1 Unità Operativa di Nefrologia e Dialisi 2 Divisione di Neurochirurgia Ospedale M. Bufalini, Cesena, Italia
Sir,
We have read with great interest the recent paper by Palmer [1] dealing with hyponatraemia (with natriuresis) developing in neurosurgical patients. Although hyponatraemia in such patients is generally attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), in most patients it is actually caused by a renal salt loss which leads to hyponatraemia and volume depletion (the so-called cerebral salt wasting syndrome [CSWS]) [2]. This creates a diagnostic dilemma where two distinct groups of patients have virtually identical clinical signs, laboratory abnormalities and overlapping associated diseases (intracranial pathology). On the other hand, distinguishing between these disorders is of paramount importance with regard to therapy, since the appropriate treatment of CSWS (fluid replacement) is quite opposite to the treatment of SIADH (fluid restriction).
As stressed by Dr Palmer, volume status may be the only contrasting variable between the euvolaemic patient with SIADH and the hypovolaemic renal salt waster with CSWS. Yet, in contrast with the optimistic statement by Dr Palmer, clinical assessment of the extracellular volume by non-invasive parameters is quite inaccurate in these patients [3].
Central venous pressure (CVP) is a reliable indicator of the blood volume in patients with normal cardiac and pulmonary functions. The placement of a central venous catheter is easily accomplished and the CVP can be determined by a simple saline manometer. By measuring CVP, we [4] were able to differentiate between the above distinct causes of hyponatraemia in 11 otherwise uncomplicated neurosurgical patients: seven patients presented euvolaemic (CVP between 610 cm of water) hyponatraemia that was attributed to SIADH; four patients had hypovolaemic (CVP less than 6 cm of water) hyponatraemia and CSWS was diagnosed. Clinical (blood pressure, urine volume) and laboratory (blood urea nitrogen, serum creatinine, serum uric acid, serum and urine electrolytes and osmolality) data obtained at the onset of hyponatraemia were not different between the two groups. Interestingly, we noted that the patients with SIADH tended to develop hyponatraemia earlier in the post-operative period than the patients with CSWS (within 6 days and between 6 and 10 days respectively). Therapeutic protocols aimed at fluid restriction (<800 ml/day) in the SIADH group and fluid replacement (normal saline 50100 ml/kg/day) in the CSWS group resulted in the prompt correction of hyponatraemia in all the patients: four patients attained normal serum sodium values within 36 h, and seven patients within 72 h.
On the basis of these observations and those of others [5], we propose a simple CVP-based algorithm as a guide for the effective (and safe) treatment of neurosurgical patients with hyponatraemia and natriuresis (Figure 1).
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Department of Internal Medicine, Southwestern Medical School, University of Texas, Dallas, TX, USA
The syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a well appreciated cause of hyponatraemia in the setting of central nervous system disease. A much less appreciated cause of hyponatraemia in this setting is the development of cerebral salt wasting (CSW). These two disorders can present with virtually identical laboratory abnormalities and have been reported to occur in many of the same disease states. Despite the overlap in cause and clinical presentation, the primary distinction between these disorders rests on assessment of effective circulatory volume [1]. SIADH is a volume expanded state while CSW is a volume depleted state. This distinction is of critical importance since the therapy of SIADH is fluid restriction while that of CSW is administration of NaCl. Inappropriate use of one therapy indicated for the other condition can result in untoward clinical outcomes.
In their letter Docci et al. agree that assessment of volume status is important in differentiating between these two disorders. They propose an algorithm that is primarily based on measurement of central venous pressure (CVP) as a means to determine whether circulatory volume is decreased (suggesting a diagnosis of CSW) or normal or increased (suggesting SIADH). While measurement of CVP can be useful in the assessment of circulatory volume, two points need to be emphasized. First, measurement of CVP with a central venous catheter is an invasive procedure that should only be performed after less invasive tools have been employed. In this regard the importance of clinically assessing the volume status of the patient should not be minimized. Findings suggesting a diagnosis of CSW should include orthostatic changes in blood pressure and pulse, dry mucous membranes, and flat neck veins. A progressive decline in weight and negative fluid balance as determined by review of hospital flow sheets are particularly useful pieces of evidence supportive of a declining ECF volume. Laboratory findings that are useful include evidence of haemoconcentration as reflected by an increased haematocrit and increased serum albumin concentration. In many, if not most, instances such an evaluation is sufficient in determining the volume status of the patient. If after a thorough review of these clinical parameters there is still ambiguity regarding the volume status of the patient, only then should consideration be given to placing a central venous catheter for measurement of CVP.
The second point is that measurement of CVP is most accurate in assessing volume status in the absence of cardiac and pulmonary disease [2,3]. Unfortunately, such diseases are common in the general population. As a result CVP measurements could be potentially misleading in a sizeable number of patients who present with disorders that are associated with either CSW or SIADH.
In summary, because of the divergent nature of CSW and SIADH therapies, accurate assessment of ECF volume is of critical importance in the approach to the hyponatraemic patient with underlying neurologic disease. Measurement of CVP can be a useful adjunct in assessing the volume status of patients with either CSW or SIADH. However, rather than being the initial step in this process, measurement of CVP should only be considered in patients without underlying pulmonary or cardiac disease and in whom less invasive clinical tools have failed to clarify the volume status. Techniques that are currently being investigated to define better the dry weight of chronic haemodialysis patients may eventually enable the clinician to define more objectively the volume status of patients in everyday practice. Such techniques include echocardiographic determination of the diameter of the inferior vena cava, bioelectric impedance measurements and measuring the circulating levels of cyclic guanosine 3'5'-monophosphate and natriuretic peptides [4,5].
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