The term cerebral salt wasting (CSW) was introduced before the syndrome of inappropriate Four years later, Schwartz et al. published their landmark paper on SIADH. . Damaraju SC, Rajshekhar V, Chandy MJ: Validation study of a central. Cerebral salt wasting (CSW) is another potential cause of hyponatremia in those with The causes and diagnosis of hyponatremia, causes and treatment of SIADH, and the general Sivakumar V, Rajshekhar V, Chandy MJ. While fluid restriction is the treatment of choice in SIADH, the treatment .. Differential diagnosis of cerebral salt wasting (CSW) vs syndrome of.
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Palmer; Hyponatraemia in a neurosurgical patient: Hyponatraemia is a common electrolyte disorder in the setting of central nervous system disease and is often attributed to the syndrome of inappropriate secretion of antidiuretic hormone SIADH. This syndrome is characterized by hyponatraemia with an inappropriately concentrated urine, increased urine sodium concentration, and evidence of normal or slightly increased intravascular volume.
By contrast, there are patients with intracranial disease who develop hyponatraemia with similar characteristics but differ in that there cerrbral clinical evidence of a contracted extracellular fluid ECF volume. This form of hyponatraemia is due to excessive renal sodium excretion resulting from a centrally mediated process and is termed cerebral salt wasting CSW.
Given cs divergent nature of the treatment and the potential for improper selection of fluid therapy to worsen the underlying clinical condition it is of paramount importance for the clinician to be able to recognize and differentiate between these two entities. A year-old black man was admitted to an outside hospital after a fall with loss of consciousness.
His past medical history was significant for chronic alcoholism complicated by alcohol withdrawal seizures and delirium tremens. On physical examination, the patient was vz to aalt a thin black man who appeared older than his stated age.
Cerebral salt wasting versus SIADH: what difference?
The remainder of the physical examination was only significant for neurological findings. He was lethargic, disoriented to person, place, and time, and had increased tremulousness.
Initial laboratory examination was unremarkable. A CT scan of the head without contrast showed evidence of a subarachnoid haemorrhage with extra axial haemorrhage adjacent to both frontal lobes. A cerebral angiogram was normal with no evidence of aneurysm or vascular malformation. The patient was transferred to Parkland Memorial Hospital and admitted to the neurosurgery va.
He was treated with librium for his tremulousness, dilantin for seizure prophylaxis, and thiamine, folate and multivitamins. Over the following days his mental status improved to baseline.
On hospital day 10 the patient was noted to be confused and hypotensive. His physical examination was notable for orthostatic changes in pulse and blood pressure. NaK 5. Other laboratory tests obtained showed a serum creatinine concentration of 0.
The uric acid was 3. Tests of both thyroid and adrenal function were normal. NaK 20, Cl In summary, this year-old man developed significant hyponatraemia in association with a recent subarachnoid haemorrhage.
Distinguishing between these disorders will be the primary focus of this review. To better understand how these disorders verebral from other causes of hyponatraemia, a brief overview on the general approach to the hyponatraemic patient will be provided.
For a more detailed discussion on this topic, the reader is referred to two recent cerebarl [ 12 ]. The initial approach to a patient with hyponatraemia is to measure the serum osmolality in order to determine whether the hyponatraemia is representative of a hypo-osmolar state Figure 1.
A normal serum osmolality would suggest the presence of pseudohyponatraemia as seen in patients with hyperglobulinaemia or hypertriglyceridaemia or an increased concentration of some other osmole such as glucose. Approach to the hyponatraemic patient EABV: If a hypo-osmolar state is confirmed the next step is to determine whether the kidney’s ability to dilute the urine is intact.
In general, because the normal kidney is able to excrete 20—30 l of water per day, it is difficult to become hyponatraemic with an intact wastingg mechanism. However, this can occur in a few rare patients who ingest water in amounts that exceed the kidney’s ability to excrete water. Siaddh unusual condition in which more modest amounts of fluid intake wxsting lead to hyponatraemia in association with a maximally dilute urine is when solute intake is extremely limited.
Cerebral salt wasting versus SIADH: what difference?
This condition is often referred to as beer potomania syndrome [ 3 ]. In addition to chronic alcoholics, this syndrome has also been described in other patients with extremely limited solid food intake [ 4 ]. In hyponatraemic patients with an inappropriately concentrated urine one needs to next assess the effective arterial blood volume EABV.
Most of the causes of hyponatraemia result from a decrease in EABV, which causes baroreceptor stimulation of arginine vasopressin secretion AVP and leads to decreased distal delivery of filtrate to the tip of the loop of Henle. Clinical determination of EABV is usually straightforward. Determining the presence or absence of a postural change in blood pressure or pulse is particularly important in this regard. Urinary electrolytes are also extremely useful in the assessment of EABV.
Patients with a low EABV will tend to have a low urinary sodium, low urinary chloride, and low fractional excretions of sodium and chloride in the urine. Patients with euvolaemic hyponatraemia, however, will be in balance and will excrete sodium and chloride at rates that reflect dietary intake of sodium and chloride. Plasma composition can also be used to assess EABV. The plasma uric acid can also be used as a sensitive index of EABV.
In patients with SIADH, serum urate is not elevated but is actually depressed as these patients are volume expanded, although it is clinically difficult to detect the degree of volume expansion.
The increased urinary sodium concentration and decreased serum uric acid suggest a volume-expanded state such as SIADH. However, as discussed below, increased urinary sodium excretion and depressed serum uric acid are also characteristic of CSW. The finding of an orthostatic change in blood pressure and pulse in this patient strongly suggests the presence of a contracted EABV and thus confirms a diagnosis of CSW.
Much less is known about the development of laboratory abnormalities in CSW. In addition there is evidence of a suppressed renin—angiotensin—aldosterone axis.
These issues are discussed below. Evidence for a volume expanded state in SIADH initially came from studies of normal individuals given exogenous pitressin [ 5 ]. In these experiments administration of pitressin resulted in an abrupt decrease in urine volume and increase in urine osmolality Figure 2. The water retention produced by this antidiuretic effect resulted in an increase in body weight and dilution of the serum sodium concentration. After several days of pitressin administration, a large increase in urine sodium and chloride excretion was noted.
This subsequent increase in urine electrolyte excretion was triggered by the progressive expansion of total ECF volume as reflected by the increase in body weight. If fluid intake was kept low during the administration of pitressin, body weight remained unchanged and urine electrolyte excretion did not increase. These findings were reproduced several years later when the first clinical cases of SIADH were described in two patients with bronchogenic carcinoma [ 6 ].
The administration of pitressin to a normal human subject results in an abrupt increase in urine osmolality U osm. As water is retained and body weight Wt increases, there is a rise in urinary sodium excretion U Na V. A fall in body weight induced by water restriction leads to a decrease in urinary sodium excretion despite the presence of a persistently concentrated urine.
During exogenous administration of vasopressin when water intake is not limited and body weight is allowed to increase a steady state is eventually reached in which urine sodium excretion stabilizes and is equal to dietary sodium intake. At this time severe dietary sodium restriction will lead to excretion of urine that is essentially sodium free whereas administration of a large isotonic sodium load is followed by rapid and almost quantitative urinary excretion of the infused solute [ 7 ].
The establishment of normal renal sodium handling despite a decreased serum sodium concentration is a characteristic feature of SIADH. In SIADH expansion of ECF volume is not typically accompanied by overt signs of hypervolaemia such as oedema or distended neck veins since only one-third of retained water is distributed in the ECF space. Nevertheless modest expansion of the intravascular volume results in increased glomerular filtration rate and increased renal plasma flow.
In addition the volume expansion leads to decreased proximal sodium reabsorption and urinary sodium excretion is increased and equal to dietary sodium intake. Substances such as uric acid and urea nitrogen, that are reabsorbed in concert with sodium proximally, also tend to be reduced because of diminished proximal reabsorption.
The concept of a CSW syndrome was first introduced by Peters and colleagues in in a report describing three patients with neurological disorders who presented with hyponatraemia, clinical evidence of volume depletion, and renal sodium wasting without an obvious disturbance in the pituitary—adrenal axis [ 8 ].
This same constellation of findings was subsequently confirmed in additional patients with widely varying forms of cerebral disease [ 910 ]. In these initial reports, it was theorized that cerebral disease could lead to renal salt wastage and subsequent depletion of ECF volume by directly influencing nervous input into the kidneys.
Only in recent years has cerebral salt wasting again come into favour as a distinct entity. Part of this new found appreciation for the diagnosis of CSW can be traced to reports in which measurement of blood and plasma volume were found to be decreased in patients who met the traditional laboratory criteria for SIADH.
As compared to neurosurgical patients without intracranial disease, 10 of the 12 patients had significant reductions in plasma volume and total blood volume. These same investigators then examined sodium balance in a monkey model of subarachnoid haemorrhage [ 12 ]. Following the haemorrhage, seven of nine animals developed hyponatraemia in association with natriuresis and negative salt balance.
There was a slight decline in plasma volume, although it was not statistically significant. In contrast, sham-operated control animals did not become hyponatraemic or natriuretic and plasma volume did not change. On an average of 7 days following the event, nine patients developed hyponatraemia that met the criteria for a diagnosis of SIADH.
Eight of nine patients were found to be in negative sodium balance, which preceded the development of hyponatraemia. Interestingly, of the 12 patients without hyponatraemia negative sodium balance developed in four patients and plasma volume decreased in eight. In one additional report of 21 neurosurgical patients with hyponatraemia associated with increased urine sodium concentration and an inappropriately concentrated urine, volume status was assessed by measurement of total blood volume and central venous pressure and determining the response to volume supplementation [ 14 ].
In summary, a substantial number of neurosurgical patients who develop hyponatraemia and otherwise meet the clinical criteria for a diagnosis of SIADH have a volume status inconsistent with that diagnosis.
Rather the evidence of negative salt balance and reductions in both plasma and total blood volume in these patients is more consistent with a diagnosis of cerebral salt wasting. The mechanism by which cerebral disease leads to renal salt wasting is not well understood. By either or both mechanisms, increased urinary sodium excretion would lead to a decrease in EABV and thus provide a baroreceptor stimulus for the release of AVP.
In turn, increased AVP levels would impair the ability of the kidney to elaborate a dilute urine. In this setting, the release of AVP is an appropriate response to the volume depletion.
A proposed mechanism for the pathogenesis of cerebral salt wasting. A likely site for depressed renal sodium absorption in CSW is the proximal nephron. Since this segment normally reabsorbs the bulk of filtered sodium, a small decrease in the efficiency of this segment would result in the delivery of large amounts of sodium to the distal nephron and ultimately into the final urine.
Decreased sympathetic input to the kidney would be a likely explanation for impaired proximal reabsorption, since the sympathetic nervous system has been shown to alter salt and water handling in this segment through a variety of both indirect and direct mechanisms. Since the sympathetic nervous system also plays an important role in the control of renin release, decreased sympathetic tone may explain the failure of circulating renin and aldosterone levels to rise in patients with CSW [ 1516 ].
The failure of serum aldosterone levels to rise in response to a decreased EABV can account for the lack of renal potassium wasting despite the large increase in distal delivery of sodium. In this regard, hypokalaemia has not been a feature of CSW and in the current case the serum potassium was actually slightly increased. In addition to decreased neural input to the kidney, release of one or more natriuretic factors may also play a role in the renal salt wasting observed in CSW.
Atrial and brain natriuretic peptide ANP, BNP have several effects that could lead to the clinical syndrome of cerebral salt wasting.