Burden of sodium abnormalities in patients hospitalized for heart failure

Hyponatremia presumably is associated with adverse clinical outcomes in patients with congestive heart failure (CHF), but risk thresholds and economic burden are less studied. The authors analyzed 115,969 patients hospitalized for CHF and grouped them by serum sodium levels (severe hyponatremia, ≤130 mEq/L; hyponatremia, 131-135 mEq/L; normonatremia, 136-145 mEq/L; hypernatremia, >145 mEq/L). Univariable and multivariable analyses on the associated clinical and economic outcomes were performed. The most common abnormality was hyponatremia (15.9%), followed by severe hyponatremia (5.3%) and hypernatremia (3.2%). Hospital mortality was highest for severe hyponatremia (7.6%), followed by hypernatremia (6.7%) and hyponatremia (4.9%) (P<.0001). Compared with normonatremia, risk-adjusted mortality was highest for severe hyponatremia (odds ratio [OR], 1.78; 95% confidence interval [CI], 1.59-1.99), followed by hypernatremia (OR, 1.55; 95% CI, 1.34-1.80) and hyponatremia (OR, 1.29; 95% CI, 1.19-1.40; all P<.0001). Risk-adjusted hospital prolongation was greater for each level of sodium abnormality than for normonatremia, ranging from 0.42 (CI, 0.26-0.60) days for hypernatremia to 1.28 (CI, 1.11-1.47) days for severe hyponatremia. Risk-adjusted attributable hospital cost increase was highest for severe hyponatremia ($1132; CI, $856-$1425; all (P<.0001). Sodium abnormalities were common in patients hospitalized for CHF. Adverse outcomes resulted not only from severe hyponatremia, but also from mild hyponatremia and hypernatremia.     

Sodium levels on admission are associated with mortality risk in hospitalized patients

AimsAbnormal sodium values are common among hospitalized patients. We aimed to investigate the association of admission sodium values and mortality.MethodsHistorical prospectively data of adult patients hospitalized to medical wards between January 2011 and December 2013. Admission sodium values were classified to five categories: severe hyponatremia (< 125 mEq/L), mild hyponatremia (125–135 mEq/L), normal sodium values (135–145 mEq/L), mild hypernatremia (145–150 mEq/L) and severe hypernatremia (> 150 mEq/L). Main outcomes were length of hospitalization, in-hospital mortality and mortality at the end-of-follow-up.ResultsThe cohort included 27,889 patients (mean age 67 ± 18 years, 52% males). The total follow-up was 1065 days. Most patients had normal sodium values (76%), 22% had hyponatremia, 3% had hypernatremia. Mean age increased with increase in severity of hyponatremia or hypernatremia. Median length of hospitalization was longer with mild and severe hypernatremia (7 and 5 days, respectively) or with mild and severe hyponatremia (4 and 4 days, respectively), compared to normal sodium levels (3 days). Compared to in-hospital mortality with normal sodium levels (5%), mortality was higher with mild and severe hyponatremia (9% and 14%, respectively) and was highest with mild (28%), and severe hypernatremia (52%). Mortality rate at the end of follow-up was 28% with normal sodium levels, 44% and 48% with mild and severe hyponatremia, 66% and 90% with mild and severe hypernatremia, respectively.ConclusionsAbnormal sodium values on admission were associated with longer hospitalization and increased short- and long-term mortality. Mortality risk was higher with hypernatremia, compared to hyponatremia.     

Disorders of fluid and electrolyte metabolism in elderly diabetics

Disorders of fluid and electrolyte metabolism in elderly diabetics were studied. High frequency of hyperkalemia (20.8%), hypomagnesemia (14.6%), hypocalcemia (13.7%), hyperphosphatemia (8.6%), hyponatremia (8.1%) and hyperchloremia (7.2%) was observed among 332 elderly diabetics. Furthermore, hyperkalemia, hyperphosphatemia, hyponatremia, hyperchloremia, hypercalcemia and hypermagnesemia were more frequent in diabetics with renal insufficiency (serum Cr greater than or equal to 1.5 mg/dl) than in diabetics with normal renal function (serum Cr less than or equal to 1.4 mg/dl). In addition, statistically significant negative correlation were observed between plasma glucose levels and serum levels of sodium and chloride in diabetics with normal renal function. These results clearly demonstrated that the most important causal factor of electrolyte disorders in elderly diabetics might be the renal dysfunction due to diabetic nephropathy and/or nephrosclerosis. Moreover, glucose intolerance is also one of the causal factors for hyponatremia and hypochloremia. Disorders of fluid and electrolyte metabolism were manifest in 31 diabetic patients with hyperosmolar non-ketotic coma. The frequency of patients with abnormally elevated serum levels of sodium, potassium and chloride, and patients with abnormally lowered serum levels of calcium was high in this morbid state. Water and sodium deficit, examined in 11 cases of hyperosmolar non-ketotic coma, was 4780 +/- 2100 ml (107 +/- 43 ml/kg body weight) and 290 +/- 170 mEq (6.8 +/- 4.2 mEq/kg body weight), respectively. However, no significant deficit of potassium was observed in the patients. Statistically significant positive correlations between water deficit and serum Cr levels and with serum effective osmolarity were observed. However, there were no significant correlations between water deficit and plasma glucose levels, serum sodium levels and serum osmolarity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prevalence and impact on outcome of sodium and potassium disorders in patients with community-acquired pneumonia: A retrospective analysis

Introduction: Disorders of sodium and potassium are common and predictors of adverse outcome. Prevalence and impact on outcome of hypokalemia, hyperkalemia, hyponatremia and hypernatremia were investigated in emergency patients with community-acquired pneumonia (CAP).Methods: Patients $\ge$18 years presenting to our emergency department between January 1st 2017 and December 31st 2018 with on-admission electrolyte measurements were included. Chart reviews were performed to identify patients with CAP.Results: 19.948 cases had measurements of sodium and potassium of which 469 had CAP (2.4%). Prevalence of hypo- and hypernatremia was significantly increased in patients with compared to those without CAP (hyponatremia: 28.8% vs. 10.5% respectively, p<0.0001; hypernatremia: 1.9% vs. 0.6% respectively, p=0.002). The prevalence of hypo- and hyperkalemia was significantly higher in patients with than without CAP (hypokalemia 15.6% vs. 11.4% respectively, p=0.004; hyperkalemia: 4.5% vs. 2.0% respectively, p=0.001). Hyponatremia was significantly associated with longer hospital stay in patients with CAP (regression coefficient 0.194, standard error 0.079, p=0.015). None of the investigated electrolyte disorders were predictive of 30-day re-admission and 180-day pneumonia recurrence rates. Use of loop diuretics was an independent predictor for 30-day re-admission (OR 2.351 (1.099-5.03). p=0.028). Pneumonia Severity Index (PSI) risk class was an independent predictor of 180-day pneumonia recurrence (OR 1.494 (1.022-2.184), p=0.038).Conclusion: Dysnatremias and dyskalemias are common findings complicating CAP in emergency patients. Prevalence of hyponatremia was highest followed by hypokalemia. Hyponatremia was an independent predictor of prolonged length of hospital stay. Loop diuretic use was associated with 30-day readmission and PSI risk class with 180-day pneumonia recurrence.     

肝硬变腹水患者钾钠氯及酸碱失衡

目的研究肝硬变腹水患者的钾、钠、氯及酸碱失衡。方法肝硬变腹水患者１５４例，血Ｋ＋、Ｎａ＋、Ｃｌ－测定采用ＥＥＬ公司自动分析仪及火焰光度计。血气及酸碱度测定采用ＩＬ１３０２型自动微机分析仪。结果低血钾者５７例，高血钾者６例，低血钠者８１例，高血钠者１２例，低血氯者３４例，高血氯者８例。２４例血气及酸碱度测定结果显示，以碱中毒者为主。依次为呼碱、呼碱＋代酸、代酸、代碱、呼酸。本组高血钾、低血钠与Ｃｈｉｌｄ分级、ＢＵＮ、Ｃｒ值相关。从本组资料表明，重症肝硬变腹水患者水盐代谢失衡多为医源性所致，且加重原有失衡。高钾血症、急性低钠血症及高钠血症大多如此，多为住院后发生，常可危及生命。结论肝硬变腹水患者的高钾血症、低钠血症和高钠血症大多在肝肾功能低下，不适当的治疗所致，是影响预后的重要因素     

Prognostic importance of hyponatremia in acute ST-elevation myocardial infarction

PURPOSE: To determine the prevalence and prognostic implications of hyponatremia in the setting of acute ST-elevation myocardial infarction. METHODS: The study sample consisted of 1047 consecutive patients presenting with acute ST-elevation myocardial infarction. Plasma sodium concentrations were obtained on admission and at 24, 48, and 72 hours thereafter. Infarct size was determined by echocardiographic examination that was performed on day 2 or 3 of hospitalization. RESULTS: Hyponatremia, defined as a plasma sodium level <135 mmol/L (<135 mEq/L), was present on admission in 131 patients (12.5%) and developed during the first 72 hours of hospitalization in 208 patients (19.9%). Plasma sodium levels decreased to < or = 130 mmol/L in 45 patients (4.3%). In a multivariate logistic regression analysis, hyponatremia was independently associated with 30-day mortality. The risk of 30-day mortality associated with hyponatremia on admission (odds ratio [OR] = 2.0; 95% confidence interval [CI]: 1.0 to 3.9; P = 0.04) was similar to that of hyponatremia developing after admission (OR = 2.4; 95% CI: 1.5 to 4.2; P = 0.002). The risk of 30-day mortality increased with the severity of hyponatremia, with an odds ratio of 2.1 in patients with sodium levels between 130 and 134 mmol/L (95% CI: 1.2 to 3.5; P = 0.007) and 3.4 in those with levels <130 mmol/L (95% CI: 1.5 to 7.8; P = 0.002). CONCLUSION: Hyponatremia on admission or early development of hyponatremia in patients with acute ST-elevation myocardial infarction is an independent predictor of 30-day mortality, and prognosis worsens with the severity of hyponatremia. Further studies are required to determine if plasma sodium levels may serve as a simple marker to identify patients at high risk.     

Effect of hyponatremia (<135 mEq/L) on outcome in patients with non-ST-elevation acute coronary syndrome

Hyponatremia is associated with adverse outcomes in patients with heart failure and ST-elevation myocardial infarction (STEMI). We evaluated the effect of hyponatremia on outcomes in patients with suspected acute coronary syndrome and non-STEMI. All patients had a sodium level determined at time of admission, at 24 and 48 hours, and at discharge. Of 1,478 patients, 341 (23.1%) were hyponatremic (sodium <135 mEq/L) on presentation. Patients who had hyponatremia on admission were significantly more likely to die or have recurrent myocardial infarction in the next 30 days (odds ratio 1.98, 95% confidence interval 1.35 to 2.89, p <0.001). This relation persisted after adjusting for factors such as age, left ventricular ejection fraction, use of diuretics before admission, hypotension on presentation, anemia, chronic renal insufficiency, pulmonary edema, and high troponin levels (odds ratio 1.7, 95% confidence interval 1.1 to 2.5, p = 0.01). In conclusion, hyponatremia on admission is associated with 30-day adverse outcome in patients presenting with suspected acute coronary syndrome/non-STEMI.     

Mortality and Serum Sodium: Do Patients Die from or with Hyponatremia?

Summary

Background and objectives

Severe hyponatremia (<120 mEq/L) in hospitalized patients has a high mortality rate. We hypothesized that underlying diseases causing hyponatremia attribute to mortality rather than hyponatremia itself.

Design, setting, participants, & measurements

The relationship between mortality and serum sodium (sNa) was examined in 45,693 patients admitted to a single community teaching hospital between January 1996 and December 2007. We conducted a comprehensive retrospective review of the medical records of 53 patients who died after developing sNa <120 mEq/L before or after admission and of 32 patients who survived after developing sNa <110 mEq/L.

Results

Mortality rates tended to increase as the sNa fell from 134 to 120 mEq/L, rising above 10% for patients with sNa of 120 to 124 mEq/L. However, below sNa of 120 mEq/L, the trend reversed, such that the mortality rate progressively decreased as sNa fell. More than two thirds of patients who died after sNa <120mEq/L had at least two additional acute severe progressive illnesses, most commonly sepsis and multiorgan failure. Three deaths (5.6%) in 12 years could plausibly be related to adverse consequences of hyponatremia, and one (1.8% of the fatal cases and 0.15% of all patients with sNa <120 mEq/L) was from cerebral edema. Most patients who survived with sNa <110 mEq/L had medication-induced hyponatremia. Severe underlying illnesses were uncommon in this group.

Conclusions

The nature of underlying illness rather than the severity of hyponatremia best explains mortality associated with hyponatremia. Neurologic complications from hyponatremia are uncommon among patients who die with hyponatremia.     

Hypernatremia and moderate-to-severe hyponatremia are independent predictors of mortality in septic patients at emergency department presentation: A sub-group analysis of the need-speed trial

Study objectiveEarly risk stratification of septic patients presenting to the emergency department (ED) is challenging. The aim of the study was to evaluate the prognostic role of plasmatic sodium level (_PNa⁺) derangements at ED presentation in septic patients.MethodsAccording to _PNa⁺ at ED presentation patients were divided in eunatremic (136–145 mEq/L), hypernatremic (>145 mEq/L) and hyponatremic (<136 mEq/L). Hyponatremic patients were subsequently divided in mild (130–135 mEq/L), moderate (125–129 mEq/L) and severe (<125 mEq/L). 7 and 30-day mortality was evaluated according to _PNa⁺ derangements and the degree of hyponatremia. The same analysis was then performed only in respiratory tract infection-related (RTI-r) sepsis patients.Results879 septic patients were included in this analysis, 40.3% had hyponatremia, 5.7% hypernatremia. Hypernatremia showed higher mortality rates at both endpoints compared to eunatremia and hyponatremia (p<0.0001 for both). Eunatremia and mild hyponatremia were compared vs. moderate-to-severe hyponatremia showing a significant difference in terms of 7 and 30-day survival (p = 0.004 and p = 0.007, respectively). The Cox proportional model identified as independent predictors of 7 and 30-day mortality moderate-to-severe hyponatremia (HR 4.89[2.38–10.03] and 1.79[1.07–3.01], respectively) and hypernatremia (HR 3.52[1.58–7.82] and 2.14[1.17–3.92], respectively). The same analysis was performed in patients with respiratory tract infection-related sepsis (n = 549), with similar results.ConclusionBoth hypernatremia and moderate-to-severe hyponatremia at ED presentation independently predict mortality in septic patients, allowing early risk stratification and suggesting more aggressive therapeutic strategies.     

Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes.

1. An attempt was made to evaluate the pathophysiology of symptoms of hyponatremia as related to changes in brain water and electrolytes. Studies were carried out in 66 hyponatremic patients and 5 groups of experimental animals. 2. In hyponatremic patients, symptoms (depression of sensorium, seizures) correlated well with plasma Na+ (r = 0.64, p less than .001), but there was substantial overlap. In patients with acute hyponatremia, all were symptomatic and 50% died. Among patients with hyponatremia of at least 3 days duration, sympatomatic patients had plasma Na+ (115 +/- 1 mEq/L) which was significantly less (p less than .001) than that of asymptomatic patients (plasma Na+ = 122 +/- 1 mEq/L). Among symptomatic patients, mortality was 12% and 8% had seizures, while none of the asymptomatic patients died or had seizures. 3. Among 14 patients with acute (less than 12 hrs) hyponatremia, the mean plasma Na+ was 112 +/- 2 mEq/L. All such patients had some depression of sensorium and four had grand male seizures. Seven of these patients were treated with hypertonic (862 mM) NaCl, while four were treated only with fluid restriction. Of the seven patients treated with hypertonic NaCl, five survived, while three of four patients treated with fluid restriction died. There was no evidence of circulatory congestion or cerebral damage in the patients treated with hypertonic NaCl. 4. Among rabbits with acute (2-3 hours) hyponatremia (plasma Na+ = 119 +/- 1 mEq/L), all had grand mal seizures and 86% died. All such animals had cerebral edema (brain H2O content 17% above control value) but brain content of Na+, K+ and Cl- was normal. 5. Rabbits with 3 1/2 days of hyponatremia (plasma Na+ = 122 +/- 2 mEq/L) appeared to be asymptomatic, even though brain water content was 7% above normal (p less than .01). 6. Rabbits with 16 days of more severe hyponatremia (plasma Na+ = 99 +/- 3 mEq/L) were weak, anorexic, lethargic and unable to walk. Brain water content was 7% above normal, although brain osmolality (218 +/- 12 mOsm/kg H2O) was similar to plasma (215 +/- 8 mOsm/kg). Brain content of Na+, K+, Cl- and osmoles was 17 to 37% less than normal values, so that the brain established osmotic equilibrium with plasma primarily by means of a loss of electrolytes. 7. These studies suggest that in patients with hyponatremia, symptoms and morbidity are only grossly correlated with either magnitude or duration of hyponatremia. Symptoms appear to correlate best with the interplay between a net increase in brain water versus a loss oof brain electrolytes. However, even asymptomatic animals have subclinical brain edema when plasma Na+ is below 125 mEq/L, and such edema may cause permanent brain damage. Thus, many patients with similar levels of plasma Na+, particularly when they are symptomatic, should probably be treated with hypertonic NaCl infusions.     

Appropriateness and complications of the use of spironolactone in patients treated in a heart failure clinic

Objectives

The widespread use of spironolactone in patients with congestive heart failure (CHF) has resulted in side effects and complications. We analyzed a cohort of patients treated by a dedicated CHF team, in order to examine the tolerability and safety of spironolactone in clinical practice.

Methods

We retrospectively evaluated data on 157 patients who were followed by the Heart Failure clinic of whom 100 patients on maximal treatment (all on β blockers, 99% on ACE inhibitors) received spironolactone. The complications following spironolactone use were defined as: hyperkalemia with serum K 5.2 mEq/l; creatinine 2.0 mg/dl; hyponatremia with serum Na 135 mEq/l, hypotension and side effects such as gynecomastia and abdominal pain.

Results

At 1 year follow-up 6 patients developed hyperkalemia (range 5.3-5.9), 4 of them had K > 5.5 mEq/l. Two patients developed hyponatremia. Six patients stopped spironolactone for: 1-gynecomastia, 2-worsening renal failure and hyperkalemia, 2-hyperkalemia (5.9 mEq/l) and 1 for bradycardia. There was an increase in mean creatinine level at 1 year (1.12 ± 0.35 vs. 1.21 ± 0.38 mg/dl, p = 0.02), however, no significant changes were found in GFR (99.9 ± 33.5 vs. 65.7 ± 27.7 ml min^− 1 1.73 m^− 2, p = ns) and potassium (4.5 ± 0.4 vs. 4.6 ± 0.5 mEq/l, p = ns). We found improvement of GFR by > 10% in 19 patients and worsening by > 10% in 38 patients. No patient was hospitalized or required urgent treatment for spironolactone-related side effects.

Conclusions

In patients with CHF on optimal therapy with ACE inhibitors and β blockers appropriate spironolactone use and close follow-up by a dedicated HF team can minimize the risk for adverse events and complications.     

Incidence of Hyponatremia with High-Dose Trimethoprim-Sulfamethoxazole Exposure

Background

Trimethoprim-sulfamethoxazole (TMP-SMX) is a commonly prescribed antibiotic used at high doses for treatment of pneumocystis pneumonia and other infections. Trimethoprim is structurally related to the potassium-sparing diuretic amiloride and has been associated with hyperkalemia and hyponatremia through blocking of epithelial sodium channels in the distal nephron. The incidence of hyponatremia in hospitalized patients treated with high-dose TMP-SMX is unknown.

Methods

We performed a single-center retrospective chart review of all hospitalized patients who received high-dose TMP-SMX (n = 235) from January 2012 to July 2014. Patients with congestive heart failure, cirrhosis, estimated glomerular filtration rate <30 mL/min/1.73 m², baseline hyponatremia, and those on other medications associated with hyponatremia were excluded. Hyponatremia was defined as a serum sodium level <136 mEq/L.

Results

Analysis was restricted to 76 unique patients who received more than 8 mg/kg/d of TMP for ≥3 days. Mean starting serum sodium at time of TMP-SMX initiation was 138.4 ± 2.1 mEq/L. Fifty-five patients (72.3%) developed hyponatremia while on therapy, of which 43.6% (n = 24) were cases of serum sodium <130 mEq/L. Mean sodium at the time of nadir was 131.6 ± 5.1 mEq/L. Hyponatremia was noted, on average, 5.5 days after initiation of therapy, with more severe hyponatremia development among African American patients. Urine sodium concentrations were available for 40.0% (22/55) of incident hyponatremia cases, with mean urinary sodium of 104.8 ± 55.9 mEq/L. Hyponatremia often resolved within 3 weeks of drug discontinuation.

Conclusions

There is a high incidence (72.3%) of hyponatremia associated with the use of high-dose TMP-SMX among hospitalized patients. This is an overlooked and potentially reversible cause of hyponatremia.     

Hyponatremia and long-term mortality in survivors of acute ST-elevation myocardial infarction

BACKGROUND: Hyponatremia, a marker of neurohormonal activation, is a common electrolyte disorder among patients with acute ST-elevation myocardial infarction. The long-term prognostic value of hyponatremia during the acute phase of infarction is not known. METHODS: We studied 978 patients with acute ST-elevation myocardial infarction and without a history of heart failure who survived the index event. During the hospital stay, sodium levels were obtained on admission and at 24, 48, and 72 hours. The median duration of follow-up after hospital discharge was 31 months (range, 9-61 months). RESULTS: Hyponatremia, defined as a mean serum sodium level less than 136 mEq/L, was present during admission in 108 patients (11.0%). In a multivariable Cox proportional hazards model adjusting for other potential clinical predictors of mortality and for left ventricular ejection fraction, hyponatremia during admission remained an independent predictor of postdischarge death (hazard ratio [HR], 2.0; 95% confidence interval [CI], 1.3-3.2; P = .002). Hyponatremia during admission was also independently associated with postdischarge readmission for heart failure (HR, 1.6; 95% CI, 1.1-2.6; P = .04). When serum sodium level was used as a continuous variable, the adjusted HR for death or heart failure was 1.12 for every 1-mEq/L decrease (95% CI, 1.07-1.18; P<.001). CONCLUSION: Hyponatremia in the early phase of ST-elevation myocardial infarction is a predictor of long-term mortality and admission for heart failure after hospital discharge, independent of other clinical predictors of adverse outcome and left ventricular ejection fraction.     

Mechanism of low serum sodium levels in Mediterranean spotted fever.

Prominent degrees of hyponatremia are detected in the severe forms of Mediterranean spotted fever and the intensity of this abnormality parallels the severity of the infectious process. In order to determine the incidence, degree and evolution of hyponatremia in 110 patients with Mediterranean spotted fever and to explore the feasible renal mechanism that could lead to this phenomenon, serum and urinary osmolality and levels of urea, creatinine and electrolytes were measured in samples obtained at selected points (up to the fifth week) in the course of the disease, and parameters of renal function were calculated. Mean serum sodium levels of 135.6 +/- 5.5 mEq/l were detected during the acute phase of the infection. At this point, 42 patients (38.2%) had sodium concentrations less than or equal to 135 mEq/l. After recovery, mean serum sodium values were 142.5 +/- 2.5. The analysis of the parameters of renal function indirectly rules out an inappropriate antidiuretic hormone secretion or renal failure as the cause of hyponatremia. As tubular incompetence to reabsorb sodium is also rejected in these patients, a shifting of sodium to the interstitial or intracellular space may account for the phenomenon.     

Hypokalaemia and ventricular fibrillation in acute myocardial infarction

Serum potassium concentrations obtained on admission to hospital were inversely related to the incidence of ventricular fibrillation in 289 women and 785 men with acute myocardial infarction, 92 of whom developed ventricular fibrillation. Hypokalaemia (serum potassium concentration less than or equal to 3.5 mmol/l) was found in 122 patients (11.4%). The incidence of ventricular fibrillation was significantly greater in patients with hypokalaemia compared with those classified as normokalaemic (serum potassium concentration greater than or equal to 3.6 mmol/l) (17.2% v 7.4%). The increased risk of ventricular fibrillation in the hypokalaemic group was about the same for women and men. While they were in hospital patients with hypokalaemia developed ventricular fibrillation significantly earlier than did normokalaemic patients (median 0.3 hours v 7 hours). Hypokalaemia was more common in women (17.3%) than in men (9.2%), and 55% of the hypokalaemic patients had been treated with diuretics before admission compared with 22% of the normokalaemic group. Hypokalaemia on admission to hospital predicts an increased likelihood and early occurrence of ventricular fibrillation in patients with acute myocardial infarction.     

Hypokalaemia and ventricular fibrillation in acute myocardial infarction.

Serum potassium concentrations obtained on admission to hospital were inversely related to the incidence of ventricular fibrillation in 289 women and 785 men with acute myocardial infarction, 92 of whom developed ventricular fibrillation. Hypokalaemia (serum potassium concentration less than or equal to 3.5 mmol/l) was found in 122 patients (11.4%). The incidence of ventricular fibrillation was significantly greater in patients with hypokalaemia compared with those classified as normokalaemic (serum potassium concentration greater than or equal to 3.6 mmol/l) (17.2% v 7.4%). The increased risk of ventricular fibrillation in the hypokalaemic group was about the same for women and men. While they were in hospital patients with hypokalaemia developed ventricular fibrillation significantly earlier than did normokalaemic patients (median 0.3 hours v 7 hours). Hypokalaemia was more common in women (17.3%) than in men (9.2%), and 55% of the hypokalaemic patients had been treated with diuretics before admission compared with 22% of the normokalaemic group. Hypokalaemia on admission to hospital predicts an increased likelihood and early occurrence of ventricular fibrillation in patients with acute myocardial infarction.     

老年脑出血与脑梗死心电图分析

目的观察老年患者不同部位脑出血及脑梗死的心电图特征。方法回顾同期住院的126例老年脑出血及151例老年脑梗死患者的心电图资料,分析其表现。结果2组心电图异常改变均主要表现为ST-T异常和(或)心律失常。脑出血组窦性心动过速、左室肥大和病死率(15.9%、15.9%和12.7%)明显高于脑梗死组(6.0%、6.0%和4.0%,P<0.01),脑梗死组的窦性心动过缓并心律不齐、房颤和期前收缩的发生率(12.6%、11.2%、11.2%)明显高于脑出血组(3.2%、7.1%、7.1%,P<0.05)。结论脑出血、脑梗死的心电图异常与疾病的严重程度密切相关。     

A patient with meningeal carcinomatosis accompanied by a small pituitary metastatic lesion from gastric cancer who developed cerebral salt wasting syndrome

A 68-year-old man with disturbed consciousness had repeatedly developed light-headedness and dizziness since the summer of 1996 and was admitted to a hospital for detailed examinations on October 8, 1996. On admission, he weighed 49 kg and showed subclinical hypothyroidism with low T3 syndrome. The adrenal function and serum electrolytes were normal. Since the stool samples were positive for occult blood, gastroscopy was performed. Examination of the biopsy specimens demonstrated gastric cancer. On October 21, blood examination showed hyponatremia (127 mEq/l). On October 22, marked disturbance of consciousness developed. On October 24, the serum Na level further decreased to 116 mEq/l. On November 8, he was referred to our hospital. On admission, his skin and tongue showed marked dehydration, and severe disturbance of consciousness and neck stiffness were observed. The central venous pressure was 4 cmH2O. In the cerebrospinal fluid, atypical cells were observed, and a diagnosis of meningeal carcinomatosis was made. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was excluded because of marked dehydration, a normal blood ADH level, and because plasma osmotic pressure was greater than urinary osmotic pressure. Considering the possibility of cerebral salt wasting syndrome (CSWS) or hypoadrenocorticism, Na supplementation and drip infusion of prednisolone (20 mg/day) were performed. The serum Na has normalized (140.1 mEq/l), and his consciousness improved. He died of aggravation of the general condition on December 16. Pathological examination demonstrated a small metastatic lesion in the infundibular part of the pituitary gland and a small metastatic lesion in the parenchyma of the bilateral adrenal glands. However, since neither hypotension nor hypoglycemia was observed before treatment, and the blood cortisol level and the serum K level were normal, hypoadrenocorticism was excluded. Hypoaldosteronism was also excluded because of a normal serum K level. CSWS has been reported to be caused by head trauma, subarachnoid hemorrhage, or trans-sphenoidal pituitary operation. This patient is a rare case of CSWS developed in the presence of meningeal carcinomatosis accompanied by a small pituitary metastatic lesion from gastric cancer. The aged with decreased ability to retain water and sodium in the body are more susceptible to CSWS than the young. In the aged with central hyponatremia, the possibility of CSWS should be considered, and early diagnosis and treatment are necessary.     

高龄脑梗死患者经静脉溶栓后早期颅内出血的相关因素分析

目的研究高龄脑梗死患者接受重组组织型纤溶酶原激活物（rt-PA）静脉溶栓后早期颅内出血（ICH）的相关因素。方法连续收集2006年7月—2011年10月上海市第一人民医院分院神经科于发病4.5 h内给予rt-PA静脉溶栓治疗的急性脑梗死患者,共175例。根据患者年龄分为年龄〈80岁组（121例）和年龄≥80岁组（54例）,对所有患者的临床资料进行回顾性分析。统计溶栓后24 h内颅内出血（ICH）和症状性颅内出血（SICH）的例数。采用改良Rankin（mRS）评分对存活的ICH患者进行随访。结果①共31例（17.7%）患者于溶栓后24 h发生ICH,年龄〈80岁组和年龄≥80岁组的ICH发生率分别为15.7%和22.2%,SICH发生率分别为5.8%和14.8%,两组患者ICH和SICH发生率的比较,差异无统计学意义,P〉0.05。②在脑白质疏松（LA）患者中,年龄〈80岁组的ICH发生率（16.7%）低于年龄≥80岁组（36.6%）,差异有统计学意义（χ2=4.643,P=0.031）;其余可能的危险因素,年龄〈80m岁组与≥80岁组的ICH发生率比较,差异无统计学意义。③共23例ICH患者好转出院。出院后90 d随访显示,年龄〈80岁组患者的基本痊愈和轻中度残疾的比例高于年龄≥80岁组,重度残疾的比例低于年龄≥80岁组,但差异无统计学意义。结论 LA可能与高龄患者溶栓后早期ICH具有相关性。     

Hyponatremia and/or hyperkalemia in patients treated with the standard dose of trimethoprim-sulfamethoxazole

OBJECTIVE: High-dose trimethoprim-sulfamethoxazole (TMP-SMX) is known to cause hyperkalemia by blocking amiloride-sensitive sodium (Na) channels in distal nephrons. The purpose of this study was to establish whether the standard dose of TMP-SMX could cause electrolyte disorders. METHODS AND PATIENTS: Serum Na, potassium (K) and creatinine (Cr) levels were examined retrospectively in 53 of 77 patients prescribed TMP-SMX, before and after taking the antibiotic combination. RESULTS: Electrolyte disorders (Na < 135 mEq/l and/or K > 5.0 mEq/l) were found in 14 of the 53 patients (26.4%) during TMP-SMX treatment. The average dose was 145.7 +/- 24.9 mg/day. The dose of TMP was significantly larger in patients with electrolyte disorders (267.7 +/- 84.2 mg vs. 101.9 +/- 9.38 mg, p = 0.0024). Electrolyte disorders were also seen in 9.1% and 22.2% of patients given the low dose (TMP < 80 mg) or standard dose (TMP 80-120 mg) of TMP-SMX, respectively. Electrolyte disorders were seen in 85.7% of patients with renal dysfunction (Cr > 1.2 mg/dl), compared with 17.5% of patients with normal renal function (p = 0.0008). Logistic regression analysis showed that the dose of TMP and the presence of renal dysfunction increased the incidence of electrolyte disorders with an odds ratio of 2.35 and 80.29, respectively. CONCLUSION: Electrolyte disorders, particularly hyperkalemia and hyponatremia can be detected in patients given TMP-SMX. These disorders are more frequent in patients given high doses, but can also be detected after low-dose administration. Renal dysfunction accelerates the incidence of electrolyte disorders induced by TMP-SMX.