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Ηλεκτρολυτικές διαταραχές σε ειδικές καταστάσεις

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Παρουσίαση με θέμα: "Ηλεκτρολυτικές διαταραχές σε ειδικές καταστάσεις"— Μεταγράφημα παρουσίασης:

1 Ηλεκτρολυτικές διαταραχές σε ειδικές καταστάσεις
Το κάλιο στην καρδιακή ανεπάρκεια Ευαγγελία Ντουνούση Ηλεκτρολυτικές διαταραχές σε ΟΝΑ Χρήστος Μπαντής Ηλεκτρολυτικές διαταραχές στο ΣΔ Μάριος Θεοδωρίδης ΗΔ στην κίρρωση και ηπατική ανεπάρκεια Μάκρω Σονικιάν ΗΔ σε χειρουργικούς ασθενείς Ευμορφία Κονδύλη Σχολιαστής Π. Πασαδάκης

2 Το κάλιο στην καρδιακή ανεπάρκεια
Ευαγγελία Ντουνούση, Λέκτορας Νεφρολογίας-Μεταμόσχευσης, Νεφρολογική Κλινική Π.Ν. Ιωαννίνων

3 Το κάλιο στην καρδιακή ανεπάρκεια
στην ΚΑ και ο ασθενής μπορεί να εμφανίσει υποκαλιαιμία (Κ+ <3,5 mEq/L), είτε υπερκαλιαιμία (K+ ορού>5,5 mEq/L)!! Η αποφυγή τους είναι δύσκολη αλλά απαραίτητη, αφού και οι δύο συνδέονται με επικίνδυνες αρρυθμίες Ακούσαμε ενδιαφέροντα πράγματα για την επιδημιολογία της ΚΑ, την σοβαρή νοσηρότητα και θνησιμότητα των ασθενών με ΚΑ. Παρά την μεγάλη βελτίωση στα καρδιαγγειακά νοσήματα (έχει μειωθεί πολύ η θνητότητα του ΟΕΜ) Η πρόγνωση της ΚΑ παραμένει άσχημη και σήμερα (50% ασθενών με ΚΑ θα πεθάνουν σε 4 χρόνια). ~ 50% των θανάτων στην ΚΑ είναι αιφνίδιοι εξαιτίας αρρυθμίας

4 Macdonald, J. E. et al. J Am Coll Cardiol 2004;43:155-161
Probability of ventricular tachycardia in relation to serum potassium concentrations (40) Macdonald, J. E. et al. J Am Coll Cardiol 2004;43: Copyright ©2004 American College of Cardiology Foundation. Restrictions may apply.

5 Υποκαλιαιμία Υπερκαλιαιμία ΗΚΓ ΗΚΓ PR: επιμήκυνση ST: πτώση
QRS: διεύρυνση, T: επιπέδωση U: εμφάνιση ΗΚΓ P: επιπέδωση ή εξαφάνιση PR: επιμήκυνση R: ελάττωση ύψους R QRS: διεύρυνση, παράταση QT, βαθύ S ST: πτώση T: ψηλά Τ (σκηνοειδή) Υπερκαλιαιμία

6 Περιστατικό Καρδ. Ανεπ. ΗΚΓ:
Γυναίκα 70-χρόνων με ΣΔ τύπου 2 από 6ετίας ήρθε στο Νοσ. για δύσπνοια μόχθου από μηνός. Δεν είχε άλλα συμπτώματα Από 4ετίας λαμβάνει Ραμιπρίλη 2,5 mg x 1, και Aldactone 25mgx2. Τελευταίες 10 ημέρες πήρε NSAIDs γα οσφυαλγία Αντικειμενική εξέταση κφ X-ray θώρακα: κφ (καρδιομεγαλία) Hyperkalemia, congestive heart failure, and aldosterone receptor antagonism. Sica DA, Gehr TW, Yancy C. Source Section of Clinical Pharmacology and Hypertension, Medical College of Virginia of Virginia Commonwealth University, MCBV Station Box , Richmond, VA , USA. Abstract Hyperkalemia is a common occurrence in patients with congestive heart failure, particularly when renal failure coexists. The level of renal function in congestive heart failure is often difficult to ascertain because good measurement tools for estimation of renal function are not available. Serum creatinine values have often been offered as a good gauge of renal function, although in most cases true renal function is appreciably lower than the estimate derived from a specific serum creatinine value. Thus, patients with congestive heart failure very commonly, particularly in the advanced stages of the disease, have moderate renal insufficiency, either due to specific heart failure-related renal perfusion changes or as the result of renal involvement from the same processes having caused the heart failure, as is the case with diabetes. It is in this setting of mild-to-moderate levels of renal failure that therapies, such as angiotensin-converting inhibitors, angiotensin-receptor blockers, and aldosterone-receptor antagonists, are administered either individually or collectively. Each of these drug classes reduces the homeostatic ability to eliminate ingested potassium loads by the renal route and increase the tendency to evolve into a hyperkalemic state. This is noteworthy because aldosterone-receptor antagonists are increasingly considered as important therapies in the long-term management of heart failure. Spironolactone has been employed in this capacity and a new aldosterone-receptor antagonist, eplerenone, will become available in the near future, which further increases the importance of evaluating and treating the hyperkalemia risk in a timely manner. Εργαστηριακά: Cr= 1.8mg%, K= 7,2mEq/L, Ca=8,5mg%, P=5.2mg% Χοληστερόλη 240 mg%, Τριγλυκερίδια 185 mg%, PH 7.34, HCO3 22 meq/L, Hb 11 gm%, WBC 12,500, ΗΚΓ:

7 Περιστατικό Καρδ. Ανεπ. Hyperkalemia, congestive heart failure, and aldosterone receptor antagonism. Sica DA, Gehr TW, Yancy C. Source Section of Clinical Pharmacology and Hypertension, Medical College of Virginia of Virginia Commonwealth University, MCBV Station Box , Richmond, VA , USA. Abstract Hyperkalemia is a common occurrence in patients with congestive heart failure, particularly when renal failure coexists. The level of renal function in congestive heart failure is often difficult to ascertain because good measurement tools for estimation of renal function are not available. Serum creatinine values have often been offered as a good gauge of renal function, although in most cases true renal function is appreciably lower than the estimate derived from a specific serum creatinine value. Thus, patients with congestive heart failure very commonly, particularly in the advanced stages of the disease, have moderate renal insufficiency, either due to specific heart failure-related renal perfusion changes or as the result of renal involvement from the same processes having caused the heart failure, as is the case with diabetes. It is in this setting of mild-to-moderate levels of renal failure that therapies, such as angiotensin-converting inhibitors, angiotensin-receptor blockers, and aldosterone-receptor antagonists, are administered either individually or collectively. Each of these drug classes reduces the homeostatic ability to eliminate ingested potassium loads by the renal route and increase the tendency to evolve into a hyperkalemic state. This is noteworthy because aldosterone-receptor antagonists are increasingly considered as important therapies in the long-term management of heart failure. Spironolactone has been employed in this capacity and a new aldosterone-receptor antagonist, eplerenone, will become available in the near future, which further increases the importance of evaluating and treating the hyperkalemia risk in a timely manner.

8 Περιστατικό Καρδ. Ανεπ. Hyperkalemia, congestive heart failure, and aldosterone receptor antagonism. Sica DA, Gehr TW, Yancy C. Source Section of Clinical Pharmacology and Hypertension, Medical College of Virginia of Virginia Commonwealth University, MCBV Station Box , Richmond, VA , USA. Abstract Hyperkalemia is a common occurrence in patients with congestive heart failure, particularly when renal failure coexists. The level of renal function in congestive heart failure is often difficult to ascertain because good measurement tools for estimation of renal function are not available. Serum creatinine values have often been offered as a good gauge of renal function, although in most cases true renal function is appreciably lower than the estimate derived from a specific serum creatinine value. Thus, patients with congestive heart failure very commonly, particularly in the advanced stages of the disease, have moderate renal insufficiency, either due to specific heart failure-related renal perfusion changes or as the result of renal involvement from the same processes having caused the heart failure, as is the case with diabetes. It is in this setting of mild-to-moderate levels of renal failure that therapies, such as angiotensin-converting inhibitors, angiotensin-receptor blockers, and aldosterone-receptor antagonists, are administered either individually or collectively. Each of these drug classes reduces the homeostatic ability to eliminate ingested potassium loads by the renal route and increase the tendency to evolve into a hyperkalemic state. This is noteworthy because aldosterone-receptor antagonists are increasingly considered as important therapies in the long-term management of heart failure. Spironolactone has been employed in this capacity and a new aldosterone-receptor antagonist, eplerenone, will become available in the near future, which further increases the importance of evaluating and treating the hyperkalemia risk in a timely manner.

9 ασθενείς με ΚΑ και υπερκαλιαιμία (K+ ορού>7,0 mEq/L),
δεν εμφανίζουν ΗΚΓκές μεταβολές ή κλινικές ενδείξεις υπερκαλιαιμίας επειδή τα ιστικά επίπεδα K+ είναι φυσιολογικά ή χαμηλά* όπως αποδεικνύεται από την ενδοκυττάρια συγκέντρωση του K+ στα ερυθρά αιμοσφαίρια (6). Hyperkalemia, congestive heart failure, and aldosterone receptor antagonism. Sica DA, Gehr TW, Yancy C. Source Section of Clinical Pharmacology and Hypertension, Medical College of Virginia of Virginia Commonwealth University, MCBV Station Box , Richmond, VA , USA. Abstract Hyperkalemia is a common occurrence in patients with congestive heart failure, particularly when renal failure coexists. The level of renal function in congestive heart failure is often difficult to ascertain because good measurement tools for estimation of renal function are not available. Serum creatinine values have often been offered as a good gauge of renal function, although in most cases true renal function is appreciably lower than the estimate derived from a specific serum creatinine value. Thus, patients with congestive heart failure very commonly, particularly in the advanced stages of the disease, have moderate renal insufficiency, either due to specific heart failure-related renal perfusion changes or as the result of renal involvement from the same processes having caused the heart failure, as is the case with diabetes. It is in this setting of mild-to-moderate levels of renal failure that therapies, such as angiotensin-converting inhibitors, angiotensin-receptor blockers, and aldosterone-receptor antagonists, are administered either individually or collectively. Each of these drug classes reduces the homeostatic ability to eliminate ingested potassium loads by the renal route and increase the tendency to evolve into a hyperkalemic state. This is noteworthy because aldosterone-receptor antagonists are increasingly considered as important therapies in the long-term management of heart failure. Spironolactone has been employed in this capacity and a new aldosterone-receptor antagonist, eplerenone, will become available in the near future, which further increases the importance of evaluating and treating the hyperkalemia risk in a timely manner. Ευαγγελία Ντουνούση * όπως αποδεικνύεται από την ΕΝΔ C K+ στα ερυθρά αιμοσφαίρια (6).

10 Hyperkalemia, congestive heart failure, and aldosterone receptor antagonism.
Sica DA, Gehr TW, Yancy C. Source Section of Clinical Pharmacology and Hypertension, Medical College of Virginia of Virginia Commonwealth University, MCBV Station Box , Richmond, VA , USA. Abstract Hyperkalemia is a common occurrence in patients with congestive heart failure, particularly when renal failure coexists. The level of renal function in congestive heart failure is often difficult to ascertain because good measurement tools for estimation of renal function are not available. Serum creatinine values have often been offered as a good gauge of renal function, although in most cases true renal function is appreciably lower than the estimate derived from a specific serum creatinine value. Thus, patients with congestive heart failure very commonly, particularly in the advanced stages of the disease, have moderate renal insufficiency, either due to specific heart failure-related renal perfusion changes or as the result of renal involvement from the same processes having caused the heart failure, as is the case with diabetes. It is in this setting of mild-to-moderate levels of renal failure that therapies, such as angiotensin-converting inhibitors, angiotensin-receptor blockers, and aldosterone-receptor antagonists, are administered either individually or collectively. Each of these drug classes reduces the homeostatic ability to eliminate ingested potassium loads by the renal route and increase the tendency to evolve into a hyperkalemic state. This is noteworthy because aldosterone-receptor antagonists are increasingly considered as important therapies in the long-term management of heart failure. Spironolactone has been employed in this capacity and a new aldosterone-receptor antagonist, eplerenone, will become available in the near future, which further increases the importance of evaluating and treating the hyperkalemia risk in a timely manner. η προτεινόμενη, επιθυμητή τιμή K+ ορού στους ασθενείς με ΚΑ είναι προς τα ανώτερα φυσιολογικά επίπεδα και συγκεκριμένα μεταξύ των ορίων: 4,5-5,0 mEq/L.

11 Η χορήγηση διουρητικών σε ΚΑ συστήνεται προκειμένου να επιτευχθεί ευβολαιμία

12 Diuretic-induced hypokalemia is best prevented by use of the lowest effective dose.
We suggest not routinely providing prophylactic therapy to prevent hypokalemia (Grade 2C).

13 Δοσοεξαρτώμενες οι ανεπιθύμητες δράσεις θειαζιδών
Metabolic complications induced by bendrofluazide in relation to daily dose (multiply by 10 to get equivalent doses of hydrochlorothiazide). Increasing the dose led to progressive hypokalemia and hyperuricemia and a greater likelihood of a mild elevation in the fasting blood glucose (FBG), all without a further reduction in the systemic blood pressure. Each treatment group contained approximately 52 patients. Data from Carlsen, JE, Kober, L, Torp-Pedersen, C, Johannsen, P, BMJ 1990; 300:975. NTRODUCTION — Hypokalemia is a relatively common problem with diuretic therapy. Profound hypokalemia (serum potassium concentrations ≤2.5 to 3.0 meq/L), however, is relatively rare, described in fewer than 10 to 15 percent of patients receiving high doses of diuretics, and generally only in those not receiving potassium supplementation [1-3]. The decrease in plasma potassium concentration following prolonged administration of 50 mg of hydrochlorothiazide per day is approximately 0.5 meq/L, whereas the same dose of long-acting chlorthalidone causes a greater fall in serum potassium concentration (0.8 meq/L) [1]. The incidence and severity of hypokalemia are dose-dependent, occurring much less frequently with lower doses [4,5]. Thus, lower doses of thiazides (eg, 12.5 to 25 mg/day of chlorthalidone or hydrochlorothiazide) are now widely used in the treatment of hypertension because they are as effective in blood pressure reduction (figure 1) with a lesser effect on electrolyte balance (figure 2) [6]. In two large hypertension trials of low-dose chlorthalidone, hypokalemia requiring therapy occurred in 7 to 8 percent of patients fasting blood glucose (FBG)

14 γ) Ανταγωνιστές της αλδοστερόνης; δ) Διουρητικά της αγκύλης;
Ποια από τις παρακάτω κατηγορίες φάρμακων δεν συστήνεται ως φάρμακο πρώτης γραμμής στη θεραπεία ΚΑ: α) α-MEA; β) β-αποκλειστές; γ) Ανταγωνιστές της αλδοστερόνης; δ) Διουρητικά της αγκύλης;

15 μελέτη δυσλειτουργίας της ΑρΚ (SOLVD) – ACE-i for NYHA II,III symptomatic HF
Specialty: Cardiology, Congestive Heart Failure. Problem: Heart failure (Symptomatic - unlike CONSENSUS which involved only NYHA class IV symptomatic patients and other SOLVD trial which involved asymptomatic patients (1992) this one involved NYHA class II and III patients) HERE IS THE LINK FOR OTHER SOLVD TRIAL WHICH LOOKED ONLY AT ASYMPTOMATIC PATIENTS. Population: 2568 patients (1256 and 1257 took Enalapril and Placebo) Inclusion criteria: Patients with congestive heart failure and ejection fractions of < 35% (0.35 or less) with mainly NYHA class II and III symptoms who were already taking drugs other than an angiotensin-converting—enzyme inhibitor as part of conventional therapy for congestive heart failure were eligible for the study. At that time only therapy most of these people were on was a diuretic and digoxin.(so only 1/4th on B-Blockers) Exclusion criteria: Above 80 years of age. Valvular heart disease Unstable angina Pulmonary disease Elevated creatinine > 2.0 Other co-morbid disease like cancer Intervention: Enalapril Control: Placebo Follow-up: Mean 41.4 months Primary endpoint: Mortality Combined end point of death or hospitalizations Secondary endpoint(s): None Details: Enalapril vs placebo (in addition to diuretics, beta-blockers, nitrates & digoxin for specific indications only) Brief Results: Reduction of death in Enalapril group = 16% reduction in death. Largest reduction of mortality in patient group with progressive heart failure = 22% reduction. No effect on deaths due to arrhythmias Overall reduction in hospitalizations. Original Paper Effect of enalapril on survival in patients with reduced left ventricular ejection fraction and congestive heart failure. 1 Aug 1991 N Engl J Med 1991; 325: CLICK HERE FOR ORIGINAL ARTICLE Here is the graph: Τα διουρητικά σχετίζονταν με αύξηση του κινδύνου εμφάνισης θανατηφόρας αρρυθμίας κατά 37%

16 Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study-EPHESUS
η επλερενόνη, σε ασθενείς με καρδιακό επεισόδιο και ενδείξεις συστολικής δυσλειτουργίας της ΑρΚ και ΚΑ, βελτιώνει την επιβίωση και τη νοσηλεία. μόλις 1% χρειάστηκε να την διακόψει εξαιτίας σοβαρής υπερκαλιαιμίας (>6 mEq/L) την καλύτερη επιβίωση έδειξαν οι ασθενείς με Κ+ ορού>4 mEq/L.

17 Aldosterone antagonist
Επικίνδυνη υπερκαλιαιμία των νέων στρατηγικών θεραπείας Καρδιακής Ανεπάρκειας HF CKD ACE-I Aldosterone antagonist + + + =

18 A diet high in fruits, vegetables, and low-fat dairy foods can help lower systolic blood pressure by more than 10 points in people with high blood pressure.

19 19

20 Ηλεκτρολυτικές διαταραχές σε ΟΝΑ
Acute kidney injury (AKI) can have both immediately recognizable consequences as well as less noticeable or delayed consequences. Fluid overload and electrolyte/acid–base abnormalities represent well known, easily recognized consequences of AKI. Contrary, impaired innate immunity and chronic kidney disease do not manifest themselves immediately.

21 Ηλεκτρολυτικές διαταραχές σε ΟΝΑ

22 Ηλεκτρολυτικές διαταραχές σε ΟΝΑ
ραβδομυόλυση, σύνδρομο λύσης όγκου, αιμόλυση ή βαρέα εγκαύματα υπερφωσφαταιμία : υπασβεστιαιμία: υπερασβεστιαμία: ραβδομυόλυση, οξεία παγκρεατίτιδα ταχεία διόρθωση μεταβολικής οξέωσης συχνή, σε υπερκαταβολικούς ή σε ΟΝΑ με αυξημένο κυτταρικό θάνατο μπορεί να παρατηρηθεί συχνότερα στη ραβδομυόλυση ή αν έχουν χορηγηθεί Ca-ούχα σκευάσματα στην φάση της υπασβεστιαιμίας ραβδομυόλυση, μετά από Ca-ούχα σκευάσματα

23 Αιτίες της ραβδομυόλυσης
Τραυματική βλάβη μυών Αύξηση δραστηριότητας μυών Εξωγενείς τοξίνες (αλκοόλ, φάρμακα) Κληρονομική μυοπάθεια, φλεγμονώδεις μυοπάθειες Υποκαλιαιμία, ΥπερΦωσφαταιμία, Υπερωσμωτικότητα

24 Jerome W. Conn (1907–1994), Primary hyperaldosteronism
Primary hyperaldosteronism has many causes, including adrenal hyperplasia and adrenal carcinoma.[2] The syndrome is due to: bilateral idiopathic adrenal hyperplasia 70 % unilateral idiopathic adrenal hyperplasia 20 % aldosterone-secreting adrenal adenoma (benign tumor, < 5%) rare forms, including disorders of the renin-angiotensin system Jerome W. Conn (1907–1994),

25

26 Οξεία νεφροπάθεια φωσφορικού
παρουσιάζεται μετά τη χρήση καθαρτικών του εντέρου με oral sodium phosphate (OSP) - αναφέρθηκε μετά από ένεμα OSP για κολονοσκόπηση το Πολλαπλές περιπτώσεις – Οξείας Νεφρικής Βλάβης (ΟΝΒ) με ειδική ιστολογική εικόνα στη βιοψία OSP was formerly sold without prescription under the brand name "Fleet Phospho-soda" (C.B. Fleet Inc.) or as a generic equivalent. OSP is currently available only by prescription in a pill form (Visicol, Osmoprep; Salix Pharmaceuticals). In both pill and liquid form, OSP is a hyperosmotic laxative that acts by drawing water into the gastrointestinal tract. Although long used as a laxative, OSP began to be used as a purgative for colonoscopy in 1990 [3]. It is frequently given in favor of standard polyethylene glycol-based lavage solutions because of the smaller required volume, which results in better patient compliance and improved colonic cleansing [4-6]. In 2006, in response to published reports, the United States Food and Drug Administration (FDA) issued a warning regarding the potential for AKI in patients who received OSP [12]. The warning was incorporated into a consensus document on bowel preparation by the American Society of Colon & Rectal Surgeons, the American Society of Gastrointestinal Endoscopy, and the Society of American Gastrointestinal & Endoscopic Surgeons [13]. In December 2008, the FDA required that a boxed warning be added to labeling of Visicol and Osmoprep, which are still available by prescription [14]. At the same time, following the recommendation of the FDA, over-the-counter preparations that contain OSP were voluntarily withdrawn from the market by the manufacturer 2006 warning for potential AKI Δεκ. 2008 boxed warning Acute phosphate nephropathy and renal failure. Desmeules S, Bergeron MJ, Isenring P N Engl J Med. 2003;349(10):1006.

27 72 ετών γυναίκα, με αιματοχεσία
ιστορικό υπέρτασης ένα επεισόδιο αιματοχεσία, υποβλήθηκε σε εξωτερική κολονοσκόπηση. εσωτερικές hemorrhoids (καυτηρίαση), 2 πολύποδες(αφαιρέθηκαν). 2 εβδομάδες αργότερα εμφάνισε προοδευτική αδυναμία και ήρθε στα ΤΕΠ. Φαρμακα που έπαιρνε lisinopril 20 mg/D και εκτάκτως ibuprofen για πόνο στις αρθρώσεις. Φυσική εξέταση : κανονική πίεση αίματος Εργαστηριακά: Κρεατινίνη ορού 3.5 mg/dL (1.0 mg/dL πριν 3 μήνες), Ουρία 120 mg/dL, K 5.2 mEq/L, Ca 8.5 mg/dL, P 7.5 mg/dL και Alb3.8 g/dL. Ούρα dipstick 1+ protein, μικροσκοπικά ουδέν Λόγω νέας αύξησης της Cr έγινε βιοψία:

28 Sunday, October 9, 2011 silver nitrate
The stain that was used is the von Kossa stain (von Kossa J (1901) The silver nitrate in the staining solution (silver ion is positive charge) binds with the anionic ionic (negative charge) portion of the salt. The silver ions react with phosphate or carbonate not calcium, by binding the positive silver ion with the negative phosphate or carbonate portion. The resulting silver salt (silver phosphate), will be seen as black. silver nitrate θετικά ιόντα Ag με το αρνητικό τμήμα φωσφορικό ή ανθρακικό. Σχηματίζουν άλας Ag (ασημένιο φωσφορικά άλατα), είναι μαύρο

29 Acute Phosphate Nephropathy
Sunday, October 9, 2011 Νεφρική βιοψία ευρήματα οξείας και χρόνιας σωληναριακής βλάβης με εναπόθεση φωσφορικού Ca. Οι επασβεστώσεις ευρίσκονται στο κυτταρόπλασμα των επιθηλιακών σωληναριακών κυττάρων και λιγότερο εντός του διαμέσου ιστού. Characterized by acute and subsequent chronic renal failure following exposure to oral sodium phosphate (OSP) bowel purgatives. Renal biopsy findings include acute and chronic tubular injury with prominent tubular and interstitial calcium phosphate deposits. The acute tubular degenerative changes involve all tubular segments from proximal to distal to collecting duct and included epithelial simplification, luminal ectasia, loss of proximal tubular brush border, enlarged reparative nuclei with prominent nucleoli, shedding of cellular fragments into the tubular lumina, and dropout of tubular epithelial cells. The tubular injury is accompanied by interstitial edema. The presence of bundant calcium phosphate deposits in distal tubules and collecting ducts The calcifications are located within the cytoplasm of tubular epithelial cells, within tubular lumina, and less prominently within the interstitium. Risk factors include older age, female gender, hypertension, chronic kidney disease (CKD), and treatment with angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and diuretics. Acute Phosphate Nephropathy

30 Ηλεκτρολυτικές Διαταραχές στο Σακχαρώδη Διαβήτη
6ο Μετεκπαιδευτικό Σεμινάριο Υγρών, Ηλεκτρολυτών και Οξεοβασικής Ισορροπίας Ηλεκτρολυτικές Διαταραχές στο Σακχαρώδη Διαβήτη Μάριος Θ. Θεοδωρίδης Νεφρολόγος , Επιμελητής Α Παν. Νεφρολογική Κλινική Π.Γ.Ν. Αλεξανδρούπολης

31 Ηλεκτρολυτικές διαταραχές στο ΣΔ
υπερνατριαιμία λόγω ωσμωτικής διούρησης διαταραγμένη ομοιοστασία Κ+ -διορθώνεται με Ins Kαλή ρύθμιση του διαβήτη αποτρέπει την υπερφωσφατουρία Ο διαβήτης σχετίζεται με υπομαγνησιαιμία

32 insulin deficiency, hypertonicity and αcidemia ………..

33 ↓ συγκέντρωση Νa στο ΕΣΑ
Υπεργλυκαιμία & Ωσμωτική διούρηση ↑[ ΓΛΥΚΟΖΗΣ ] στο ΕΣΑ ↓ Επαναρρόφηση ύδατος ↓ συγκέντρωση Νa στο ΕΣΑ ↑ απέκκριση Νa ↑ αποβολή ύδατος back diffusion of Na+ from interstitial to tubular fluid (paracellular) a. Increased water excretion Mechanism: osmotic diuresis (explained before) FM’s urinary specific gravity is <1.005 (range ) This SG is at the lower end of the range and, given the high rates of excretion of glucose (urinary [glucose] >1000 mg/dl), Na+ (420 mEq/24 hr), & K+ (260 mEq/24 hr), he must be drinking large volumes of water to have that low a specific gravity. Thirst mechanism driven by  vascular volume,  plasma osmolality Increased Na+ excretion osmotic diuresis  Na+ reabsorption from proximal tubule  Na+ delivery to distal nephron  Na+ reabsorption from collecting duct and  Na+ excretion c. Increased K+ excretion i. Osmotic diuresis  collecting duct flow rate  tubular fluid [K+]  cell to tubule [K+] gradient  K+ secretion and excretion ii. Vascular volume depletion   sympathetic activity and  afferent arteriole bp  renin,  angiotensin,  aldosterone  K+ secretion and excretion iii. Unreabsorbable anions in collecting duct (CD) CD fluid contains acetoacetate &  hydroxybutyrate because they have exceeded their proximal tubule Tm Ketoacids not reabsorbed in CD (Cl- is)  CD lumen more negative   K+ secretion and excretion ↑ απέκκριση K 4. Conclusion Συνήθεις απώλειες γλυκόζη ≈ mmol/L Na+ ≈ 40 mmol/L K+ ≈ 20 mmol/L.

34 In all 4 patients the plasma electrolyte values were fallaciously low.
Moderately raised serum lipids and lipoproteins often are found in adults with diabetes mellitusI-3 and in diabetic children4- both before and after treatment. Severe hyperlipidaemia in association with diabetes is however much less common.7 We describe 4 children with insulin-dependent diabetes who developed massive hyperlipidaemia associated with a variable degree of metabolic decompensation. In all 4 patients the plasma electrolyte values were fallaciously low. In all 4 patients the plasma electrolyte values were fallaciously low.

35 Pseudohyponatremia occurs when a quantitative serum Na+ measurement is performed on a given volume of plasma that contains a greater-than-normal amount of water-excluding particles, such as lipid or protein. In this setting, plasma water (which contains the Na+) composes a smaller fraction of the plasma volume, leading to a factitiously low serum Na+ concentration (when expressed in mEq/L). The Na+ concentration in plasma water is normal, and therefore patients are asymptomatic. Attention should be directed to hyperlipidemia or hyperproteinemia.

36 σοβαρές κράμπες στα πόδια
42 ετών γυναίκα, διαβητική για 10 χρόνια , Ιστορικό: κόπωση, απώλεια βάρους, ναυτία, έμετος, πολυουρία, πολυδιψία, σωματικοί πόνοι, και πόνος στα κάτω άκρα. Πτωχός γλυκαιμικός έλεγχος: 4 μήνες FPG 280mg%,PLPG 360mg% Από 6μήνου Νυκτουρία. Φάρμακα: glibenclamide 10mg x 2, Tab. metformin 500mg x 2. During this period she noticed weight loss, increasing thirst and fatigue. About a month back she complained of body ache and pains in her lower limbs. For this she consulted her family physician who prescribed NSAIDS. This gave her only marginal relief. Later she noticed that she had difficulty in getting up from the squating position, and needed support. The pains and weakness persisted and were gradually increasing. Fifteen days prior to admission she complained of nausea and occasional vomiting. Her weakness, fatigue and weight loss had all increased. A plasma glucose done one week prior to admission was fasting 240mg% with urine sugar of +++ and post lunch 340mg% with urine sugar of ++++, Urinary ketones were absent. O/E she appeared ill and weak. She had signs suggestive of dehydration like a dry tongue and diminished skin turgor. She was pale with no evidence of clubbing, cynosis or icterus. Her pulse was 88/min and regular and the BP was 160/90 mmHg. There was no pedal oedema. Her cardiac and respiratory systems did not reveal any abnormality. FPG fasting plasma glucose, PLPG post lunch plasma glucose

37 σοβαρές κράμπες στα πόδια
Πριν από ένα μήνα ο οικογενειακός γιατρός της έγραψε NSAIDS για πόνο στο σώμα και τα πόδια με μικρή ανακούφιση. Στη συνέχεια παρουσίασε αδυναμία έγερσης από καθιστή θέση. Οι πόνοι και η αδυναμία συνεχίστηκαν με σταδιακή αύξηση. 15 ημέρες πριν ναυτία, έμετοι. 7 ημέρες πριν Εργαστηριακά: FPG 240mg%, PLPG 340mg%, γλυκόζη ούρων +++, ketones --. During this period she noticed weight loss, increasing thirst and fatigue. About a month back she complained of body ache and pains in her lower limbs. For this she consulted her family physician who prescribed NSAIDS. This gave her only marginal relief. Later she noticed that she had difficulty in getting up from the squating position, and needed support. The pains and weakness persisted and were gradually increasing. Fifteen days prior to admission she complained of nausea and occasional vomiting. Her weakness, fatigue and weight loss had all increased. A plasma glucose done one week prior to admission was fasting 240mg% with urine sugar of +++ and post lunch 340mg% with urine sugar of ++++, Urinary ketones were absent. O/E she appeared ill and weak. She had signs suggestive of dehydration like a dry tongue and diminished skin turgor. She was pale with no evidence of clubbing, cynosis or icterus. Her pulse was 88/min and regular and the BP was 160/90 mmHg. There was no pedal oedema. Her cardiac and respiratory systems did not reveal any abnormality.

38 σοβαρές κράμπες στα πόδια
Αντικειμενική Εξέταση: Είχε συμπτώματα αφυδάτωσης. Σφύξεις 88/min, ρυθμικές, BP = 160/90 mmHg. Καρδιά – Αναπνευστικό κφ. ECG : Επιπέδωση Τ During this period she noticed weight loss, increasing thirst and fatigue. About a month back she complained of body ache and pains in her lower limbs. For this she consulted her family physician who prescribed NSAIDS. This gave her only marginal relief. Later she noticed that she had difficulty in getting up from the squating position, and needed support. The pains and weakness persisted and were gradually increasing. Fifteen days prior to admission she complained of nausea and occasional vomiting. Her weakness, fatigue and weight loss had all increased. A plasma glucose done one week prior to admission was fasting 240mg% with urine sugar of +++ and post lunch 340mg% with urine sugar of ++++, Urinary ketones were absent. O/E she appeared ill and weak. She had signs suggestive of dehydration like a dry tongue and diminished skin turgor. She was pale with no evidence of clubbing, cynosis or icterus. Her pulse was 88/min and regular and the BP was 160/90 mmHg. There was no pedal oedema. Her cardiac and respiratory systems did not reveal any abnormality. The liver was palpable 3 cm below the coastal margin, was smooth and nontender; the spleen was not palpable. On neurological examination, her higher functions were intact with no evidence of any cranial nerve involvement. Her fundus examination was normal with no evidence of a diabetic retinopathy. Power in the upper limbs was normal. Lower limbs showed normal power distally, tested at the ankle and knee. Proximally at the hip power was reduced to grade 4. She had difficulty in getting up from squatting position and had the Gower’s sign positive. But once up she could walk without support. She had no involuntary movements or ataxia, co-ordination as tested by the finger-nose-finger and the knee-heelknee tests was normal.Her sensory system was normal to touch, pain and temperature, vibration sense was impaired at the ankles and her ankle reflexes were not elicitable. The planters were flexors. She had no evidence of an autonomic neuropathy.

39 Κατά την εισαγωγή Τυχαίο σάκχαρο αίματος: 350 mg %,
Ουρά (spot): Glucose ++++, Protein – trace, Ketones +++; Ηλεκτρολύτες: Na 134; K 1.7; CI 99, Ουρία 110 mg%, Cr 1.5 mg%, Chol 240 mg%, TGl 350 mg%, pH 7.34, HCO3 20 mEq/L, Ca 8.5 mg%, P 4 gm% Hb 10 gm%, WBC 12,500, X-ray κφ At admission Spot urine test done using multistix showed Glucose ++++, Protein – trace, Ketones +++; ECG : Flattening of T waves, Random Blood sugars: 350mg%, electrolytes: Na 134; K 1.7; CI 99, BUN 55 mg%, Creatinine 1.5 mg%, Cholesterol 240 mg%, Triglycerides 350 mg%, PH 7.34, HCO320 meq/I, Ca 8.5 mg%, P 4 gm% Hb 10 gm%, WBC 12,500, X-ray Chest – normal. Treatment for DKA instituted with KCI included in the drip Tribasic Calcium phosphate tablets were started. KCI 200 mmol given in the first 24 hours. Έναρξη Θεραπείας για DKA με KCI – KCl δόθηκαν 200 mEq τις πρώτες 24h

40 Ημέρα 2η Σάκχαρο 117mg%, Ketones: ίχνη,
Electrolytes: Na 135; K 2.7; CI 108, Ουρία 56mg%. Την νύχτα παρουσίασε έντονο πόνο στα κάτω άκρων με κράμπες. Οι πόνοι ήταν αρκετά σοβαροί ώστε να την κάνουν να κραυγάζει με αγωνία ΝΕΥΡΟΛΟΓΙΚΗ ΕΞΕΤΑΣΗ: Η αδυναμία είχε αυξηθεί. ΌΧΙ σημεία μηνιγγίτιδας. Άνω άκρα κφ. Η ασθενής δεν μπορεί να σηκώσει τa πόδιa, στο κρεβάτι. Τα αντανακλαστικά στα κάτω άκρα δεν παράγονταν. Ο πόνος στα κάτω άκρα γενικεύτηκε. Δεν υπήρχαν μυϊκοί σπασμοί, αλλά επώδυνες κράμπες. On Day 2 Blood sugar was 117mg%, Ketones: trace, Electrolytes: Na 135; K 2.7; CI 108, BUN 28mg%. At this point, KCI 100 mmol was given. Evening of 2nd day, the blood sugar was 140mg%, Ketones: absent, Electrolytes: Na 136; K2.6; CI 108. At night patient developed severe pain in the lower limbs with cramps. The pains were severe enough to make her scream with agony. O/E Pulse 100/min, BP 140/90 mm of Hg, Chest was clear. Neurologically her weakness had increased. She could not sit up by herself even holding the rails of the bed. There was no meningeal signs. Power in the upper limbs was normal. She could not lift her leg while in bed. The pain in the lower limbs was generalised with no locally palpable tenderness. There were no spasms, but the pains were cramp like. Reflexes in the lower limbs were not elicitable; and the planters were flexors. Blood was collected for serum magnesium and an injection of magnesium sulphate was given. Within a few minutes of the injection the patients’ limb

41 σοβαρές κράμπες στα πόδια
Eξετάστηκε το μαγνήσιο ορού και Δόθηκε μια ένεση Θειικό Μαγνήσιο. Μέσα σε λίγα λεπτά εξαφανίστηκε ο πόνος των άκρων και η ασθενής μπόρεσε να κοιμηθεί. On Day 3 Patient was very cheerful, Proximal muscle weakness had improved dramatically, she was able to walk and go to the toilet. Blood sugar: 125 mg%, Ketones: Absent, Electrolytes: Na 138; K 3.5; CI 108, Ca 8.5 mg%, P 3.5 mg%, Mg 0.8 mg%. Discussion Magnesium deficiency in diabetic ketoacidosis is well described but it is generally not given due importance in the routine management of diabetic ketoacidosis. This patients’ cramps and proximal and truncal muscle weakness was obviously due to magnesium deficiency, since treatment with magnesium sulphate alleviated all these symptoms. Her persistently low potassium levels was also probably due to magnesium deficiency. Hypomagnesemia enhances potassium losses in the urine by increased production of aldosterone and administration of magnesium salts can correct this abnormality. Conclusion Magnesium deficiency is more common than is believed, but its presentation with such severe cramps and pronounced proximal and truncal weakness is very unusual. Magnesium deficiency should always be included in the differential diagnosis of patients who present with persistent or severe muscle pains, spasms or weakness, and magnesium supplementation should be routinely considered in severe cases of diabetic ketoacidosis. ΣΥΜΠΕΡΑΣΜΑ Οι σοβαρές κράμπες στα πόδια σχετίζονταν με σοβαρή μυϊκή αδυναμία λόγω ανεπάρκειας μαγνησίου.

42 ΗΛΕΚΤΡΟΛΥΤΙΚΕΣ ΔΙΑΤΑΡΑΧΕΣ ΣE ΚΙΡΡΩΣΗ - ΗΠΑΤΙΚΗ ΑΝΕΠΑΡΚΕΙΑ
Μάκρω Σονικιάν Νεφρολογικό τμήμα ΓΝΜ “Α. Φλέμινγκ”

43 ΗΔ στην κίρρωση και ηπατική ανεπάρκεια
Επιπλοκές Κίρρωσης Κιρσοί οισοφάγου Ηπατική εγκεφαλοπάθεια Άλλες επιπλοκές

44 ΗΔ στην κίρρωση και ηπατική ανεπάρκεια
υποNατριαιμία λόγω διουρητικών για τον ασκίτη, πρόσληψη μεγάλων ποσοτήτων υγρών με χαμηλό Na+ υποKαλιαιμία λόγω απώλειας Κ+ στα ούρα υποΦωσφαταιμία σε αλκοολικούς με χρόνια ηπατική ανεπάρκεια Υπομαγνησιαιμία Μπορεί να εμφανιστεί θεωρητικά σε ασθενείς με ηπατική κίρρωση/ανεπάρκεια και φυσιολογική νεφρική λειτουργία, που παρουσιάζουν χρόνια διάρροια, υποσιτισμό ή λαμβάνουν μακροχρόνια θεραπεία με διουρητικά της αγκύλης ή θειαζίδες. Επί απώλειας Mg2+ η ημερήσια απέκκρισή του στα ούρα είναι >10-30 mg και η κλασματική του απέκκριση >2%. Επί εξωνεφρικής απώλειας η κλασματική απέκκριση Mg2+ φθάνει το 2,7% και επί νεφρικής το 4-48%(34).

45 ΗΔ στην κίρρωση και ηπατική ανεπάρκεια
υποΝατριαιμία λόγω κατακράτησης ύδατος (αυξ. έκκριση ADH, μείωση RBF-νεφρική αγγειοσύσπαση) κατανάλωση ποσοτήτων υγρών με χαμηλό Na+ διουρητικά α) Περιορισμός υγρών < Vu β) Διόρθωση συνυπάρχουσας υποΚ γ) Χορήγηση ανταγωνιστών V2-ADH δ) Δεμεκλοκυκλίνη ε) Υπέρτονο NaCl 3% Στη χρόνια υπονατριαιμία της κίρρωσης και προς αποφυγή εγκεφαλικού οιδήματος υπάρχει αντιρροπιστική έξοδος από τα εγκεφαλικά κύτταρα Κ+, γλουταμίνης, μυοϊνοσιτόλης και άλλων ενδοκυτταρίων ουσιών, η οποία επισυμβαίνει προοδευτικά σε διάστημα 48 ωρών. Χορήγηση ανταγωνιστών των υποδοχέων βαζοπρεσσίνης: Οι ανταγωνιστές των V2 υποδοχέων της βαζοπρεσσίνης τολβαπτάνη, σαταβαπτάνη, λυξιβαπτάνη χρησιμοποιούνται από το στόμα. Ο ανταγωνιστής των V2 και V1a υποδοχέων κονιβαπτάνη χρησιμοποιείται ενδοφλέβια. Ο τελευταίος προκαλεί μείωση της ήδη χαμηλής αρτηριακής πίεσης και αυξάνει τον κίνδυνο αιμορραγίας των κιρσών του οισοφάγου (η βαζοπρεσσίνη είναι αποτελεσματική στη θεραπεία των αιμοραγούντων κιρσών)(23). Επίσης, η κονιβαπτάνη μπορεί να επιδεινώσει τη νεφρική λειτουργία (ο V1α αγωνιστής τερλιπρεσσίνη βελτιώνει τη νεφρική λειτουργία σε κίρρωση με ασκίτη)(24). Συμπερασματικά, η κονιβαπτάνη πρέπει να χρησιμοποιείται με μεγάλη προσοχή. Η απάντηση της υπονατριαιμίας στην τολβαπτάνη στους ασθενείς με κίρρωση/ηπατική ανεπάρκεια είναι ασθενέστερη σε σχέση με τους ασθενείς με καρδιακή ανεπάρκεια και σύνδρομο απρόσφορης έκκρισης αντιδιουρητικής ορμόνης (μελέτη SALTWATER)(25). Οι κύριες ανεπιθύμητες ενέργειες ήταν συχνουρία, πολυουρία, δίψα, ξηροστομία, κόπωση και οδήγησαν σε διακοπή της θεραπείας στο 5,4% των 111 ασθενών. Η νοσηλεία είναι υποχρεωτική για την έναρξη ή επανέναρξη της θεραπείας, διότι μπορεί να προκληθεί υπερταχεία διόρθωση της υπονατριαιμίας V2: τολβαπτάνη, σαταβαπτάνη, λυξιβαπτάνη V1a: κονιβαπτάνη ΕΦ

46 αλκοολικοί με χρόνια ηπατική ανεπάρκεια
Υποφωσφαταιμία συνηθέστερη εκδήλωση (P < 1 mg/dl), είναι η μυοπάθεια* η μυοπάθεια μπορεί να οδηγήσει σε ραβδομυόλυση, οπότε αντισταθμιστικά απελευθερώνεται PO43- από τους πάσχοντες μύες. Υποψία πιθανού ενδοκυτταρίου ελλείμματος Mg2+ τίθεται επί ανθεκτικής υποκαλιαιμίας με κοιλιακές αρρυθμίες, οπότε πρέπει να χορηγηθούν 50 mEq Mg2+ στάγδην ενδοφλέβια μέσα σε 8-24 ώρες. Επί χορήγησης θειαζιδικών διουρητικών ή διουρητικών της αγκύλης, αυτά μπορούν να αντικατασταθούν από καλιοσυντηρητικά διουρητικά που αυξάνουν την επαναρρόφηση του Mg2+ στο φλοιϊκό αθροιστικό σωληνάριο. * μπορεί να οφείλεται στο έλλειμμα PO43 ‘η/και στο αλκοόλ.

47 αλκοολική κίρρωση Ανδρας 47 ετών προσεκομίσθη με από 3-ημέρου αδυναμία, ανορεξία, δύσπνοια καθώς και μια πρόσφατη πτώση. Ιστορικό: πεπτικό έλκος, υπέρταση και αλκοολική κίρρωση. Οικογενειακό ιστορικό ελεύθερο. Αναφέρει κάπνισμα 2 πακέτων ημερησίως, και κατανάλωση μπύρες την ημέρα τα τελευταία 20 χρόνια. Introduction Cirrhosis of the liver commonly leads to a state of chronic hypervolemic hyponatremia. Profound exacerbation of the hyponatremic state may occur in patients with decompensated cirrhosis in conjunction with acute stressors such as infection or binge alcohol ingestion. A 47-year-old Caucasian male was admitted with a 3-day history of shortness of breath, weakness, anorexia, and unsteady gait, including a recent fall. The patient had a medical history significant for peptic ulcer disease, hypertension, and alcoholic cirrhosis. His family history was not significant. He reported smoking 2 packs per day and drinking 8-12 beers per day for the past 20 years. Over the previous 6 months, the patient had been unemployed and reported increased alcohol consumption. On physical exam, the patient was noted to have marked ascites with a prominent fluid wave and bulging flanks, bilateral pitting edema above the knees, and crackles as well as dullness to percussion in the left lower lobes. In addition, chest radiographs revealed a left lower lobe pneumonia. Significant laboratory studies included a WBC of 19.4 × 109/L, AST of 107 U/L, ALT of 66 U/L, and serum sodium concentration of 105 meq/L. The patient was treated with IV furosemide (40 mg × 1 dose) and 3% NaCl in addition to fluid restriction because of his symptomatic and profound hyponatremia. His serum sodium concentration increased to 120 meq/L over 48 hours and 130 meq/L over 96 hours with the use of 3% NaCl and fluid restriction, and his weakness, anorexia, and unsteady gate improved. His pneumonia was treated with Vancomycin (1 g IV every 12 hrs) and Piperacillin/Tazobactam (3.375 mg IV every 6 hrs) which resulted in symptomatic and radiographic improvement. He was discharged from the hospital on oral spironolactone (200 mg/day) and furosemide (40 mg/day) with recommendations for abstinence from alcohol, a low sodium diet, and fluid restriction.

48 αλκοολική κίρρωση ΦΥΣΙΚΗ ΕΞΕΤΑΣΗ:
σημαντικός ασκίτης, οίδημα ζυμώδες πάνω από τα γόνατα άμφω, αμβλύτητα και ρόγχοι στον αριστερό κάτω πνευμονικό λοβό. Θώρακος x-ray: Πνευμονία* αριστερού κάτω λοβού. Εργαστηριακά:WBC =19.400/L, AST =107 U/L, ALT =66 U/L, Να ορού 105 meq/L. Introduction Cirrhosis of the liver commonly leads to a state of chronic hypervolemic hyponatremia. Profound exacerbation of the hyponatremic state may occur in patients with decompensated cirrhosis in conjunction with acute stressors such as infection or binge alcohol ingestion. A 47-year-old Caucasian male was admitted with a 3-day history of shortness of breath, weakness, anorexia, and unsteady gait, including a recent fall. The patient had a medical history significant for peptic ulcer disease, hypertension, and alcoholic cirrhosis. His family history was not significant. He reported smoking 2 packs per day and drinking 8-12 beers per day for the past 20 years. Over the previous 6 months, the patient had been unemployed and reported increased alcohol consumption. On physical exam, the patient was noted to have marked ascites with a prominent fluid wave and bulging flanks, bilateral pitting edema above the knees, and crackles as well as dullness to percussion in the left lower lobes. In addition, chest radiographs revealed a left lower lobe pneumonia. Significant laboratory studies included a WBC of 19.4 × 109/L, AST of 107 U/L, ALT of 66 U/L, and serum sodium concentration of 105 meq/L. The patient was treated with IV furosemide (40 mg × 1 dose) and 3% NaCl in addition to fluid restriction because of his symptomatic and profound hyponatremia. His serum sodium concentration increased to 120 meq/L over 48 hours and 130 meq/L over 96 hours with the use of 3% NaCl and fluid restriction, and his weakness, anorexia, and unsteady gate improved. His pneumonia was treated with Vancomycin (1 g IV every 12 hrs) and Piperacillin/Tazobactam (3.375 mg IV every 6 hrs) which resulted in symptomatic and radiographic improvement. He was discharged from the hospital on oral spironolactone (200 mg/day) and furosemide (40 mg/day) with recommendations for abstinence from alcohol, a low sodium diet, and fluid restriction. *Vancomycin (1 g IV χ 2) Piperacillin/Tazobactam (3.375 mg IV χ 4)

49 αλκοολική κίρρωση ΘΕΡΑΠΕΙΑ: IV Lasix (40 mg × 1) και 3% NaCl με επιπρόσθετο περιορισμό υγρών εξαιτίας της σημαντικής και συπτωματικής ΥΠΟΝΑΤΡΙΑΙΜΙΑΣ. Το Να ορού αυξήθηκε στο 120 meq/L σε 48 hours και 130 meq/L σε 96 ώρες, και η αδυναμία, ανορεξία και ασταθής κατάσταση βελτιώθηκε. ρυθμός διόρθωσης της υπονατριαιμίας Discussion Chronic hyponatremia (defined as a serum sodium concentration below 130 meq/L) occurs in up to 22 percent of people with cirrhosis [5], and is often asymptomatic if the serum sodium concentration is above 120 meq/L [6,7]. The percent of people with cirrhosis affected by chronic hyponatremia increases to 50 percent if a cutoff for serum sodium concentration of 135 meq/L, the lower limit of normal, is used [5]. The frequency of such profound hyponatremia as seen at presentation in the patient in this case (serum sodium concentration of 105 meq/L) is unclear; a population survey reported that the prevalence of patients with cirrhosis and serum sodium concentrations less than or equal to 120 meq/L is 1.2 percent [6]. The most common reason for chronic hyponatremia in cirrhosis is impairment in renal solute-free water secretion due to increased antidiuretic hormone secretion and decreased effective arterial volume [5,8]. The brain is able to compensate for the increased osmolar pressure (which leads to cerebral edema) in chronic hyponatremia by extruding intracellular osmolytes, such as potassium, glutamine and myoinositol, which can take 48 hours for full effect [5,7,9]. This adaptive mechanism explains why patients with chronic hyponatremia and serum sodium concentrations above 120 meq/L are often asymptomatic. If there is an acute exacerbating condition however, such as infection or binge drinking as in this patient, the serum sodium concentration can rapidly drop to dangerously low levels for which the brain is unable to compensate acutely. Acute worsening of chronic hyponatremia may have various etiologic factors, including: generalized haemodynamic derangement with low peripheral resistance, reduced effective arterial volume, hypothalamic overproduction of antidiuretic hormone, elevated renin and angiotensin, hypotonic fluid ingestion and reduced glomerular filtration, all of which may lead to marked water retention [5,7,8]. The ingestion of large amounts of alcohol, a hypotonic fluid containing little sodium, may worsen the underlying chronic hyponatremia present in cirrhosis [2] and is believed to be a factor for the acute decompensation seen in this patient. Common symptoms of chronic hyponatremia include fatigue, nausea, dizziness, lethargy, confusion, and gait disturbances [10,11]. In the setting of acute hyponatremia, or acute on chronic hyponatremia, seizures, coma, and respiratory arrest may occur [10]. It should be noted that the symptoms experienced by the patient presented in this report are likely multifactorial and due to both the profound hyponatremia and comorbid lobar pneumonia. Treatment of hyponatremia in patients with cirrhosis includes sodium and fluid restriction and continued treatments with spironolactone and loop diuretics. However, care must be taken when administering diuretics as they can exacerbate the reduction in tissue perfusion that occurs in cirrhosis, further impairing the ability to excrete free water [12]. Bolus infusions of 3% NaCl are reserved for patients with profound hyponatremia and severe symptoms [13]. Vasopressin receptor antagonists are newer therapies and their precise role in treating hypervolemic hyponatremia in patients with cirrhosis is not well-defined [5,7]. The serum sodium concentration in symptomatic hyponatremia should be corrected at a rate no more than 10 meq/L in the first 24 hours, 18 meq/L in the first 48 hours, and 20 meq/L in the first 72 hours to prevent iatrogenic brain injury and central pontine myelinolysis [13,14]. In patients with cirrhosis, it is important to recognize the symptoms of hyponatremia, identify and treat any exacerbating conditions early in their course, and correct the serum sodium concentration slowly with frequent monitoring. Abbreviations ALT: alanine transaminase; AST: aspartate transaminase; IV: intravenous; NaCl: Sodium Chloride; WBC: white blood cell count. Consent <10 mEq/L τις 24 ώρες και <18 mEq/L τις 48 ώρες για την αποφυγή ωσμωτικού απομυελινωτικού συνδρόμου

50 αλκοολική κίρρωση ΕΞΙΤΗΡΙΟ από το Νοσοκομείο
ΣΤ spironolactone (200 mg/Η) & furosemide (40 mg/Η) αποχή από το αλκοόλ, δίαιτα χαμηλή Να και περιορισμό υγρών. Discussion Chronic hyponatremia (defined as a serum sodium concentration below 130 meq/L) occurs in up to 22 percent of people with cirrhosis [5], and is often asymptomatic if the serum sodium concentration is above 120 meq/L [6,7]. The percent of people with cirrhosis affected by chronic hyponatremia increases to 50 percent if a cutoff for serum sodium concentration of 135 meq/L, the lower limit of normal, is used [5]. The frequency of such profound hyponatremia as seen at presentation in the patient in this case (serum sodium concentration of 105 meq/L) is unclear; a population survey reported that the prevalence of patients with cirrhosis and serum sodium concentrations less than or equal to 120 meq/L is 1.2 percent [6]. The most common reason for chronic hyponatremia in cirrhosis is impairment in renal solute-free water secretion due to increased antidiuretic hormone secretion and decreased effective arterial volume [5,8]. The brain is able to compensate for the increased osmolar pressure (which leads to cerebral edema) in chronic hyponatremia by extruding intracellular osmolytes, such as potassium, glutamine and myoinositol, which can take 48 hours for full effect [5,7,9]. This adaptive mechanism explains why patients with chronic hyponatremia and serum sodium concentrations above 120 meq/L are often asymptomatic. If there is an acute exacerbating condition however, such as infection or binge drinking as in this patient, the serum sodium concentration can rapidly drop to dangerously low levels for which the brain is unable to compensate acutely. Acute worsening of chronic hyponatremia may have various etiologic factors, including: generalized haemodynamic derangement with low peripheral resistance, reduced effective arterial volume, hypothalamic overproduction of antidiuretic hormone, elevated renin and angiotensin, hypotonic fluid ingestion and reduced glomerular filtration, all of which may lead to marked water retention [5,7,8]. The ingestion of large amounts of alcohol, a hypotonic fluid containing little sodium, may worsen the underlying chronic hyponatremia present in cirrhosis [2] and is believed to be a factor for the acute decompensation seen in this patient. Common symptoms of chronic hyponatremia include fatigue, nausea, dizziness, lethargy, confusion, and gait disturbances [10,11]. In the setting of acute hyponatremia, or acute on chronic hyponatremia, seizures, coma, and respiratory arrest may occur [10]. It should be noted that the symptoms experienced by the patient presented in this report are likely multifactorial and due to both the profound hyponatremia and comorbid lobar pneumonia. Treatment of hyponatremia in patients with cirrhosis includes sodium and fluid restriction and continued treatments with spironolactone and loop diuretics. However, care must be taken when administering diuretics as they can exacerbate the reduction in tissue perfusion that occurs in cirrhosis, further impairing the ability to excrete free water [12]. Bolus infusions of 3% NaCl are reserved for patients with profound hyponatremia and severe symptoms [13]. Vasopressin receptor antagonists are newer therapies and their precise role in treating hypervolemic hyponatremia in patients with cirrhosis is not well-defined [5,7]. The serum sodium concentration in symptomatic hyponatremia should be corrected at a rate no more than 10 meq/L in the first 24 hours, 18 meq/L in the first 48 hours, and 20 meq/L in the first 72 hours to prevent iatrogenic brain injury and central pontine myelinolysis [13,14]. In patients with cirrhosis, it is important to recognize the symptoms of hyponatremia, identify and treat any exacerbating conditions early in their course, and correct the serum sodium concentration slowly with frequent monitoring. Abbreviations ALT: alanine transaminase; AST: aspartate transaminase; IV: intravenous; NaCl: Sodium Chloride; WBC: white blood cell count. Consent

51 Η υπομαγνησιαιμία της κίρρωσης οφείλεται:
α) Στη χρόνια διάρροια; β) Στον υποσιτισμό; γ) Στη μακροχρόνια λήψη διουρητικών; δ) Σε όλα τα παραπάνω;

52 Διαταραχές ηλεκτρολυτών σε χειρουργικούς ασθενείς
Κονδύλη Ευμορφία Επίκουρη καθηγήτρια Εντατικής Ιατρικής ΜΕΘ - ΠΑΓΝΗ

53 Physiological Aspects of Fluid and Electrolyte Balance
The 1999 UK National Confidential Enquiry into Perioperative Deaths report (Callum, Gray et al. 1999) has found that fluid imbalance contributes to serious postoperative morbidity and mortality and has recommended that “training in fluid management, for medical and nursing staff, is required to increase awareness and spread good practice”. An earlier retrospective study (Stoneham and Hill 1997) showed that perioperative fluid prescriptions are extremely variable, with some patients receiving as much as 5 L fluid and 740 mmol sodium per day. Dileep N. Lobo MB, BS, MS, Dip. NB, FRCS (Gen Surg) University of Nottingham, October 2002

54 Provision of guidelines or teaching on fluid and electrolyte prescribing

55 ΗΔ σε χειρουργικούς ασθενείς
Υπονατριαιμία= μία από τις συνηθέστερες διαταραχές. Υπερφωσφαταιμία** συχνότερα σε ασθενείς με σοβαρή νεφρική νόσο, υποπαραθυρεοειδισμό, τραύμα, ραβδομυόλυση ή εκσεσημασμένα αυξημένο κυτταρικό μεταβολισμό. *μπορεί να είναι σοβαρά επηρεασμένη σε χειρουργικούς αρρώστους **Κλινικά εκδηλώσεις της υποκείμενης νόσου ή της συνυπάρχουσας υποασβεστιαιμίας

56 ΗΔ σε χειρουργικούς ασθενείς
οι μετεγχειρητικοί ασθενείς τις πρώτες μετεγχειρητικές ημέρες πολύ συχνά βρίσκονται σε θετικό ισοζύγιο υγρών (> 7 L) και Na+ ( 700 mmol) Αρχικά, η απάντηση στο στρες και τον πόνο προκαλεί αντιδιούρηση και ολιγουρία (ADH, αυξ. κατεχολαμίνες, ενεργ. RAA). Συχνά εκλαμβάνεται ως υπογκαιμία και αντιμετωπίζεται με χορήγηση υγρών πλούσιων σε Na+. Αρχικά, η απάντηση στο στρες και τον πόνο προκαλεί αντιδιούρηση και ολιγουρία ως αποτέλεσμα της δράσης της ADH, των αυξημένων κατεχολαμινών και της ενεργοποίησης του άξονα RAA. Αυτό οδηγεί όχι μόνο σε αύξηση του κυκλοφορούντος όγκου, αλλά και του διάμεσου υγρού προκαλώντας οίδημα, αύξηση του σωματικού βάρους και αιμοαρραίωση

57 ΒΑΣΙΚΕΣ καθημερινές ΑΠΑΙΤΗΣΕΙΣ ΜΕΤΕΓΧΕΙΡΗΤΙΚΟΥ ΑΣΘΕΝΗ
για τους νεαρούς ενήλικες (περίπου) 30 ml/kg Η2Ο, mmol/kg Na mmol/kg K.

58 Υποτασικός ασθενής με επισκληρίδιο
αποκλεισμός ελλείματος υγρών. Η υπόταση Δεν οφείλεται οπωσδήποτε στην επισκληρίδιο. αποφυγή υπερβολικής χορήγησης υγρών σε ασθενείς που είναι ενυδατωμένοι.* vasodilating effects of epidural analgesia. The ideal way of tackling problems with fluid and electrolyte balance is to avoid them in the first place. Appropriate monitoring strategies are discussed in section 2.4. The patient’s fluid status and electrolyte balance need to be estimated, taking into consideration: unusual losses as the result of the surgical problem prior to assessment continuing surgical-related losses usual maintenance needs vasodilating effects of epidural analgesia.

59 Ποια είναι η πιθανή αιτία της υποΝα?
Γυναίκα 38-ετών νοσηλεύεται μετά από ετερόπλευρη χειρουργική μαστεκτομή. Εργασηριακά 1ης μετεγχειρητικής ημέρας: Ουρία 26 mg/dL, Κρεατινίνη 1.2 mg/dL, με Na+ ορού 127 mEq/L, ουρικό οξύ 3mg/dL, Απέκκριση Na+ > 40mEq/L, Ωσμωτικότητα ούρων > 100 mosmol/kg* Hyponatremia in the setting of bacterial meningitis (or any pathologic CNS process) is usually due to SIADH. SIADH is a form of hyponatremia involving sustained or spiking levels of ADH that are inappropriate for the osmotic or volume stimuli that normally affect ADH secretion. Urinary Na+ excretion exceeds 20 mEq/L unless the patient is wasting, and it improves with fluid restriction. In most cases, restriction of fluids to mL/day is all that is needed. SIADH

60 βασικά σημεία για διάγνωση της SIADH
ΥποΝατριαιμία ΥποΩσμωτικότητα (Sosm mosmol/kg) Ωσμωτικότητα ούρων > 100 mosmol/kg* Απέκκριση Na+ > 40mEq/L Φυσιολογική Οξεοβασική Ισορροπία και Ισορροπία Κ Φυσιολογική λειτουργία νεφρών, θυρεοειδούς, επινεφριδίων Χαμηλό ουρικό οξύ (συνήθως) The normal response to hyponatremia (which is maintained in primary polydipsia) is to markedly suppress ADH secretion, resulting in the excretion of a maximally dilute urine with an osmolality below 100 mosmol/kg and a specific gravity ≤ Values above this level indicate an inability to normally excrete free water, most commonly because of persistent 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 higher. The primary causes of persistent ADH release are effective circulating volume depletion (true hypovolemia, heart failure, and cirrhosis) and the syndrome of inappropriate ADH secretion (SIADH). Serum uric acid and urea concentrations — The initial water retention and volume expansion in the SIADH is frequently associated with hypouricemia (serum uric acid concentration less than 4 mg/dL or 238 micromol/L) due to increased uric acid excretion in the urine [11,13-15]. It is presumed that the early volume expansion diminishes proximal sodium reabsorption, leading to a secondary decline in the net reabsorption of uric acid and increased uric acid excretion. However, stimulation of the vasopressor V1a receptor (which primarily causes vasoconstriction) may also contribute to the uric acid wasting via an uncertain mechanism. If hyponatremia is induced in normal volunteers with desmopressin (dDAVP), an agent that stimulates the V2 receptor (which primarily mediates the antidiuretic response) but not the V1a receptor, the serum uric acid concentration does not fall as much (29 versus 53 percent) as it does in patients with a similar degree of hyponatremia caused by the SIADH (in which the native hormone stimulates both the V1a and V2 receptors) [16]. ** μεγαλύτερη από την αναμενόμενη για τον βαθμό της ΥποΝατριαιμίας

61 ΦΑΝΑΡΙ ΡΟΔΟΠΗΣ 2D. Hypokalemia impairs insulin release. Hormonal mechanisms (involving insulin, β-adrenergic agonists, and aldosterone) modulate potassium (K) distribution by promoting rapid transfer of K across the cell membrane. In patients with hypokalemia, mineralocorticoid status is an important consideration. In addition, sodium ion delivery changes to the distal nephron, and inherited and acquired defects of the distal nephron function, can all lead to hypokalemia.


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