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Eur J Cardiothorac Surg 2004;26:306-310
© 2004 Elsevier Science NL
a Department of General Intensive Care, Rabin Medical Center, Campus Beilinson, Petah Tikva 49100, Israel
b Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
c Department of Cardiothoracic Surgery, Rabin Medical Center, Campus Beilinson, Petah Tikva 49100, Israel
Received 14 December 2003; received in revised form 6 March 2004; accepted 8 March 2004.
* Corresponding author. Address: Department of General Intensive Care, Rabin Medical Center, Campus Beilinson, Petah Tikva 49100, Israel. Tel.: +972-3-937-6525; fax: +972-3-923-2333
e-mail: jonatanc{at}clalit.org.il
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Abstract |
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 Top Abstract 1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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Key Words: Hypophosphatemia • Postoperative • Major cardiac surgery
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1. Introduction |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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The incidence of hypophosphatemia, and in particular the possible consequences thereof, are less well described in patients following cardiac surgery [4,5]. Interestingly, many of the major reported complications following cardiac surgery [6] including respiratory failure requiring prolonged mechanical ventilatory support (in 3.4–5.6% of patients) and myocardial dysfunction (1.3%), are also amongst the common clinical manifestations of hypophosphatemia [7]. Since the occurrence of major postoperative complications after cardiac surgery may have profound consequences for both the patient (altered functional status and quality of life) and the health care system (increased utilization of scarce resources and costs), much research has focused on identifying patient and intraoperative factors predisposing to major morbidity [6,7]. However, hypophosphatemia has not been specifically targeted as a possible reversible cause for these complications.
We therefore performed a prospective study in patients undergoing elective major cardiac surgery to assess the incidence and possible clinical consequences of significant hypophosphatemia (SH).
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2. Materials and methods |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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2.2. Surgery and postoperative care
All patients received standardized anesthesia. Cardiopulmonary bypass was performed using a membrane oxygenator. Cardiac arrest was achieved by multiple administrations of anterograde and/or retrograde blood cardioplegia. In almost all cases, core temperature was around 30 °C. All patients were rewarmed to 37 °C before discontinuation of cardiopulmonary bypass. After completion of surgery, all patients were returned to the cardiothoracic ICU while still intubated.
Standardized postoperative care consisted of mechanical ventilation in the assist-control mode, cardioactive drugs (dopamine and/or noradrenaline) to maintain the mean arterial pressure between 60 and 80 mmHg, the use of warm air heaters to maintain normothermia, and analgesia with IV morphine boluses as required. Criteria for weaning from the ventilator included hemodynamic stability (no or decreasing use of cardioactive drugs), absence of significant bleeding (<100 ml/h), absence of significant arrhythmias, adequate urine output (>1 cm3/kg per h), and oxygen saturation >95% with fractional concentration of inspired oxygen <0.50; the patient also needed to be sufficiently awake to follow commands. Patients fulfilling these criteria were placed on pressure support ventilation for 20–30 min, and in the absence of respiratory or cardiac distress, extubation was performed immediately thereafter. Patients were discharged from the ICU to the ward at least 4–6 h after extubation. During this period, any increasing requirement for cardioactive drugs, or significant decrease in oxygen saturation (<90% despite oxygen mask), urine output, or level of consciousness, was considered a contraindication for discharge.
Patients were discharged from the hospital when they were physically independent, not requiring any intravenous medications, were in sinus rhythm and there was no evidence of wound infection.
2.3. Blood sampling and data collection
Serum electrolytes, including phosphate, potassium, magnesium, and ionized calcium were measured at three time periods: on the morning prior to surgery, immediately after admission to the ICU and on the first postoperative day (Hitachi 747 Automatic Analyzer, Boehringer Mannheim, Germany).
In order to assess the incidence, possible causes and consequences of postoperative hypophosphatemia, we differentiated patients into two groups according to the serum phosphate level measured immediately after surgery: those with SH, defined as a level of <0.48 mmol/l, and a control group. The normal value for serum phosphate at our institution ranges from 0.80 to 1.45 mmol/l.
In all patients, the type of procedure performed, 2000 Bernstein–Parsonnet preoperative risk estimate score [8], duration of cross-clamping and bypass, amount of intraoperative fluids administered, and units of packed red cells, fresh frozen plasma and platelets transfused, were analyzed. The postoperative variables analyzed included duration of mechanical ventilation, presence of atrial fibrillation, cardioactive drug requirements (on admission to the ICU, and at 4, 12–24, and >24 h after admission), duration of ICU and hospital stay, and in-hospital mortality.
2.4. Interventions
All patients with SH received intravenous phosphate replacement either in the form of sodium or potassium phosphate (if the serum potassium was <3.5 mmol/l) given at a dose of 0.8 mmol/kg body weight over 6–12 h [1].
2.5. Statistical analysis
Data are presented as mean±SD. Comparison of baseline characteristics was performed using an unpaired Student's t-test. Serological data before, immediately after and 24 h following surgery were compared using the Wilcoxon signed rank test. A P value equal or less than 0.05 was considered significant. Analysis was performed using SPSS 8.0 for Windows (SPSS, Chicago, IL).
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3. Results |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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The phosphate levels measured preoperatively and on the first postoperative day were not significantly different in the SH and control group (Table 1). The mean potassium value was significantly lower for the total group in the sample obtained immediately after surgery (P=0.03).
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4. Discussion |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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Hypophosphatemia has been described following major surgery, including hepatic surgery [2,3,10], elective abdominal aortic bypass surgery [11] and general surgery [1], and typically occurs on the second postoperative day. Recognized risk factors include sepsis, and the use of diuretics, antacids and total parenteral nutrition [1–3]. In our patients, SH was already evident in the immediate postoperative period. This finding has also been noted in a recent study [4] in which phosphate levels measured upon admission to the ICU were significantly lower in patients undergoing cardiac surgery than in a control group who had undergone various other surgical procedures (0.49±0.2 versus 0.92±0.32 mmol/l, P<0.01). Risk factors for developing hypophosphatemia in patients undergoing cardiac surgery are not well-defined. However, the onset in the immediate postoperative period suggests a causal relationship to the intraoperative course. In fact, the surgical procedure appears to particularly predispose to hypophosphatemia. Thus, catecholamines, which are invariably required during such procedures, and were used intraoperatively in 80% of our patients, may result in an intracellular shift of phosphate via beta-adrenergic receptor mediated stimulation of phosphate uptake [12], which appears to be dose-dependent. Cardiac surgery with cardiopulmonary bypass has been shown to induce an acute-phase reaction, with elevated levels of interleukin-6 and other pro-inflammatory cytokines [13]. High levels of these cytokines may result in the shift of phosphate from the intra- to extravascular space, further aggravating hypophosphatemia [14]. In the study of Giovanni et al. in patients undergoing hepatectomy [3], SH was found to anticipate clinical evidence of postoperative complications. The authors found a strong inverse relationship between phosphate levels and the APACHE II score and they suggested that SH was a humoral marker of an intense acute-phase response. An additional cause for SH in patients undergoing cardiac surgery is the effect of hypothermia. Thus, it has been shown that plasma phosphate levels decreased significantly in patients undergoing moderate hypothermia (32–33 °C) as part of the treatment for brain injury [15]. The authors postulated that the mechanism was related to sympathetic activation after moderate hypothermia resulting in hyperglycemia and insulin release, driving phosphate into the intracellular space with glucose. The decrease in serum potassium seen post-surgery may also be explained by the release of endogenous catecholamines and hypothermia [16].
The reason for the SH in our series is not obvious. However, patients in the SH group required more blood products, especially platelets (6.2±2.4 versus 2.1±1.3 units, P=0.01) and were receiving more cardioactive drugs at the time of admission to the ICU (42.3 versus 28.2%, P=0.05). This suggests that the intraoperative course was more traumatic in these patients so that the SH may have been catecholamine and cytokine mediated.
The potential consequences of hypophosphatemia may be particularly deleterious to patients following cardiac surgery. In our series, patients developing SH required significantly more prolonged mechanical ventilation and cardioactive drug support than did the normophosphatemic controls. Hypophosphatemia has been shown to impair diaphragmatic contractility [17] leading to respiratory muscle dysfunction, and the result may be a requirement for prolonged mechanical ventilation. Repletion of phosphorus stores may reverse the failure to wean [18]. The cardiovascular system may also be affected, and possible effects include cardiac arrhythmias [19] and altered myocardial function [20]. Again, once recognized, these effects may be reversed by the administration of phosphate. Two additional potential consequences of SH need to be mentioned, particularly in the context of cardiac surgery. Abnormalities in leukocyte function, including depression of chemotactic, phagocytic and bactericidal activity have been reported [21]. These effects may have considerable implications in patients at risk for developing sepsis. SH may also result in glucose intolerance, probably as a result of tissue insensitivity [22]; this is again particularly relevant for patients after cardiac surgery where hyperglycemia has been shown to result in increased infectious complications [23].
In view of the possible adverse consequences of SH, there are strong reasons for restoring normal levels as quickly as possible. In our patients, phosphate replacement was initiated in the postoperative period for serum phosphate levels below 0.48 mmol/l. The early initiation of therapy may have prevented any increased mortality from SH. However, complications were common. This is probably related to inadequate replacement, as levels on the first postoperative day had not returned to normal. A high failure rate of adequate phosphate repletion (20–70%) and the need for additional phosphate administration has been reported in Ref. [24]. This may be due to the fact that ICU patients have many physiological derangements, which increase the amount required for repletion. These include an increased volume of distribution for phosphate, and the use of insulin, glucose, and catecholamine infusions which all tend to decrease the phosphate level even further. For this reason, a recent paper [25] has suggested using a more rapid infusion of phosphate (30 mmol of potassium phosphate in 50 ml of saline given over 2 h). They showed an overall efficacy of 98% by the end of the infusion, no adverse events were reported and the need for resupplementation over the entire study period was 28%, which is a lower rate than reported in other studies. We are presently conducting a prospective study measuring phosphate levels during the surgical procedure to determine at what stage SH appears with a view to instituting intraoperative supplementation and so possibly avoiding the postoperative complications.
4.1. Conclusion
We have shown that hypophosphatemia is common after major cardiac surgery, occurs in the immediate postoperative period and is associated with significant respiratory and cardiac morbidity. We suggest that phosphate levels be routinely measured after surgery, especially in patients having a complicated intraoperative course, so that appropriate replacement therapy may be started in a timely manner.
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References |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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