of the US findings (13/16 in episodes of peritonitis and 5/8 exit site infections were localized to segment 4, that is, to the internal cuff region. Apart from a significant increase in width in all infected segments versus a normal tunnel, no differences in size were seen between peritonitis, exit-site, or tunnel infections, nor were there any differences in size and localization in these infections when comparing the offending organism (Gram-positive, negative, or culture negative). CONCLUSIONS: We conclude that peritonitis and exit-site infections are frequently accompanied by involvement of the catheter tract. The localization of infection to the internal cuff region in cases of exit-site infection probably occurred as a result of downward migration along the catheter tract. This supports the notion that ideally the exit site should be pointing caudally or that the peritoneal catheter have a swan-neck configuration. With regard to peritonitis, infection within the peritoneal cavity appears to extend and involve the internal cuff region. Thus both the internal and external cuffs do not seem to pose an effective barrier against the spread of infection.. Based on our data, we recommend that US be performed as a routine investigation in all cases of exit-site infection and in cases of refractory or relapsing peritonitis.

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The existence of diurnal variation in CAPD remains controversial. We therefore attempted to delineate the blood-pressure (BP) pattern in CAPD patients by ambulatory blood-pressure monitoring (ABPM). Initially ABPM was performed in 31 patients (21 M, 10 F), mean age 65.4 years (26-87) using the Spacelabs model 90207. The maximal normal BP preset on the recorder was 140/90 mmHg. Daytime and night-time readings, recorded every 30 min, were defined as those from 0600 to 2100 and 2100 to 0600 hours respectively. Mean duration of dialysis was 15.2 months (3-76). There were 14 hypertensive patients, defined as a basal BP > 140/90 mmHg, or those on antihypertensive medications. Taking the group as a whole a significant difference between day and night-time readings was found as regards minimal systolic BP (118 versus 107.6 mmHg), maximal systolic BP (181.6 versus 171.2 mmHg), mean diastolic BP (83.9 versus 79.6 mmHg), and maximal diastolic BP (121.7 versus 104.5 mmHg), P < 0.05. Diurnal variation, defined in the initial study as a 10% decrease of MAP occurring during any consecutive 4-h period, was present in 21 patients. In three the diurnal variation manifested as a paradoxical reduction of BP during the day. The only significant difference between those with diurnal variation and those without was the duration of dialysis, being 19.2 +/- 19.9 versus 13.3 +/- 17.3 months respectively, (P < 0.05). In a second study 18 hypertensive CAPD patients were subjected to ABPM. Nine of them had participated in the first study. These patients were specifically asked to detail their periods of sleep and arousal.(ABSTRACT TRUNCATED AT 250 WORDS)

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Serum uric acid has been described as being increased in the prediabetic stage of diabetes mellitus and as being decreased in overt diabetes. In this study we compared the serum uric acid levels of patients with insulin-dependent diabetes mellitus (IDDM) to those of controls matched for sex, age and ethnic origin. Also the correlation between serum uric acid levels and the fractional excretion of uric acid in IDDM patients was investigated, as well as the correlation between glycosuria and the fractional excretion of uric acid. The mean serum uric acid was lower in IDDM patients than in normal controls (4.0 +/- 1.3 vs. 4.3 +/- 1.3 mg/100 ml; p less than 0.03), mainly due to significantly lower levels in male and Ashkenazi IDDM patients, as compared to their respective controls. The fractional excretion of uric acid was found to be elevated in IDDM patients: 13.0 +/- 8.6% (mean +/- SD). A significant negative correlation was found between serum uric acid levels and the fractional excretion of uric acid in IDDM patients (p less than 0.001), although not when the males were examined separately. We found no correlation between the fractional excretion of uric acid and the degree of glycosuria in IDDM patients. In addition, the prevalence of hypouricemia (serum uric acid less than 2.5 mg%) was the same in IDDM patients and controls.

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Body weight reduction in the overweight hypertensive patient was found to reduce blood pressure, irrespective of the daily urinary sodium excretion. Significant blood pressure reductions were achieved while the urine sodium excretion was between 165-185 mEq/day. Salt restriction resulting in a significant decrease of the 24-hour urine sodium from 192-110 mEq/24-hours did not change the blood pressure. Some of the studies indicating a reduction in blood pressure, did not take into account the changes in body weight, while on sodium restriction. Thus sodium restriction in the treatment of hypertension has not been uniformly found to reduce the blood pressure. Although there is much evidence in favour of the involvement of sodium in the regulation of blood pressure, there is no convincing evidence that dietary sodium restriction can be of use as a therapeutic modality in the treatment of hypertension in the overweight hypertensive patient.

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Elevated serum lactic dehydrogenase (LDH) levels, 595 to 615 microns/ml (normal less than 225 microns/ml) with predominance of LDH isoenzymes 2 and 3 was the early and only sign of occult malignant lymphoma in three patients. In the first patient, overt lymphoma appeared clinically only 2 months after the finding of elevated serum LDH levels, whereas in the other two asymptomatic patients, pathologic LDH levels were the only clues to the need for further diagnostic investigation. It is concluded that LDH may have a diagnostic value in the preclinical stage of malignant lymphoma. Thus, a patient with no apparent cause for elevated serum LDH levels warrants a thorough work-up including abdominal CT scan and even explorative laparotomy.

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Plasma viscosity was measured by the capillary method in 108 patients with ischemic heart disease. The highest value of plasma viscosity was found in 11 patients with severe unstable angina (1.66 +/- 0.068), while in 18 patients with less severe unstable angina plasma viscosity was lower (1.61 +/- 0.056; p less than 0.025). In 43 patients with acute myocardial infarction plasma viscosity was 1.53 +/- 0.10, significantly lower than in the two groups with unstable angina (p less than 0.005). In 36 patients with stable angina plasma viscosity was 1.42 +/- 0.089, similar to that found in 100 normal subjects. Plasma viscosity did not increase in 30 ischemic heart disease patients during exercise-induced myocardial ischemia. It is suggested that the elevated plasma viscosity in unstable angina demonstrated in this study compromises the oxygen delivery to the myocardium and coronary blood flow and therefore may possibly be a factor in the pathophysiology of this syndrome.

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A 15-year-old boy who suffered from leg edema of unknown origin is described. The exclusion of any other cause for the edema, the clinical features, and the results of the dynamic tests performed suggested the diagnosis of "idiopathic edema," a syndrome described previously in women only. Spironolactone therapy brought about the disappearance of the edema and enabled the patient to return to his normal activities. This case report suggests that "idiopathic edema" is a syndrome common to both sexes, and is therefore not related to estrogen disturbances.

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The incidence, in-hospital evolution, and long-term follow-up were studied in patients who developed acute deviation of the mean (frontal) QRS axis to the right during an acute myocardial infarction (AMI). Among 3,160 patients evaluated, 13 (0.41 percent) developed left posterior hemiblock (LPHB) and 57 (1.8 percent) developed an incomplete form of LPHB, the right axis deviation group (RAD). Patients in the LPHB group had a statistically significant higher incidence of in-hospital morbidity (69 percent incidence of congestive heart failure) and mortality (38.5 percent). Follow-up revealed a statistically significant higher incidence of cardiac symptomatology (angina pectoris and congestive heart failure) in the RAD group than in the control group, mainly in patients in whom RAD persisted for more than 24 hours. Patients developing LPHB during AMI constitute a high risk population with a high incidence of morbidity and mortality. Patients developing RAD constitute an intermediate group (between the LPHB and the control group) characterized by a high incidence of cardiac symptoms at the time of follow-up.

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Low values of serum creatine phosphokinase (CPK) were found in a group of 27 patients suffering from acute viral hepatitis. The values were significantly lower than CPK values in a group of 25 patients with extra hepatic obstructive jaundice (23.3 +/- 32.1 versus 163 +/- 43 U/L, p less than 0.001). CPK values in the hepatitis group when recovered (6 months after hospitalization) were much higher than the mean CPK levels in the same group during the acute illness (178 +/- 28 versus 23.3 +/- 32.1 U/L, p less than 0.001) and were the same as a control group of 26 healthy volunteers (179 +/- 28 versus 179 +/- 20.9 U/L). Similar results were found when the groups were divided into separate male and female groups. Serum CPK values, thus, were found to be a useful diagnostic tool to distinguish between patients with intrahepatic jaundice due to acute viral hepatitis and patients with extra hepatic obstructive jaundice.

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Seven cases of procainamide-induced polymorphous ventricular tachycardia are presented. In four patients, polymorphous ventricular tachycardia appeared after intravenous administration of 200 to 400 mg of procainamide for the treatment of sustained ventricular tachycardia. In the remaining three patients, procainamide was administered orally for treatment of chronic premature ventricular contractions or atrial flutter. These patients had Q-T prolongation and recurrent syncope due to polymorphous ventricular tachycardia. In four patients, the arrhythmia was rapidly diagnosed and treated with disappearance of further episodes of the arrhythmia. In two patients, the arrhythmia degenerated into irreversible ventricular fibrillation and both patients died. In the seventh patient, a permanent ventricular pacemaker was inserted and, despite continuation of procainamide therapy, polymorphous ventricular tachycardia did not reoccur. These seven cases demonstrate that procainamide can produce an acquired prolonged Q-T syndrome with polymorphous ventricular tachycardia.

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