Yoğun Bakımda Sıvı, Elektrolit, Asit-Baz Prof. Dr. Reha Erkoç YYÜ Tıp Fakültesi, İç Hastalıkları AD, Nefroloji BD, Van

Hiperpotasemi Bazen böbrek yetersizliğinden beklenmeyen derecede şiddetli olabilir Genelde 7 mEq/l üzerinde semptomatik olur En belirgin şikayet kas güçsüzlüğüdür, Alt ekstremitelerden başlar, gövde ve kollara yayılır-flask paraliziolur! Solunum kasları işin içine girince alveolar hipoventilasyon ve mekanik ventilasyon desteği gerekebilir. Nörolojik muayenede: Sfinkterler sağlam ve kafa çiftleri normaldir Severe muscle weakness or paralysis — Muscle weakness usually begins with the lower extremities and progresses to the trunk and upper extremities. If severe, it can progress to flaccid paralysis [4,5]. It is rare to have respiratory muscle weakness, and patients usually have intact sphincter tone and normal cranial nerve exam. Weakness resolves with correction of the hyperkalemia

İlk olarak sivri T ve kısa QT Sonra PR ve QRS genişler Sonuçta sine dalgası oluşur Cardiac conduction abnormality — A tall peaked T wave with shortened QT interval is the first change seen on the ECG in a patient with hyperkalemia (figure 1). This is followed by progressive lengthening of the PR interval and QRS duration. The P wave may disappear, and ultimately the QRS widens further to a "sine wave." Ventricular standstill with a flat line on the ECG ensues with complete absence of electrical activity. Ventricular fibrillation or standstill are the most severe consequences. A variety of other conduction disturbances, including right bundle branch block, left bundle branch block, bifascicular block, and advanced atrioventricular block may also be seen [6]. In addition, a pseudoinfarct pattern has been reported [7]. There is large interpatient variability in the actual potassium level leading to progression of ECG changes with worsening hyperkalemia, in part related to the presence or absence of concomitant hypocalcemia, acidemia, rapidity of hyperkalemia onset, or hyponatremia [1,8]. Thus, monitoring of the ECG is essential [1]. (See "ECG tutorial: Miscellaneous diagnoses", section on 'Hyperkalemia'.)

Hasta asemptomatik ve K<6 Hasta asemptomatik ve K<6.5 ise (EKG bulgusu yok ise) sadece Ca Polystrene Sulfonate (antipotasyum toz) yeterli olur. In comparison, an asymptomatic patient with a plasma potassium concentration of 6.5 meq/L whose electrocardiogram does not manifest signs of hyperkalemia can be treated only with a cation exchange resin (Kayexalate®), while patients with a value below 6 meq/L can often be treated with a low potassium diet and diuretics. In addition, any extra source of potassium intake (such as salt substitutes or potassium supplements) should be eliminated and any potentiating drugs (such as nonsteroidal antiinflammatory drugs or angiotensin converting enzyme inhibitors) should be discontinued

K<6 mEq/l ise: Sadece düşük potasyumlu diyet, K atıcı diüretikler- loop thiazide, K içeren serumların (Kadaleks, İsolyte vb) ACEi, AT2 bloker, NSAID, spironolaktone, triamterene, amiloride, potasyum içeren hazır tuzların-SelDiyet vb- kesilmesi yeterli olur.

.K>7 ise şiddetli kas güçsüzlüğü veya EKG değişiklikleri varsa acil tedavi gerekir . At plasma potassium concentrations above 7.0 or greater, severe muscle weakness, or marked electrocardiographic changes are potentially life-threatening and require immediate treatment. Immediate therapy is warranted if electrocardiographic changes or peripheral neuromuscular abnormalities are present, regardless of the degree of hyperkalemia [10]. (See "ECG tutorial: Miscellaneous diagnoses", section on 'Hyperkalemia'.)

Tedavi: Ca Gluconate iv. Potasyumun hücre membranındaki etkilerinin antagonize edilmesi: Sadece şiddetli hiperkalemide EKG de QRS genişlemesi veya p dalga kaybı varsa yapılmalı! Kalsiyum glukonat amp 1 amp min 2-3 dk da iv verilir İğne damarda iken EKG düzelir Etki süresi 30 dk Specific treatment of hyperkalemia is directed at antagonizing the membrane effects of potassium, driving extracellular potassium into the cells, or removing excess potassium from the body

İnsulin-dextrose İv 10 Ü insulin ve 100 cc %20 dextroz ve daha sonra da 500 ml %20 dextroz yavaşça gidecek şekilde verilir. Alternatif olarak sadece yukarıdaki glukoz Veya %20 dextroz içinde 5-10 ü insulin verilebilir. Insulin and glucose — Increasing the availability of insulin lowers the plasma potassium concentration by driving potassium into the cells, apparently by enhancing the activity of the Na-K-ATPase pump in skeletal muscle [13]. Hyperinsulinemia can be induced in either by giving insulin (10 units plus 50 mL of a 50 percent glucose solution as a intravenous bolus followed by a glucose infusion to prevent hypoglycemia) or by the intravenous administration of glucose alone (50 mL of a 50 percent glucose solution), which will rapidly enhance endogenous insulin secretion.

Etki 15 dakikada başlar, 60. dakikada max olur Saatlerce devam eder. Bu tedavi ile K 0.5-1.5 düşer Etki 15 dakikada başlar, 60. dakikada max olur Saatlerce devam eder. ]. Effective therapy usually leads to a 0.5 to 1.5 meq/L fall in the plasma potassium concentration, an effect that begins in 15 minutes, peaks at 60 minutes, and lasts for several hours

Albuterol 10-20 mg 4 ml izotonikle nebul 10 dk da 0.5 mg iv infüzyon Sc terbutalin de kullanılmöış Anginayı presipite edebilir, ritim bozukluğu yapabilir. The following doses have been used: albuterol (10 to 20 mg in 4 mL of saline by nebulization over 10 minutes or 0.5 mg by intravenous infusion), or epinephrine (0.05 µg/kg per minute by intravenous infusion). The peak effect is seen within 30 minutes with intravenous infusion, but occurs at 90 minutes with nebulization [25]. Subcutaneous terbutaline has also been used successfully in end-stage renal disease [26].

Antipotasyum 15 g şase Ca polystrene sulfonat 4x1 po yemeklerle Lavman 60-120 g Geç ama güçlü etki

Ca polystrene Sulfonate Klasik olarak sorbitolle kullanılıyor ülkemizde oral sorbitol yok ancak lavmanla da kullanımı riskli Post op hasta ve renal transplanlılarda kullanılmamalı 4x5-10 g po sorbitolsüz kullanılabilir toleransı daha iyi. , SPS in sorbitol should probably not be used in postoperative patients and in renal transplant recipients. (See "Gastrointestinal disease in dialysis patients", section on 'Kayexalate induced colonic necrosis'.) SPS can be given either orally or as a retention enema; oral dosing is probably more effective if intestinal motility is not impaired. The oral dose is usually 15 to 30 grams, and is typically provided in 60 to 120 mL of a 20 percent sorbitol solution (to prevent constipation), but a powdered form is available. The dose can be repeated every four to six hours as necessary. Lower doses (5 or 10 grams) are generally well tolerated (no nausea or constipation) and can be given one to three times per day to control chronic mild hyperkalemia in patients with renal insufficiency, often without the necessity of concurrent laxative therapy.

2-4 saatte bir tekrarlanabilir. 150 ml su ve 60 g antipotasyum (4 poşet) kolonda en az 30-60 dk (tercihan 2-3 saat) kalacak şekilde 2-4 saatte bir tekrarlanabilir. When given as an enema, 50 g of resin is mixed with 150 mL of tap water (NOT sorbitol); this solution should be kept in the colon for at least 30 to 60 minutes and preferably two to four hours. The enema can be repeated every two to four hours.

Bikarbonat 5 ampul mediflekste min 5 dakikada verilir. Etkisi zayıftır ama asidotik hastada faydalı olur. Ca ile aynı şişede olmamalıdır.

Hiponatremi Na <135 meq/L Renal Yetersizlik Uygunsuz ADH Hipovolemik durumlar Hiperglisemi Sürrenal yetmezlik Hipotiroidi INTRODUCTION — In virtually all patients, hyponatremia reflects water retention due to an inability to match water excretion with water ingestion. In most patients who do not have advanced renal failure, this defect represents the syndrome of inappropriate ADH secretion (SIADH), one of the hypovolemic states, or hyperglycemia. Although the definition may vary among different clinical laboratories, hyponatremia is commonly defined as a serum sodium concentration ≤135 meq/L [1].

Anemnez, fm Sıvıkaybı öyküsü,bulgusu Ödem veya asit Uygunsuz ADH sendromuna neden olabilecek hastalık Sürrenal yetersizliği veya hipotiroidi bulguları A history of fluid loss (eg, vomiting, diarrhea, diuretic therapy) and, on examination, signs of extracellular volume depletion, such as decreased skin turgor and a low jugular venous pressure. (See "Clinical manifestations and diagnosis of volume depletion in adults".) Signs of peripheral edema and/or ascites, which can be due to heart failure, cirrhosis, or renal failure. (See "Clinical manifestations and diagnosis of edema in adults" and "Evaluation of the patient with suspected heart failure" and "Diagnostic approach to the patient with cirrhosis".) A history consistent with one of the causes of SIADH, such as small cell carcinoma or central nervous system disease. (See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)".) Symptoms and signs suggestive of adrenal insufficiency or hypothyroidism. (See "Diagnosis of adrenal insufficiency in adults" and "Diagnosis of and screening for hypothyroidism".)

lab Plazma ozmolaritesi İdrar ozmolaritesi İdrar Sodyumu Laboratory tests — Three laboratory tests provide important initial information in the differential diagnosis of hyponatremia [2]: Plasma osmolality Urine osmolality Urine sodium concentration

Plazma ozmolal GAP Hiponatremi ve normal plazma ozmolaritesi-pseudohiponatremi In some cases, however, the plasma osmolality is either normal or elevated, possibly resulting in a plasmal osmolal gap. (See "Plasma osmolal gap".) Hyponatremia with a normal plasma osmolality may be due to hyperlipidemia or hyperproteinemia (called pseudohyponatremia since it represents a laboratory artifact), or it may follow the infusion of sucrose and maltose-containing IgG formulations or the absorption of isotonic glycine during urological or gynecological procedures. (See "Hyponatremia following transurethral resection or hysteroscopy".)

Hiperglisemi Mannitol Renal failure presents a different problem since the blood urea nitrogen (BUN) is elevated but urea is an ineffective osmole. The effective plasma osmolality is calculated from the measured value minus the BUN/2.8 or minus the blood urea if measured in mmol/L. Because of the elevation in BUN, the plasma osmolality may be normal or even elevated, but the effective osmolality is reduced. As a result, these patients have true hyponatremia. Hyponatremia with a high plasma osmolality may be seen with hyperglycemia or the administration of hypertonic mannitol, both of which induce osmotic water movement out of the cells and lower the plasma sodium concentration by dilution [2,5-8]. However, this effect is at least in part counteracted by the osmotic diuresis that typically occurs in such patients. By causing water loss in excess of sodium and potassium, the osmotic diuresis can raise the plasma sodium concentration to normal or even high values. (See "Clinical features and diagnosis of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults", section on Plasma sodium concentration

Böbrek yetersizliği: Ozmolarite yüksektir ancak üre efektif bir ozmolar değildir Renal failure presents a different problem since the blood urea nitrogen (BUN) is elevated but urea is an ineffective osmole. The effective plasma osmolality is calculated from the measured value minus the BUN/2.8 or minus the blood urea if measured in mmol/L. Because of the elevation in BUN, the plasma osmolality may be normal or even elevated, but the effective osmolality is reduced. As a result, these patients have true hyponatremia.

İyon selektif elektrotla dilusyonsuz ölçülürse hiperlipidemi veya hiperproteinemi pseudohiponatremiye yol açmaz In patients with hyperlipidemia or hyperproteinemia who present with a low serum sodium concentration but a normal plasma osmolality (called pseudohyponatremia), ion-selective electrodes will reveal a normal serum sodium concentration if an instrument employing direct potentiometry is used. Many laboratory analyzers that measure sodium with ion-selective electrodes utilize indirect potentiometry in which the serum or plasma sample is diluted before measurement; these will report a low sodium concentration. To understand why this occurs, consider an instrument that dilutes the serum specimen 1:100 [6]. Suppose that the plasma water (with a normal sodium concentration of 150 meq/L) constitutes 80 percent of the plasma in a patient with hyperlipidemia. In this setting, each L of plasma contains 120 meq of sodium. If this is now diluted to a total volume of 100 L, there will be only 120 meq of sodium present and, correcting for dilution, the measured sodium concentration will appear reduced at 120 meq/L.

İdrar ozmolaritesi Primer polidipsiyi ayırmada kullanılır Primer polidipside idrar dansitesi<1003 yani osmol<100 olur, idrar maximal dilüedir. Diğer durumlarda idrar osm genelde 300 veya üzeridir İki istisnası şunlardır: Urine osmolality — In patients with hyponatremia and a low plasma osmolality, the urine osmolality can be used to distinguish between impaired water excretion (which is present in almost all cases) and primary polydipsia, in which water excretion is normal but intake is so high that it exceeds excretory capacity. The normal response to hyponatremia (which is maintained in primary polydipsia) is to completely suppress ADH secretion, resulting in the excretion of a maximally dilute urine with an osmolality below 100 mosmol/kg and a specific gravity ≤1.003. Values above this level indicate an inability to normally excrete free water, most commonly because of continued secretion of ADH. Most hyponatremic patients have a relatively marked impairment in urinary dilution that is sufficient to maintain the urine osmolality at 300 mosmol/kg or greater. There are two hyponatremic disorders other than primary polydipsia in which the urine osmolality may be below 100 mosmol/kg:

Malnütrisyon Reset ozmostat Malnutrition, described primarily in beer drinkers (called beer drinkers potomania), in which dietary solute intake (sodium, potassium, protein) and therefore solute excretion is so low that the rate of water excretion is markedly diminished even though urinary dilution is intact. (See "Causes of hyponatremia", section on 'Low dietary solute intake'.) Reset osmostat after a water load appropriately suppresses ADH release. The major clinical clue to the presence of this disorder is a moderately reduced plasma sodium concentration (usually between 125 and 135 meq/L) that is stable on multiple measurements. (See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat", section on 'Reset osmostat'.)

Hipovolemide de düşük olabilir, bunu süratle Na un normalleşmesi izler The urine osmolality may be below 100 mosmol/kg if it is measured after the reason for water retention has been eliminated (eg following volume expansion with isotonic saline in a patient with hypovolemic hyponatremia); in this case, the low urine osmolality heralds the spontaneous and rapid correction of hyponatremia.

İdrar sodyumu Efektif arteriel dolumu ayırmada kullanılabilir Hipovolemide Na 25 mEq/L altındadır istisnaları: Renal tuz kaybı, adrenal yetm, serebral tuz kaybı İdrar sodyumu>40 mEq/L Uygunsuz ADH, Urine sodium concentration — In patients with hyponatremia, hypoosmolality, and an inappropriately concentrated urine, the urine sodium concentration can be used to distinguish between hyponatremia caused by a decreased effective arterial blood volume and euvolemic hyponatremia [2]: The urine sodium concentration is usually below 25 meq/L in hypovolemia, unless there is renal salt-wasting, due most often to diuretic therapy and infrequently to adrenal insufficiency or cerebral salt-wasting. (See "Cerebral salt-wasting".) The urine sodium concentration is usually above 40 meq/L in patients with the SIADH who are normovolemic and whose rate of sodium excretion is determined by sodium intake, as it is in normal subjects [10-12].

Uygunsuz ADH Plazma ozmolaritesi düşlüktür İdrar ozmolaritesi uygunsuz şekilde yüksektir (>100,sıklıkla >300) İdrar sodyumu >40 mEq/L BUN ve ürik asit düşüktür Kreatinin normal Asit baz K dengesi normaldir Adrenal ve tiroid fonksiyonu normaldir Findings in SIADH — Given the importance of diagnosing the SIADH in patients with hyponatremia, it is worthwhile to summarize the general findings in this disorder and the laboratory tests that should be performed [20]: A low plasma osmolality An inappropriately elevated urine osmolality (above 100 mosmol/kg and usually above 300 mosmol/kg) A urine sodium concentration usually above 40 meq/L Low BUN and serum uric acid concentration A relatively normal plasma creatinine concentration Normal acid-base and potassium balance Normal adrenal and thyroid function

Çoğu olguda kronik hiponatremi vardır, Na 120 üzeridir. Most patients with hyponatremia have chronic (ie, gradual onset) hyponatremia, a serum sodium concentration above 120 meq/L, and appear asymptomatic, although subtle neurologic abnormalities may be present when the serum sodium is between 120 and 130 meq/L. (See 'Necessity for therapy' below.)

Bu hafif vakalarda tedavi: Sıvı kısıtlaması 800ml/gün Serbest tuz oral alımı Semtomatik hastalarda daha agrezif tedavi gerekir. (Na<110-115) Hipertonik NaCl verilmelidir. Initial treatment in such patients typically consists of slow correction of the hyponatremia via fluid restriction or, if volume depletion is present, the administration of isotonic saline (or oral salt tablets) [1-3]. Vasopressin receptor antagonists also may be helpful. Among patients with SIADH, isotonic saline may worsen the hyponatremia. (See 'SIADH' below.) More aggressive therapy is indicated in patients who have symptomatic or severe hyponatremia (serum sodium concentration below 110 to 115 meq/L). In this setting, initial therapy usually consists of hypertonic saline with or without vasopressin receptor antagonists.

Hiponatremik hastanın tedavisinde şunlar göz önüne alınır Na’u yükseltecek optimum yöntem Sodyum açığının hesaplanması Düzeltme hızı When considering the treatment of patients with hyponatremia, the following issues will be reviewed here: The optimal method of raising the serum sodium concentration, which varies with the cause of hyponatremia Estimation of the sodium deficit if sodium is to be given The optimal rate of correction

Hızlı düzelme! Altta yatan olay hızla düzelebilir; örnek volüm açığı, ilaca bağlı hiponatremi, sürrenal yetmezliği There are several circumstances in which the underlying disease can be corrected quickly, possibly leading to overly rapid correction of the hyponatremia (see 'Avoid overly rapid correction' below: The administration of saline to patients with true volume depletion. In this setting, restoration of euvolemia will suppress the release of ADH (which has a half-life of only 15 to 20 minutes), thereby allowing rapid excretion of the excess water. (See 'True volume depletion' below.) The administration of glucocorticoids to patients with adrenal insufficiency, which will directly suppress the release of ADH. (See "Hyponatremia and hyperkalemia in adrenal insufficiency".) Relatively rapid reversal of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). This can occur with self-limited disease (eg, nausea, pain, surgery) and with cessation of therapy with certain drugs that cause SIADH such as desmopressin and selective serotonin reuptake inhibitors (eg, fluoxetine, sertraline).

Tedavinin etkisi: Na da yükselme: (İnfüzat Na-SNa) ÷ (Total Vücut Suyu + 1) TVS: Ağırlık X 0.5(kadın) veya x0.6 (erkek)

Potasyumun etkisi Ozmotik olarak Na gibi etkili olduğundan verilince Na u yükseltir Effect of potassium — Potassium is as osmotically active as sodium. As a result, giving potassium (usually for concurrent hypokalemia) can raise the serum sodium concentration and osmolality in hyponatremic patients [7,8,11,12]. Since most of the excess potassium enters the cells, electroneutrality is maintained in one of three ways, each of which will raise the serum sodium concentration:

Sodyum Açığı= TVSx(İstenen Na seviyesi-Mevcut Na) Sodium deficit = TBW x (desired serum Na - actual serum Na TBW is estimated as lean body weight times 0.5 for women and 0.6 for men. Change in serum Na = (Infusate minus serum Na) / (TBW + 1)

Düzeltme hızı Hiponatremi akut mu kronik mi ? Hasta semptomatik mi ? Optimum düzeltme hızı nedir ? RATE OF CORRECTION General issues — There are several general issues that must be addressed before discussing specific therapies: Is the hyponatremia acute or chronic? Is the patient symptomatic or asymptomatic? What is the optimal rate of correction?

Beyin korunma mekanizmaları Günler içinde maksimum olur Düzeltilmesi sorun olabilir Acute versus chronic hyponatremia — Patients with acute hyponatremia are more likely to develop neurologic symptoms resulting from cerebral edema induced by water movement into the brain. However, the brain has a protective response that reduces the degree of cerebral edema; this response begins on the first day and is complete within several days. The net effect of this adaptation is that the clinical manifestations of hyponatremia are reduced, with the potential disadvantage of increasing the susceptibility to osmotic demyelination with overly rapid correction of the hyponatremia

Ozmotik demyelinizasyon sendromu Şiddetli ve irreverzibldir Premenapozal kadın özellikle risk altındadır

Genelde ilk gün 10-12 mmol/L den veya ilk 48 saat 18mmol den fazla artışlarda olur Hedef ilk 24 saatte 10 mmol yükselme İlk 48 saatte 18 mmol/L altında yükselme olmalıdır

Deneysel çalışmalar saatlik artışlardan çok 24 saatlik değişikliğin etkisini göstermektedir. General principles — As described above, there are a variety of modalities used in the treatment of hyponatremia. The choice among them varies with the severity and underlying cause of the hyponatremia. (See 'Methods of raising the serum sodium' above.) With true volume depletion, the administration of saline can correct the hypovolemia, thereby removing the stimulus to the release of antidiuretic hormone (ADH) and allowing the excess water to be excreted in the urine. Correction of the underlying disorder can also be achieved with certain causes of SIADH (eg, glucocorticoids for adrenal insufficiency or the cessation of offending drugs).

Uygunsuz ADH da tedavi Sıvı kısıtlaması ve oral tuz ve idrar ozmolaritesi plazmanın 2 katından fazla ise loop diüretikleridir The following discussion will provide an overview of the approach to therapy according to the presence or absence of symptoms that are attributable to the hyponatremia. The treatment of hyponatremia due to specific causes is discussed in detail separately: For SIADH, in which the mainstay of chronic therapy is fluid restriction with, if necessary, the addition of oral salt tablets and, if the urine osmolality is more than twice the plasma osmolality and the serum sodium concentration is below goal, a loop diuretic

Kalb yetersizliği ve Siroz 130! For heart failure and cirrhosis, in which serum sodium concentrations below 130 meq/L are typically associated with close to end-stage disease (see "Hyponatremia in heart failure" and "Hyponatremia in cirrhosis").

Şiddetli semptomatik hiponatremi Hipertonik NaCl Beyin herniasyonu önlenebilir! Severe symptoms — Hypertonic saline is warranted in patients with severe and often acute hyponatremia (serum sodium usually below 120 meq/L) who present with seizures or other severe neurologic abnormalities or with symptomatic hyponatremia in patients with intracerebral diseases that have been associated with brain herniation

1-2 kez daha 10 dakika aralarla tekrarlanabilir 100ml %3 Na>Cl iv Na 2-3 mEq yükselir 1-2 kez daha 10 dakika aralarla tekrarlanabilir One hypertonic saline regimen that we have used was initially described in hyponatremic athletes participating in endurance events such as marathon races. It consists of 100 mL of 3 percent saline given as an intravenous bolus, which should acutely raise the serum sodium concentration by 2 to 3 meq/L, thereby reducing the degree of cerebral edema; if neurologic symptoms persist or worsen, a 100 mL bolus of 3 percent saline can be repeated one or two more times at ten minute intervals

Burada tedavideki sorun başlangıçtaki Na yükselmesini daha sonra Na un böbrekle atılması ile tekrar düşme izlemesidir. The treatment of symptomatic hyponatremia due to SIADH is complicated by the fact that, in patients with a highly concentrated urine (eg, greater than 500 to 600 mosmol/kg), the initial elevation in serum sodium induced by hypertonic saline will fall back toward baseline as the administered sodium is excreted in the urine

Orta derecede semptomatik Konfüzyon letarji %3 NaCl 1ml/kg saat infüzyon Moderate symptoms — For the purposes of this discussion, moderate symptoms are defined as confusion and/or lethargy. Some of these patients, particularly those with SIADH, may benefit from hypertonic saline, but do not require the aggressive approach suggested in the preceding section for those with severe neurologic symptoms. (See 'Severe symptoms' above.) In patients with SIADH and moderate symptoms, initial hypertonic saline therapy to raise the serum sodium at rates up to 1 meq/L per hour may be justified in the first three to four hours. This can generally be achieved by administering hypertonic (3 percent) saline at a rate of 1 mL/kg lean body weight per hour. Such calculations are only estimates and the serum sodium should be measured at two to three hours. The total elevation in serum sodium in the first 24 hours should.. be less than 10 meq/L

Hızlı düzelme! Özellikle hipovolemide beklenebir Bu durumda dezmopressin önerilir! +-Dextroz! Although hyponatremia is initially corrected slowly with isotonic saline in hypovolemic patients, ADH release will be appropriately suppressed once near euvolemia is restored. This will lead to a marked water diuresis and patients with an initial serum sodium below 120 meq/L might be at risk for overly rapid correction and possible osmotic demyelination. In such patients, desmopressin with or without dextrose in water may be considered to either prevent or treat overly rapidly correction

Hafif semptomlar Unutkanlık denge bozukluğu vb Sıvı kısıtlaması ve tuz Mild symptoms — Patients with SIADH or hypovolemia who have only mild symptoms (eg, dizziness, forgetfulness, gait disturbance) should be treated with less aggressive therapy, such as fluid restriction and oral salt tablets in SIADH or, with hypovolemia, isotonic saline and treatment of the cause of fluid loss.

Asemptomatik hiponatremi Asymptomatic hyponatremia — Patients who have asymptomatic hyponatremia should be corrected slowly, since rapid correction is not necessary and may be harmful. (See 'Avoid overly rapid correction' above.) Treatment varies with the underlying disease. Among patients with SIADH, isotonic saline may, via a mechanism described above, lower the serum sodium when the urine osmolality is well above 300 mosmol/kg. Thus, if fluid restriction is not sufficient, subsequent therapy includes salt tablets and, if necessary, a loop diuretic if the urine osmolality is more than twice that of the plasma.

Kalb yetersizliği ve sirozda hiponatremi tedavisi? Anlamsız Little benefit would be provided in patients with hyponatremia due to heart failure or cirrhosis in whom a serum sodium concentration persistently below 130 meq/L is a marker of end-stage disease and a poor prognosis unless transplantation or some equivalent intervention is performed.

Ozmotik demiyelinizasyon Dizartri disfaji paraparezi, quadriparezi, davranış bozuklukları, letarji, koma Nadiren konvulziyonlar Na düzeldikten 2-6 gün sonra çıkarlar The symptoms of osmotic demyelination include dysarthria, dysphagia, paraparesis or quadriparesis, behavioral disturbances, lethargy, and coma; seizures may also be seen but are less common. Clinical manifestations are usually delayed for two to six days after the elevation in the plasma sodium concentration and are often irreversible or only partially reversible. (See 'Clinical manifestations' above.)

Risk faktörleri Hız Alkolizm Malnutrisyon KC hastalığı Hipokalemi Na<105 The most important risk factor for the development of osmotic demyelination syndrome is the rate of correction of the hyponatremia. Other risk factors that are less important include alcoholism, malnutrition, liver disease, plasma sodium ≤105 meq/L, and hypokalemia

Hız günlük 20 üzerinde veya 140 ı geçmişse risk fazla The daily, rather than hourly, rate of correction determines risk. Osmotic demyelination occurs in patients in whom the plasma sodium concentration increases more than 10 to 12 meq/L in the first 24 hours or more than 18 meq/L in the first 48 hours. The risk is highest for those patients in whom the plasma sodium concentration is raised more than 20 meq/L in the first 24 hours or is overcorrected to above 140 meq/L. (See 'Rapid rate of correction' above.)

tanı CT MR Bulgular 4 haftaya gecikebilir! The demyelinating lesions can be detected by CT scanning or preferably magnetic resonance imaging. These tests may not become positive for as long as four weeks after disease onset. Thus, an initially negative test does NOT exclude osmotic demyelination. (See 'Detection' above.)

tedavi semptomatik There is no proven treatment for osmotic demyelination syndrome. Aggressive supportive therapy should be continued for at least six to eight weeks for all patients who were functional before the onset of osmotic demyelination syndrome, since recovery from seemingly hopeless neurological deficits are not rare. (

korunma Saatte 0.5 den hızlı düzelme ve su diürezi varsa (idrar ozmolaritesi <200) dezmopressin 2-4 mcg iv/sc Prevention of an overly rapid increase in plasma sodium is critical in preventing osmotic demyelination, primarily in patients with a plasma sodium below 110 to 115 meq/L who are at greatest risk. We initiate preventive measures in patients who have not exceeded the 24 hour goal (less than 10 meq/L increase in plasma sodium), but are correcting the plasma sodium more rapidly than desired (goal less than 0.5 meq/L per hour) in association with the development of a water diuresis (ie, urine osmolality less than 200 mosmol/kg). In such patients, we suggest desmopressin (2 to 4 micrograms intravenously or subcutaneously) plus water restriction (Grade 2C)

1.Desmopressin 6-8 saatte bir 10-30 ml/saat hipertonik NaCl Na 4-6 satte bir ölçülmeli Na 125-130 a kadar devam edilir Two different regimens have been suggested: - One regimen is to give desmopressin every six to eight hours. Since desmopressin produces a concentrated urine, correction of the hyponatremia will slow down or cease. If necessary, a slow infusion of hypertonic saline can be added (10 to 30 mL per hour) to produce a rise in plasma sodium at the desired rate. The plasma sodium should be measured every four to six hours. Desmopressin and, if used, hypertonic saline are continued until the plasma sodium reaches 125 to 130 meq/L

2. rejim Tek doz dezmopressin Na hızlı yukselir veya idrar çok artarsa ek doz Saatlik idrar debisi takip edilmelidir Sık serum Na takibi - A second regimen is to begin with one dose of desmopressin. Subsequent doses may be given after six to eight hours (or more) if the plasma sodium is again rising too quickly or the urine output has increased dramatically. The urine output should be monitored hourly, since escape from the antidiuretic effect of desmopressin can be sudden and unpredictable, and the plasma sodium measured should every two to three hours.

Na 24 saatte 12 den fazla artmışsa: 24 satte 18 den fazla artmışsa: Dezmopressin ve 6 ml/kg Dextrozla düşürme For patients who have already raised the plasma sodium by more than 10 to 12 meq/L in the first 24 hours or 18 meq/L in the first 48 hours, we suggest relowering of the plasma sodium with desmopressin plus individual doses of D5W at a rate of 6 mL/kg lean body weight over one to two hours (Grade 2C). The plasma sodium should be measured after each dose. Desmopressin should be repeated every six hours until the plasma sodium falls to a level below the level of overcorrection. The usual dose is 2 to 4 micrograms intravenously or subcutaneously.

Reset ozmostat Uygunsuz ADH varyantı RESET OSMOSTAT — In normal individuals, plasma antidiuretic hormone (ADH, arginine vasopressin) levels are very low when the plasma osmolality is below 280 mosmol /kg, thereby permitting excretion of ingested water, and increase progressively as the plasma osmolality rises above 280 mosmol/kg (graph 2). Hyponatremia due to downward resetting of osmostat is one form of the SIADH [1,29-31]. (See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)", section on 'Patterns of ADH secretion'.) Downward resetting of the osmostat can also occur in hypovolemic states (in which the baroreceptor stimulus to ADH release is superimposed upon osmoreceptor function), quadriplegia (in which effective volume depletion may result from venous pooling in the legs), psychosis, tuberculosis, and chronic malnutrition [1,29]. The serum sodium concentration also falls by about 5 meq/L in normal pregnancy. No therapy is required. (See "Renal and urinary tract physiology in pregnant women".) The presence of a reset osmostat should be suspected in any patient with apparent SIADH who has mild hyponatremia (usually between 125 and 135 meq/L) that is stable over many days despite variations in sodium and water intake. The diagnosis can be confirmed clinically by observing the response to a water load (10 to 15 mL/kg given orally or intravenously). Normal subjects and those with a reset osmostat should excrete more than 80 percent of the water load within four hours, while excretion will be impaired in the SIADH [1]. Identification of a reset osmostat is important because the above therapeutic recommendations for the SIADH may not apply [1,29,32]. These patients have mild to moderate asymptomatic hyponatremia in which there is downward resetting of the threshold for both ADH release and thirst. Since osmoreceptor function is normal around the new baseline, attempting to raise the serum sodium concentration will increase ADH levels and make the patient thirsty, a response that is similar to that seen with fluid restriction in normal subjects. Thus, attempting to raise the serum sodium concentration may be unnecessary (given the apparent lack of symptoms and lack of risk of more severe hyponatremia) and likely to be ineffective (due to increased thirst). Treatment should be primarily directed at the underlying disease, such as tuberculosis [33].

Serebral Tuz Kaybı Cerebral salt wasting (CSW) is characterized by hyponatremia and extracellular fluid depletion due to inappropriate sodium wasting in the urine, in the setting of acute disease in central nervous system (CNS), usually subarachnoid hemorrhage. CSW is a much less common cause of hyponatremia in patients with cerebral injury than the syndrome of inappropriate ADH secretion (SIADH). (See 'Introduction' above and 'Epidemiology and causes' above.)

Azalmış santral sempatik aktivite sonucu Na kaybı BNP Azalmış santral sempatik aktivite sonucu Na kaybı The pathophysiology of CSW is related to impaired sodium reabsorption, possibly due to the release of brain natriuretic peptide and/or diminished central sympathetic activity. Regardless of the mechanism, sodium-wasting can lead sequentially to volume depletion, increased ADH release, hyponatremia due to the associated water retention, and possibly increased neurologic injury. (See 'Pathophysiology' above.)

Sıvı kaybı farkıdır Some authorities contend that CSW does not exist and that the laboratory findings are due to SIADH. However, we feel that CSW is a distinct entity. (See 'Is cerebral salt-wasting real?' above.) Specific laboratory findings include hyponatremia with a low plasma osmolality, an inappropriately elevated urine osmolality (above 100 mosmol/kg and usually above 300 mosmol/kg), a urine sodium concentration above 40 meq/L, and a low serum uric acid concentration due to urate wasting in the urine. Since CSW is associated with extracellular fluid depletion, hypotension and decreased skin turgor may also be observed. (See 'Clinical features' above.)

Fark izotonik verilince düzelmesidir. İdrar tedaviyle dilüedir Na kaybetmez Ancak uygunsuz ADH ile birlikte olabilir CSW mimics all of the laboratory findings in the SIADH. The only clue to the presence of CSW rather than SIADH is clinical evidence of extracellular volume depletion, such as hypotension and decreased skin turgor, and/or increased hematocrit, in a patient with a urine sodium concentration above 40 meq/L. Unlike SIADH, volume repletion in CSW leads to a dilute urine, due to removal of the hypovolemic stimulus to ADH release, and subsequent correction of the hyponatremia. This finding has not been convincingly demonstrated which could reflect concurrent SIADH due to the CNS disease. (See 'Differential diagnosis' above.)

Tedavide İzotonik NaCl verilir In the setting of CNS disease, accurate distinction between CSW and SIADH is essential since the two disorders are managed differently, with possible adverse consequences if the incorrect therapeutic strategy is administered. In patients with a clinical picture compatible with CSW, we recommend initial therapy with isotonic saline to correct the volume depletion and possibly reverse the hyponatremia. (See 'Treatment' above.)

Asit Baz Dengesi Güçlü İyonlar ve Stewart Yaklaşımı

Ana tema bikarbonatın bağımlı değişken olması ve pH yı etkilememesidir Fark yapanlar : Güçlü İyon farkı Nonvolatil zayıf asitler veya tamponlar Arteriel karbondioksittir The cardinal tenet of the strong ion difference or Stewart approach to acid-base analysis is that the serum bicarbonate concentration does not alter blood pH. Instead, the independent variables responsible for changes in acid-base balance are the strong ion difference (SID), plasma concentration of nonvolatile weak acids or buffers (ATot), and arterial carbon dioxide tension (PaCO2). (See 'Strong ion difference' above.)

6 ana asit baz denge bozukluğu tanımlar Because clinically important acid-base derangements are thought to result from changes in PaCO2, SID, and ATot, the strong ion approach distinguishes six primary acid-base disturbances. These are respiratory acidosis, respiratory alkalosis, strong ion acidosis, strong ion alkalosis, nonvolatile buffer ion acidosis, and nonvolatile buffer ion alkalosis. (See 'Strong ion difference' above.)

Belirgin Güçlü İyon Farkı: Güçlü anyonlarla katyonların farkıdır The apparent SID (SIDapp) is defined as the difference in net charge between the sum of the strong cations and the sum of the major strong anions present in health.

Hesaplanan güçlü iyon farkı: pH ve zayıf asit fonksiyonudur Efektif Güçlü iyon farkı olarak adlandırılır pH alb ve fosfattan hesaplanır The calculated SID value, which is a function of pH and ATot, is called the effective strong ion difference or SIDeff. It can be calculated from measured values of pH, serum albumin, and phosphate (see 'Strong ion gap' above).

Güçlü iyon GAP: Belirgin Güçlü İyon Farkı ile Effektif olanın farkıdır Sıfır olmalıdır Pozitif olması serumda organik bir asit olduğunu gösterir The difference between SIDapp and SIDeff is the strong ion gap, which should be zero. A positive value suggests that an organic acidosis may be present. (See 'Strong ion gap' above.)

Konvansiyonel AG dan farkı işin içine albuminin girmesidir AG için alb hesaplanırsa belirgin bir fark kalmaz Alb de 4.4 e göre her 1 g düşüş AG ı 2.4 azaltır The major practical difference between the Stewart approach and the conventional approach to acid-base disturbances is the inclusion of the serum albumin concentration in the Stewart approach. However, if changes in serum albumin concentration are accounted for in measurement of the anion gap, the more complex Stewart approach does not appear to offer a clinically significant advantage over the traditional Schwartz-Bartter approach to acid-base disturbances. Each 1.0 g/dL decrease or increase in serum albumin below or above 4.4 g/dL respectively lowers or raises the actual concentration of unmeasured anions by approximately 2.3 to 2.5 meq/L. (See 'Relative diagnostic efficacy' above.)

Metabolik asidozda yaklaşım Asit üretiminde artma Bikarbonat kaybı Renal asit atılımında azalma Approach to the adult with metabolic acidosis Authors Increased acid generation (eg, ketoacidosis and lactic acidosis) (see "Causes of lactic acidosis") Loss of bicarbonate (eg, diarrhea or type 2 [proximal renal tubular acidosis]) or a bicarbonate precursor (eg, ketoacid anion loss in ketoacidosis) (see "The Δanion gap/ΔHCO3 in metabolic acidosis") Diminished renal acid excretion (eg, renal failure or type 1 [distal] renal tubular acidosis)

Respiratuar kompansasyon Bikarbonattaki her 1 meq/L düşmeye karşı pCO2 1.1-1.2mmHg düşer 1 satte başlar 12 24 saatte tamamlanır The respiratory compensation results in a 1.1 to 1.2 mmHg fall in the PCO2 for every 1 meq/L reduction in the plasma bicarbonate concentration [3,5]. This response begins in the first hour and is complete by 12 to 24 hours [6]. Respiratory failure is suggested by the inability to generate such a response

AG Öçülen katyonlar- Ölçülen anyonlar AG: Na- (Cl+HCO3) Determination of the plasma anion gap (AG) is an important step in approaching the differential diagnosis of metabolic acidosis (table 1) [1,3,10]. The plasma AG is calculated from the following formula: AG = Measured cations - measured anions Since Na is the primary measured cation and Cl and HCO3 are the primary measured anions: AG = Na - (Cl + HCO3)

Yeni otoanalizörlerde 3-11 olabilir, yüksek Cl den dolayı Normali 7-13 arasındadır Yeni otoanalizörlerde 3-11 olabilir, yüksek Cl den dolayı In normal subjects, the AG is primarily determined by the negative charges on the plasma proteins, particularly albumin. As a result, the expected normal values for the AG must be adjusted downward in patients with hypoalbuminemia, with the AG falling by 2.3 to 2.5 meq/L for every 1 g/dL (10 g/L) reduction in the plasma albumin concentration [1,11]. The In normal subjects, the AG is primarily determined by the negative charges on the plasma proteins, particularly albumin. As a result, the expected normal values for the AG must be adjusted downward in patients with hypoalbuminemia, with the AG falling by 2.3 to 2.5 meq/L for every 1 g/dL (10 g/L) reduction in the plasma albumin concentration [1,11]. normal plasma AG had been considered to range between 7 and 13 meq/L. However, the normal AG may be as low as 3 to 11 meq/L (averaging 6 meq/L) due to a higher chloride concentration measured with the newer autoanalyzers [4,10]. As a result, knowing the normal range in a particular laboratory is essential if the AG is to be interpreted properly [10].

AG ölçülmeyen Ca ve Mg düşmesi ile Ölçülmeyen anyonların-albumin veya organik asit- artması ile artabilir aLBUMİNİN düşebilir ALB ARTMASI İLE AZALABİLİR. Thus, an increase in the AG can be induced by a fall in unmeasured cations (hypocalcemia or hypomagnesemia) or, more commonly and more markedly, by a rise in unmeasured anions (as with hyperalbuminemia due to volume contraction or the accumulation of an organic anion in metabolic acidosis) [10

Sebepleri Laktik asidoz Ketoasidoz The major causes of a high AG metabolic acidosis include [1,3,10]: Lactic acidosis, usually due to marked systemic hypoperfusion or to malignancy. (See "Bicarbonate therapy in lactic acidosis".) Ketoacidosis due to diabetes mellitus, alcohol, or fasting, in which beta-hydroxybutyrate is the primary unmeasured anion. (See "Clinical features and diagnosis of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults"

Metanol glikolat ve oxalat entox Etilen glikol Aspirin Renal yetersizlik Metanol glikolat ve oxalat entox Etilen glikol Aspirin Most patients with renal failure, in whom there is retention of both hydrogen and anions, such as sulfate, phosphate, and urate [3,14]. (See "Treatment of metabolic acidosis in chronic kidney disease".) Ingestions, in which the major retained anions are formate with methanol, glycolate and oxalate with ethylene glycol, and ketones and lactate with aspirin. However, metabolic acidosis may be absent and the anion gap may be normal in methanol or ethylene glycol intoxication if there is concurrent alcohol ingestion; the latter will compete for the enzyme alcohol dehydrogenase, thereby minimizing the metabolism of methanol or ethylene glycol to their toxic metabolites. (

AG 25 üzerinde ise tanısal gücü artar The diagnostic utility of a high AG is greatest when the AG is above 25 meq/L; in this setting, one of the above conditions will almost always be present

Tedavi genel prensipler pH<7.20 olmadıkça tedavi altta yatana yönelik General principles — The aim of therapy in metabolic acidosis is restoration of a normal extracellular pH. The normal renal response in this setting is to markedly increase acid excretion, primarily as ammonium. Thus, exogenous alkali may not be required if the acidemia is not severe (arterial pH >7.20), the patient is asymptomatic, and the underlying process, such as diarrhea, can be controlled. In other settings, correction of the acidemia can be achieved more rapidly by the administration of sodium bicarbonate. The initial aim of therapy is to raise the systemic pH above 7.20; this is a level at which the major consequences of severe acidemia should not be observed, although there is some uncertainty about the absolute benefits of achieving this level (table 1) [27,28].

HCO3 eksiği:Bikarb boşluğu x bikarb defisiti/l Bikarbonat defisiti : HCO3 10-12 hedeftir HCO3 eksiği:Bikarb boşluğu x bikarb defisiti/l Calculation of bicarbonate deficit — Assuming that respiratory function is normal, attainment of a pH of 7.20 usually requires raising the plasma bicarbonate to 10 to 12 meq/L [25]. The quantity of bicarbonate required can be estimated from the bicarbonate deficit: HCO3 deficit = HCO3 space x HCO3 deficit per liter The apparent bicarbonate space is a reflection of total body buffering capacity, which includes extracellular bicarbonate, intracellular proteins, and bone carbonate [29,30]. At a normal to moderately reduced plasma bicarbonate concentration, excess hydrogen ions are buffered proportionately through the total body water and the apparent bicarbonate space is approximately 55 percent of lean body weight.

Normalde %55 vücut ağırlığı Bikarbonat boşluğu: = [0.4 + (2.6 ÷ [HCO3])] x vücut ağırlığı( kg) However, the bicarbonate space rises in severe metabolic acidosis, since the fall in the plasma bicarbonate concentration means that there is an ever increasing contribution from the cells and bone, which have a virtually limitless supply of buffer. Thus, the bicarbonate space can reach 70 percent when the plasma bicarbonate concentration falls below 10 meq/L and may exceed 100 percent at levels below 5 meq/L [6]. The bicarbonate space at a given plasma bicarbonate concentration can be estimated from the following formula [30]: Bicarbonate space = [0.4 + (2.6 ÷ [HCO3])] x body weight (in kg)

THAM Tromethamine — Tromethamine (tris-hydroxymethyl aminomethane; THAM; trometamol) is an inert amino alcohol which buffers acids and CO2 by virtue of its amine (-NH2) moiety via the following reactions [10]: THAM-NH2 + H+ = THAM-NH3+ THAM-NH2 + H2O + CO2 = THAM-NH3+ + HCO3- Protonated THAM is excreted in the urine at a slightly higher rate than creatinine clearance in conjunction with either chloride or bicarbonate. Thus, THAM supplements the buffering capacity of blood without generating carbon dioxide but is less effective in anuric patients. Reported toxicities include hyperkalemia, hypoglycemia, and respiratory depression; the last complication probably results from the ability of THAM to rapidly increase the pH and decrease the PCO2 in the central nervous system. (See "Control of ventilation".)

Carbicarb — It has been proposed that a more effective alternative to sodium bicarbonate may be the administration of carbicarb, which is an equimolar mixture of sodium carbonate (Na2CO3) and sodium bicarbonate [3,7]. Sodium carbonate uses carbonic acid (H2CO3) to generate bicarbonate via the following reaction [12]: CO3(2-) + H2CO3 = 2 HCO3 RECOMMENDATIONS — In summary, the efficacy of and indications for alkali administration in hypoperfusion-induced lactic acidosis remains unresolved [18]. The primary aim of therapy must be reversal of the underlying disease. At best, raising the extracellular pH will only be of benefit if there is a parallel rise in intracellular pH [15]. This goal does not appear to be achieved with bicarbonate administration during cardiopulmonary resuscitation (CPR) [14,15]. (See "Therapies of uncertain benefit in basic and advanced cardiac life support".) Preliminary studies in patients with shock-induced lactic acidosis have not demonstrated any improvement in cardiac output or systemic blood pressure with the acute administration of sodium bicarbonate (when compared to an infusion of an equivalent amount of sodium chloride) [8]. Because acidemia is only one of many factors affecting the mortality of these critically ill patients, very large numbers will have to be assessed to determine if there is a therapeutic role for alkali. Partial elevations in both extracellular and intracellular pH can be achieved in patients being ventilated by increasing the rate of ventilation, thereby lowering the PCO2 [15]. Most physicians would limit the use of sodium bicarbonate to patients with severe metabolic acidemia (arterial pH below 7.10 to 7.15), with the aim being to maintain the pH above 7.15 until the primary process can be reversed. There is at present no evidence that alkali therapy is beneficial during CPR [15].

DeltaAG/DeltaHCO3 1-2 arası olmalıdır 1 in altında ise yani AG deki değişiklik HCO3 azalmasından az ise üriner keton kaybı İlave AG artmamış asidoz Oran>2 ise HCO3 AG göre çok düşmüştür İlave metab alkaloz