Hiponatremia Merupakan Salah Satu Masalah Yang Bisa Ditemui Dalam Perawatan Pasien Neurologi

5/21/2018 Hiponatremia Merupakan Salah Satu Masalah Yang Bisa Ditemui Dalam Perawatan Pasi...

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Hiponatremia merupakan salah satu masalah yang bisa ditemui dalam perawatan pasien

neurologi. Meskipun sekilas tampaknya sederhana, namun diagnosis yang tepat dan terapi yang

efektif untuk hiponatremia dapat menjadi kompleks. Kesulitan utama yang sering ditemui adalah

menentukan apa yang menyebabkan penurunan konsentrasi Natrium serum. Cerebral Salt-

Wasting Syndrome (CSWS) merupakan kelainan pengaturan Natrium dan air, yang terjadi

sebagai akibat penyakit serebral tanpa disertai kelainan fungsi ginjal. CSWS ditandai adanya

hiponatremia yang berkaitan dengan hipovolemia, yang sesuai dengan namanya, disebabkan oleh

natriuresis. Dalam praktik klinik, terdapat kesulitan dalam membedakan kondisi CSWS dengan

Syndrome of inappropriate secretion of Antidiuretic Hormone (SIADH). Meskipun demikian,

sangatlah penting untuk membedakan kedua keadaan tersebut oleh karena prinsip terapi yang

secara fundamental berbeda.

DO-Cerebral Salt Wasting Pathophysiology Diagnosis and Treatment-Neurosurgery Clinics of

NA-2010

Mekanisme penyakit serebral yang menyebabkan CSWS masih belum dimengerti sepenuhnya.

Kemungkinan besar proses tersebut melibatkan gangguan input saraf ke ginjal dan/atau

penyebaran sentral faktor faktor natriuretik dalam sirkulasi. Pada kedua mekanisme tersebut,

terjadi peningkatan ekskresi Natrium urin, yang dapat menyebabkan penurunanEffective Arterial

Blood Volume(EABV), dan hal ini kemudian merangsang baroreseptor sehingga terjadi sekresi

Arginine Vasopressin (AVP). Dalam hal ini, peningkatan kadar AVP dapat mengganggu

kemampuan ginjal dalam menguraikan urin cair. Dapat dikatakan bahwa sekresi AVP dalam

keadaan ini merupakan respons yang sesuai terhadap deplesi volume. Sebaliknya, sekresi AVP

pada SIADH tidaklah sesuai, karena EABV meningkat.



Kemungkinan lokasi terjadinya penurunan absorbsi Natrium ginjal pada CSWS terdapat pada

nefron proksimal. Hal tersebut disebabkan oleh karena pada segmen tersebut secara normal

terjadi reabsorbsi sebagian besar Natrium yang tersaring. Sedikit saja penurunan efisiensi pada

segmen tersebut dapat menyebabkan pelepasan sejumlah besar Natrium menuju nefron distal,

dan pada akhirnya keluar bersama sama urin. Penurunan input simpatis ke ginjal merupakan

faktor yang memyebabkan terganggunya reabsorbsi nefron proksimal. Sistem saraf simpatis

dapat merubah pengaturan garam dan air pada segmen nefron proksimal melalui berbagai

mekanisme langsung dan tidak langsung. Sistem saraf simpatis juga berperan dalam kontrol

pelepasan rennin, sehingga penurunan tonus simpatis merupakan penjelasan terjadinya kegagalan

peningkatan kadar rennin dan aldosteron sirkulasi pada pasien CSWS. Kegagalan peningkatan

kadar aldosteron serum sebagai respons terhadap menurunnya EABV dapat menjelaskan

mengapa pada CSWS tidak terjadi ekskresi berlebihan Kalium, meskipun terjadi pelepasan

berlebihan Natrium ke nefron distal. Dengan demikian, hipokalemia bukan merupakan bagian

dari CSWS.

Selain penurunan input saraf ke ginjal, pelepasan satu atau lebih faktor faktor natriuretik juga

berperan dalam mekanisme ekskresi berlebihan garam pada CSWS. Efek Atrial Natriuretic

Peptide(ANP) danBrain Natriuretic Peptide(BNP) dapat menyebabkan gambarangambaran

klinis CSWS. Sebagai contoh,

. For example, infusion of either of these

peptides into normal human subjects results in a natriuretic

response that is unrelated to changes in blood pressure [22].

The ability of these compounds to increaseGFRaccounts for

some of the natriuresis; however, even in the absence of a



change inGFR, urinaryNaexcretionincreases because of a

direct inhibitory effect on Na transport in the inner

medullary collecting duct [22]. These peptides can also

increase urinary Na excretion without causing hypokalemia.

For example, ANP and BNP are associated with

decreased circulating levels of aldosterone because of direct

inhibitory effects on renin release in the juxtaglomerular cellsof thekidneyanddirect

inhibitoryeffects onaldosteronerelease in the adrenal gland. In addition, inhibition of Na

reabsorption in the inner medullary collecting duct would

not be expected to cause renal K wasting, because thissegment is distal to the predominantK secretory site in the

cortical collecting duct. AsECF volume becomes contracted,

proximal Na reabsorption would increase, resulting in less

distal delivery of Na to the collecting duct. Decreased Nadelivery protects against K wasting in the setting of high

circulating levels of aldosterone.

ANP and BNP can also directly decrease autonomicoutflowthrough effects at the level of the brain stem[22,23].

In this manner, natriuretic peptides can act synergistically

withCNSdisease todecreaseneural input to the kidney.The

evidence both for and against ANP and a circulatingouabain-like factor as important factors in the development

of CSWhas recently been reviewed [24].

BNP in humans is found primarily in the cardiac

ventricles, but also in the brain [22,25]. It is not known

whether either brain or cardiac tissue or both contribute to

the increased BNP concentrations found in these patients

with subarachnoid hemorrhage. Increased release of

cardiac BNP could be part of a generalized stress response

to the underlying illness, whereas increased intracranial

pressure could provide a signal for brain BNP release. In



this regard, one could speculate that the development of

renal salt wasting and resultant volume depletion in the

setting of intracranial disease is a protective measure,

limiting extreme rises in intracranial pressure. In

addition, the vasodilatory properties of these natriuretic

peptides might decrease the tendency for vasospasm in

disorders such as subarachnoid hemorrhage.

Differentiation of SIADH and CSW

Distinguishing between CSW and SIADH in clinical

practice can be difficult, given the similarity in laboratory

values and the overlap in associated intracranial diseases.

Determination of ECF volume remains the primary means

of distinguishing these disorders (Table 1). ECF volume is

increased in SIADH, whereas it is low in CSW. Physical

findings that support a diagnosis of CSW include orthostatic

changes in blood pressure and pulse, dry mucous

membranes and flat neck veins. Weight loss or negative

fluid balance as determined by a review of hospital flow

sheets are particularly good pieces of evidence in support

of a declining ECF volume. Laboratory findings that are

useful include evidence of hemoconcentration, as reflected

by an increased hematocrit and increased serum albumin



concentration, and the finding of a raised serum bicarbonate

concentration, because decreased ECF volume is

an important factor in the maintenance of metabolic

alkalosis.

Normally, the serum level of uric acid would be a useful

tool in this situation. As previously mentioned, uric acid

levels are depressed in patients with SIADH, which

reflects the slight increase in ECF volume. By contrast,

uric acid levels in patients with hyponatremia occurring in

the setting of decreased ECF volume are either normal or

slightly increased. Although not well studied, serum uric

acid levels inCSWtend to be unexpectedly low [26]. In fact,

hypouricemia and increased fractional urate excretion

might be a common feature of intracranial disease in

general [26,27]. Maesaka et al. [28] studied 29 consecutive

neurosurgical patients with a variety of intracranial

diseases. Eighteen of the patients had fractional excretion

of urate values .10% of normal and 16 of the patients had

a serum urate concentration #4 mg dl21. Only one patient

in the series had coexistent hyponatremia. In this patient,

the hypouricemia and increased fractional urate excretion

persisted after correction of the serum Na concentration.

Although not always accompanied by hyponatremia,



hypouricemia and increased renal uric acid excretion

have also been noted in patients with Alzheimers disease

and in patients with AIDS [27,29]. Although correction of

the serum Na concentration in SIADH leads to a normalization of uric acid handling by the

kidney [30],

hypouricemia and increased renal uric acid excretion

remain persistent findings following the correction of the

serum sodium concentration in CSW

Treatment of CSW and SIADH

Making the distinction between CSW and SIADH is of

particular importance with regard to treatment [31]. Fluid

restriction is employed in SIADH because the primary

abnormality is expansion of the ECF volume with water.

Administration of NaCl is indicated in CSW because ECF

volume is decreased as a result of renal salt wasting.

Failure to distinguish properly between these disorders so

that treatment indicated for one disorder is inappropriately

used for the other can potentially result in an adverse

outcome.



SIADH versus CSW



Serum sodium levels in critically ill patients can be altered by many factors. The

human body is 60% to 70% water, with approximately 30% of that water as

extracellular fluid and sodium chloride as the major electrolyte (135-145 mEq/L).

Hypo natremia occurs when a persons serum sodium level is less than 135 mEq/L;

it is the most common electrolyte abnormality among hospitalized patients, occurring

in up to 30% of patients in the intensive care unit (ICU).1 A sodium level lessthan 125 mEq/L is an independent predictor of mortality, especially among criticallyill patients, and should be avoided or corrected when it occurs.2

Syndrome of inappropriate antidiuretic hormone (SIADH) and cerebral salt

wasting (CSW) represent a particularly challenging subset of hyponatremias.These conditions are exceedingly common in patients with an intracranial disorder

and neurosurgical patients but also may be seen in other critically ill populations.

In the neurosurgical population, 62% of hyponatremias are caused by

SIADH, and 4.8% to 31.5% are caused by CSW.3 These 2 conditions are verysimilar and may be hard to differentiate in critically ill patients.

Pathophysiology

Hyponatremia can be associated with high, low, or normal serum osmolality.

Normal serum osmolality is between 280 and 295 mOsm/L. It can be measured inthe serum or calculated using the following formula: [2 _ sodium] _ [blood urea

nitrogen/2.8] _ [glucose/18]. Determining osmolality is the first step in evaluating

hyponatremias.Normal and High Osmolality

Low sodium with normal osmolality is usually referred to as pseudohyponatremia

or false hyponatremia. The causes of pseudohyponatremia include hyperlipidemia,

an excess of plasma proteins, and laboratory error.4,5 Hyponatremiawith high osmolality indicates an excess of solute other than sodium, including

glucose, mannitol, and propylene glycol (an ingredient found in some intravenous

[IV] medications). Excess osmolality from hyperglycemia or other substancesin the urine in SIADH does not change.7,10 The

causes of SIADH include CNS disorders, pulmonary

disorders, malignancy, surgery, andmedications (Table 1).7

Symptoms

Symptoms of hyponatremia typically depend

on the acuity and severity of the decrease in sodium.

A slower or mild decrease in the serumsodium level can be associated with anorexia,

headache, irritability, and muscle weakness.

A significant subset of patients is asymptomatic.More severe symptoms following a rapid

decrease in sodium or a serum sodium level

less than 120 mEq/L include cerebral edema,nausea, vomiting, delirium, hallucinations,


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lethargy, seizures, respiratory arrest, and potentially

death.11 Volume status also affects

other symptoms that the patient experiences.Assessment of volume status is important to

help determine the cause of hyponatremia and

optimal treatment.7ACC233

Hyponatremia (sodium level of



primary distinction between CSWS

and SIADH is volume status.10 Indications

of volume depletion (hypotension,weight loss, and decreased skin

turgor) occur with CSWS, whereas

indications of volume expansionoccur with SIADH (decreased urineoutput and generalized weight gain

due to fluid retention).

Treatment. Determining the cause(SIADH or CSWS) of hyponatremia

in trauma patients is important.

SIADH requires strict fluid restriction

and/or slow, judicious administrationof hypertonic saline, whereas

CSWS requires replacement of fluid

volume with physiological salineand intravenous replacement with

hypertonic 3% sodium chloride

solution. As in treatment of SIADH,

hypertonic solutions (3% sodiumchloride) must be administered

slowly because too-rapid correction

of hyponatremia can result in centralpontine myelinolysis.3,13 In patients

who tolerate oral intake, fluid can

be replaced orally, often with salt

tablet supplements.Restriction of fluids is contraindicated

in patients with CSWS. If fluids

are restricted, patients will be atrisk for cerebral vasospasm, cerebral

ischemia, and/or infarction.3 Other

medical interventions may includetreatment with fludrocortisone

acetate to increase absorption of

sodium by the renal tubules.14

Nursing Management.Nursing

management of patients with CSWSis comparable to that of patients with

CNDI or SIADH. Isotonic or hypertonic

fluids are administered intravenouslyto obtain positive fluid balance and correct volume depletion.

Sodium can also be replaced



orally. Cardiac status should be

monitored to detect side effects of

medications and fluid volume status.

The goal of treatment of CSWS

is to replace sodium and fluid volume

with intravenous saline or salt

tablets. Fluid restriction is definitely

contraindicated and can worsen

neurological outcomes.

C1222

Hiponatremia Merupakan Salah Satu Masalah Yang Bisa Ditemui Dalam Perawatan Pasien Neurologi

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