Severe electrolyte disorders following cardiac surgery: a prospective controlled observational study

Introduction

Electrolyte disorders are an important cause of ventricular and supraventricular arrhythmias as well as various other complications in the intensive care unit. Patients undergoing cardiac surgery are at risk for development of tachyarrhythmias, especially in the period during and immediately after surgical intervention. Preventing electrolyte disorders is thus an important goal of therapy in such patients. However, although levels of potassium are usually measured regularly in these patients, other electrolytes such as magnesium, phosphate and calcium are measured far less frequently. We hypothesized that patients undergoing cardiac surgical procedures might be at risk for electrolyte depletion, and we therefore conducted the present study to assess electrolyte levels in such patients.

Methods

Levels of magnesium, phosphate, potassium, calcium and sodium were measured in 500 consecutive patients undergoing various cardiac surgical procedures who required extracorporeal circulation (group 1). A total of 250 patients admitted to the intensive care unit following other major surgical procedures served as control individuals (group 2). Urine electrolyte excretion was measured in a subgroup of 50 patients in both groups.

Results

All cardiac patients received 1 l cardioplegia solution containing 16 mmol potassium and 16 mmol magnesium. In addition, intravenous potassium supplementation was greater in cardiac surgery patients (mean ± standard error: 10.2 ± 4.8 mmol/hour in cardiac surgery patients versus 1.3 ± 1.0 in control individuals; P < 0.01), and most (76% versus 2%; P < 0.01) received one or more doses of magnesium (on average 2.1 g) for clinical reasons, mostly intraoperative arrhythmia. Despite these differences in supplementation, electrolyte levels decreased significantly in cardiac surgery patients, most of whom (88% of cardiac surgery patients versus 20% of control individuals; P < 0.001) met criteria for clinical deficiency in one or more electrolytes. Electrolyte levels were as follows (mmol/l [mean ± standard error]; cardiac patients versus control individuals): phosphate 0.43 ± 0.22 versus 0.92 ± 0.32 (P < 0.001); magnesium 0.62 ± 0.24 versus 0.95 ± 0.27 (P < 0.001); calcium 1.96 ± 0.41 versus 2.12 ± 0.33 (P < 0.001); and potassium 3.6 ± 0.70 versus 3.9 ± 0.63 (P < 0.01). Magnesium levels in patients who had not received supplementation were 0.47 ± 0.16 mmol/l in group 1 and 0.95 ± 0.26 mmol/l in group 2 (P < 0.001). Urinary excretion of potassium, magnesium and phosphate was high in group 1 (data not shown), but this alone could not completely account for the observed electrolyte depletion.

Conclusion

Patients undergoing cardiac surgery with extracorporeal circulation are at high risk for electrolyte depletion, despite supplementation of some electrolytes, such as potassium. The probable mechanism is a combination of increased urinary excretion and intracellular shift induced by a combination of extracorporeal circulation and decreased body temperature during surgery (hypothermia induced diuresis). Our findings may partly explain the high risk of tachyarrhythmia in patients who have undergone cardiac surgery. Prophylactic supplementation of potassium, magnesium and phosphate should be seriously considered in all patients undergoing cardiac surgical procedures, both during surgery and in the immediate postoperative period. Levels of these electrolytes should be monitored frequently in such patients.     

The use of real-time PCR to identify Entamoeba histolytica and E. dispar infections in prisoners and primary-school children in Ethiopia

In Ethiopia, it is generally unknown what proportion of the amoebic infections commonly found, by microscopy, in humans are caused by non-invasive Entamoeba dispar rather than the potentially invasive E. histolytica. Faecal samples were therefore collected from 363 primary-school students and 409 prisoners from various regions of Ethiopia. Each of these samples was checked for Entamoeba infection by the microscopical examination of formol-ether concentrates. DNA was then extracted from the 213 samples (27.6%) found Entamoeba-positive, and run in a real-time PCR with primers, based on the SSU-rRNA gene sequences of E. histolytica and E. dispar, that allow DNA from the two species to be distinguished. Although E. dispar DNA was identified in 195 (91.5%) of the 213 samples checked by PCR, no E. histolytica DNA was detected. This finding is consistent with the conclusion of a previous, smaller investigation: that many amoebic infections in Ethiopia are incorrectly attributed to E. histolytica and then treated, unnecessarily, with amoebicidal drugs.     

Neuroprotection in acute brain injury: an up-to-date review

Neuroprotective strategies that limit secondary tissue loss and/or improve functional outcomes have been identified in multiple animal models of ischemic, hemorrhagic, traumatic and nontraumatic cerebral lesions. However, use of these potential interventions in human randomized controlled studies has generally given disappointing results. In this paper, we summarize the current status in terms of neuroprotective strategies, both in the immediate and later stages of acute brain injury in adults. We also review potential new strategies and highlight areas for future research.     

Polymerase chain reaction-based differential diagnosis of Ancylostoma duodenale and Necator americanus infections in humans in northern Ghana

We evaluated a two-step semi-nested polymerase chain reaction (PCR)-based approach for the specific detection of Ancylostoma duodenale DNA in human faeces. The test was used to determine to what extent this species of hookworm is present in the regions of Bolgatanga and Garu of northern Ghana. Initially, the sensitivity and specificity of the PCR were tested using a range of well-defined control samples. Subsequently, a total of 378 human faecal DNA samples from Bolgatanga and Garu were subjected to the PCR. The results were compared with those obtained using a previously established PCR for the specific detection of Necator americanus DNA in human faeces. Infection with A. duodenale was recorded in 74 (19.6%) samples and N. americanus in 278 (73.5%), of which 64 (16.9%), represented co-infections with both species. While A. duodenale was predominantly detected in the samples from Bolgatanga, infections in Garu related almost exclusively to N. americanus. The results showed that the present PCR approach is a valuable complementary tool for the diagnosis of A. duodenale infection in humans in Ghana, having implications for epidemiological studies and for the monitoring of the success of control programmes in regions in Africa.     

Sudden unexpected death in children with a previously diagnosed cardiovascular disorder

BACKGROUND: It is known that children with previously diagnosed heart defects die suddenly. The causes of death are often unknown. OBJECTIVE: The aim of the study was to identify all infants and children within the Netherlands with previously diagnosed heart disease who had a sudden unexpected death (SUD), and to identify the possible cause of death. DESIGN: Retrospective, cross-sectional study. PATIENTS AND SETTING: All children (<19 years) with a previously diagnosed heart defect and SUD between January 1990 and June 2001 in seven out of eight tertiary centres in the Netherlands were identified using the hospital databases. We excluded patients receiving compassionate care. Diagnoses, clinical status and circumstances of death were sought from case notes and post mortem reports. Deaths were classified as of cardiac or non-cardiac origin. RESULTS: We identified 150 cases of SUD (89 male) at a median age of 2.3 years (range 18 days-18.9 years); 49/150 patients (33%) were 相似文献   

Intraobserver and interobserver variation of ultrasound diagnosis of Oesophagostomum bifurcum colon lesions

Infection by the nematode Oesophagostomum bifurcum is focally distributed in Africa and causes a syndrome of abdominal pain, obstruction, or abdominal mass because of its predilection for invasion of colonic mucosa. To determine the reliability of ultrasound for the detection of colon pathology induced by this parasite, three studies to assess the intraobserver and interobserver variation of the technique were performed. In an area of northern Ghana endemic for O. bifurcum, 181 people from a low-prevalence village and 62 people from a high-prevalence village were examined twice by the same observer, and 111 people were independently examined by two observers in a moderately endemic village. The kappa statistics for the prevalence observations in the three studies were 0.82, 0.87, and 0.81, respectively, and kappa values for the intensity observations were 0.66, 0.63, and 0.71, respectively. The upper 95% confidence intervals of the average absolute difference in nodule size measurements in Study 1 and Study 3 were 3.6 and 4.5 mm, respectively. Therefore, ultrasound is useful in the diagnosis and management of O. bifurcum colon infection.     

Of ions and temperature: the complicated interplay of temperature,fluids, and electrolytes on myocardial function

This article discusses the potential of levosimendan to treat calcium-induced myocardial dysfunction associated with deep hypothermia. Moderate hypothermia (30 to 34°C) usually improves myocardial contractility and stabilizes heart rhythm, but deep hypothermia can cause severe myocardial dysfunction, which is mediated by intracellular calcium overload. In experimental studies, levosimendan appears effective in reversing this. Clinical studies are needed to confirm these findings and to determine whether levosimendan could also be used for accidental hypothermia and perhaps to mitigate diastolic dysfunction under moderate hypothermia.Lowering core temperature has complex and divergent effects on the myocardium, stimulating or inhibiting contractility and heart rhythm through several different mechanisms. The effects vary with the depth of hypothermia and are influenced by volume status, heart rate (which itself is affected by hypothermia), endocrine factors, and (crucially) extracellular and intracellular electrolyte concentrations. In general, moderate hypothermia (30 to 34°C) improves myocardial contractility whereas deep hypothermia (<28°C) has the opposite effect. Under specific circumstances (presence of tachycardia, hypovolemia, or electrolyte disorders), moderate hypothermia can also cause myocardial dysfunction.Electrolytes, particularly calcium, play a key role in maintaining myocardial contractility through mechanisms that are also temperature-dependent. In the previous issue of Critical Care, Rungatscher and colleagues [1] present the results of a study on a key issue affecting deep hypothermic circulatory arrest (DHCA): reversing calcium-mediated persistent myocardial dysfunction after rewarming from DHCA.Moderate hypothermia (30 to 34°C) increases intracellular Ca²⁺ transients in a dose-dependent fashion, thereby increasing myocardial contractility [2]. However, deep hypothermia (<28°C) can lead to intracellular calcium overload, especially when hypothermia is maintained for more than 30 minutes [3-5]. Intracellular hypercalcemia is corrected only slowly during and after rewarming from deep hypothermia, often leading to persistent myocardial dysfunction [3-5]. In addition, deep hypothermia can induce calcium desensitization, which usually develops during rewarming after DHCA. Diastolic relaxation, in turn, is rate-limited by removal of Ca²⁺ from the cytoplasm and the rate of cross-bridge detachment [6].These issues are further complicated by hypothermia-induced changes in excretion of calcium and other electrolyte levels as well as on electrolyte shifts and changes in intracellular pH. Urinary electrolyte excretion can increase markedly during induction of hypothermia, and a pronounced intracellular shift of potassium, magnesium, phosphate, calcium, and (to a lesser extent) sodium will occur [7-9]. This intracellular shift is reversed when the patient is rewarmed [7,8]. All this can have profound effects on the myocardium; this applies in particular to hypocalcemia, which can cause myocardial dysfunction, hypotension, arrhythmias, and failure to respond to drugs that act through calcium-mediated mechanisms (norepinephrine, dopamine, digoxin, and so on). Deficiencies of magnesium, potassium, and phosphate can also induce myocardial dysfunction and arrhythmias [7]. Conversely, intracellular influx of magnesium can help stabilize cellular membranes, improve intracellular energy management, and mitigate effects of calcium overload (which can occur during deep hypothermia but also during ischemia) [7,8]. In addition, intracellular pH increases during hypothermia, potentially enhancing myocardial contractility by offsetting the calcium-desensitizing effect of hypothermia [10,11]. Intracellular Na⁺ can also increase, leading to increased production of reactive oxygen species (ROS) in the mitochondria [12]. This may initially improve intracellular homeostasis through more effective intracellular signaling and energy management [13], but when the rise is excessive, ROS can severely damage intracellular structures [7,13]. However, in yet another twist, mild hypothermia itself mitigates excessive ROS production, countering the potentially dangerous nitric oxide synthase toxicity [7].Thus, the effects of moderate hypothermia on electrolytes in general and on calcium in particular are convoluted, with numerous and often conflicting effects on myocardial tissue. However, with deep hypothermia, some myocardial dysfunction will almost invariably occur, which is mediated to a substantial degree by intracellular calcium overload.Epinephrin is the drug most commonly used to treat refractory hypotension in this situation. Rungatscher and colleagues [1] compared epinephrine with the calcium sensitizer levosimendan to reverse myocardial dysfunction after rewarming from DHCA in a rat model. They report that levosimendan was significantly more effective in reversing systolic and diastolic myocardial dysfunction, independent of volume status. Levosimendan also improved ventricular relaxation, better preserved myocardial ATP content, and reduced plasma lactate concentrations [1].The same authors previously reported that levosimendan has better inotropic and lusitropic effects than epinephrine during rewarming from DHCA [14]. Others have published similar findings, with positive inotropic effects of levosimendan irrespective of the temperature.Given these experimental data, levosimendan appears to be a highly promising drug to improve myocardial function during and after deep hypothermia, with a number of theoretical advantages over the commonly used epinephrine. The drug now needs to be evaluated in clinical studies, not just in DHCA but also for accidental hypothermia, in which rewarming is often complicated by major hemodynamic problems.Given the mechanisms outlined above, hemodynamic effects of hypothermia can be hard to predict. Moderate hypothermia (30 to 34°C), induced under controlled conditions (euvolemia, preventing discomfort through sedation or other means, preserving normal serum electrolyte levels), will usually decrease heart rate, reduce risk of arrhythmias, markedly improve systolic function, and induce mild diastolic dysfunction. Under optimal conditions, the diastolic dysfunction has only minimal effects on myocardial performance, and the overall effect of cooling will be an improvement in myocardial contractility, increase in stroke volume, reduction in cardiac output (CO) because of the decrease in heart rate, and stabilization or slight increase in blood pressure [7]. Indeed, several clinical studies have reported the successful use of hypothermia to treat refractory cardiac shock [7]. The balance between metabolic supply and demand improves because the decrease in metabolic demand (7% to 10% per °C decrease in core temperature) exceeds the drop in CO [7].However, under different conditions (especially the presence of tachycardia), myocardial contractility may be adversely affected even under moderate hypothermia [7]. Several studies have shown that increasing heart rate under normothermic conditions improves myocardial contractility and CO but that increasing heart rate under hypothermic conditions decreases myocardial contractility [7,15]. There is also a dichotomy in temperature effect on heart rhythm: membrane stabilization and decreased risk of arrhythmias with moderate hypothermia, increased risk of arrhythmias with deep hypothermia (<28°C) [7].The results of the study by Rungatscher and colleagues [1] for deep hypothermia suggest that levosimendan could potentially also be used to reverse the mild diastolic dysfunction that occurs in many patients during moderate hypothermia. However, it is too early to recommend the use of this promising drug outside the context of clinical trials.     

Treatment failure in trichomoniasis and persistence of the parasite after Lactobacillus immunotherapy; two case reports

This report describes the clinical and laboratory observations on two patients with a Trichomonas vaginalis infection resistant to metronidazole. The metronidazole resistance was confirmed in in vitro cultures under aerobic conditions, after in vitro cultivation of the strains. Trichomonas infection persisted during high-dose intravenous metronidazole administration and Lactobacillus immunotherapy was unsuccessful in both patients.