Emergency in Nephrology

Emergency in Nephrology
Bancha Satirapoj, MD Division of Nephrology Department of Medicine Phramongkutklao Hospital and College of Medicine

Outlines Acute kidney injury Hypokalemia Hyperkalemia Hyponatremia

KDIGO 2012: Definition AKI is defined as any of the following :
Increase in SCr ≥0.3 mg/dl within 48 hours Increase in SCr ≥1.5 times baseline, which is presumed to have occurred within the prior 7 days Urine volume < 0.5 ml/kg/h for 6 hours

Staging of AKI Only after volume status had been optimized
Stage Serum creatinine Urine output 1 ≥ 0.3 mg/dL OR ≥ times baseline < 0.5 ml/kg/hr for 6-12 hrs 2 times baseline < 0.5 ml/kg/hr for ≥ 12 hrs 3 3.0 times baseline OR ≥ 4 mg/dL OR initiation of RRT OR in patient<18 yrs, decrease in eGFR<35 mL/min/1.73 m3 < 0.3 ml/kg/hr for ≥ 24 hrs Anuria for ≥ 12 hrs Only after volume status had been optimized Urinary tract obstruction needed to be excluded

Approach to AKI Yes Yes Yes Yes Yes Azotemia Pseudoazotemia
Correct cause No Yes CKD No Yes Postrenal AKI No Yes Intrinsic AKI No Yes Prerenal vs ATN

INTERPRETING BUN & Cr CREATININE BUN Raised Reduced GFR
Larged muscle bulk Rhabdomyolysis Reduced tubular secretion (trimethoprim, cimetidine, probenecid) Reduced Small muscle mass Pregnancy Raised Reduced GFR Dehydration UGI bleeding Corticosteroid Hypercatabolic state High-protein diet Reduced Liver disease Starvation/Anabolic state

Correct cause No Yes CKD Treatment No Yes Postrenal AKI No Yes Intrinsic AKI No Yes Prerenal vs ATN

Differentiating AKI and CKD
Previous Serum Cr Chronic uremic symptoms/signs :fatigue, cramps, nocturia, hypertension Broad casts

Renal Ultrasound Small shrunken kidneys (usually < 7-8 cm in length) Thin cortex Increase renal echogenicity

X-ray Bone: Rugger-jersey spine Subperiosteal erosions on radial site of 2nd and 3rd fingers Resorption of the distal clavicles

Correct cause No Yes CKD Treatment No Retain foley’s catheter and Ultrasound kidney Yes Postrenal AKI No Yes Intrinsic AKI No Yes Prerenal vs ATN

Obstructive Uropathy Normal Severe Moderate Severe Hydronephrosis

Correct cause No Yes CKD Treatment No Yes Retain foley’s catheter and Ultrasound kidney Postrenal AKI No Yes Intrinsic AKI Treatment No Yes Prerenal vs ATN

Acute Kidney Injury (AKI)
Prerenal (55%) Intrinsic renal 40% Post renal cause 5% AIN 10% ATN (85%) AGN 5% Ischemic ATN (50%) Nephrotoxic ATN (35%)

Urinalysis in Acute Kidney Injury
Normal/bland Abnormal sediment Hematuria RBC casts proteinuria WBC WBC casts Eosinophils RTE cells Pigmented casts Crystalluria Non- albumin proteinuria Glomerulopathy Vasculitis Thrombotic MA AIN Atheroembolic AKI Uric acid Toxins Drugs Prerenal Postrenal Oncotic AKI Pyelonephritis Interstitial nephritis ATN Myoglobin Hemoglobin Plasma cell dyscrasia

Kidney biopsy

Indications for Renal Biopsy in AKI
Tissue examination via LM/EM/IF Acute nephritic syndrome Unexplained AKI Uncertain or multiple competing DDX Young pts with AKI often are considered based on long-term renal survival outcomes maximized with definitive dx

Clinical findings urinary indices
Approach to AKI Azotemia Yes Pseudoazotemia Correct cause No Yes CKD Treatment No Yes Postrenal AKI Ultrasound kidney No Yes Intrinsic AKI Treatment No Yes Clinical findings urinary indices Prerenal vs ATN

Acute Kidney Injury (AKI)
Prerenal (55%) Intrinsic renal 40% Post renal cause 5% AIN 10% ATN (85%) AGN 5% Ischemic ATN (50%) Nephrotoxic ATN (35%)

Acute Tubular Necrosis
Toxic ATN Ischemic ATN Sepsis Drug Pigment Injury -Myoglobinuria, Hemoglobinuria Crystal Induced Injury -Uric acid nephropathy, -Oxalate nephropathy Metabolic Causes -Hypercalcemia, Myeloma protein, -Light-chain nephropathy Prolong prerenal/ischemia Shock

Prerenal azotemia VS ATN
1. BUN/Cr >20:1 10:1 2. Urine Sp. Gr >1.018 1.010 3. Uosm > 500 4. Urine Na+ < 20 ** >40 5. FE Na+ < 1%** > 1%** 6. RF index <1 >1 7. FE urea <35% >50% 8. UA sediment Hyaline cast Muddy brown cast 9. Respond to Rx Decrease in hr No respond or delay

FE Na FE Na >1% FE Na <1% Prerenal azotemia
Early obstructive uropathy Acute glomerulonephritis Contrast induce AKI NSAIDs, ACEI/ARB 10-15% nonoliguric ATN ATN Late obstructive uropathy Prerenal azotemia Non reabsorbable solute Mineralocorticoid deficiency CKD Diuretic use

Urinalysis in Acute Kidney Injury
Normal/bland Abnormal sediment Hematuria RBC casts proteinuria WBC WBC casts Eosinophils RTE cells Pigmented casts Crystalluria Non- albumin proteinuria Glomerulopathy Vasculitis Thrombotic MA AIN Atheroembolic AKI Uric acid Toxins Drugs Prerenal Postrenal Oncotic AKI Pyelonephritis Interstitial nephritis ATN Myoglobin Hemoglobin Plasma cell dyscrasia

Management of AKI Treatment cause Supportive care
Balance fluid intake and output Intake = urine output + insensible loss +extrarenal loss Avoid nephrotoxic drug Correct metabolic complication Closed follow up clinical and lab Dialysis if indicated

Stage-Based Management of AKI
High risk Discontinue all nephrotoxic agents when possible Ensure volume status and perfusion pressure Consider functional hemodynamic monitoring Monitor serum creatinine and urine output Avoid hyperglycemia Consider alternatives to radiocontrast procedures Non-invasive diagnostic workup Consider invasive diagnostic workup Check for changes in drug dosing Consider Renal replacement therapy Consider ICU addmission Avoid subclavian catheters if possible

Aminoglycosides induce AKI
Not using aminoglycosides (2A) Single dose daily rather than multiple-dose daily treatment regimens (2B) Using topical or local applications of aminoglycosides rather than i.v. application (2B) KDIGO. Kidney International Supplements (2012) 2, 8–12

Contrast-induced AKI Assess the risk for CI-AKI in particular renal impairment Consider alternative imaging methods Lowest possible dose of contrast medium Iso-osmolar or low-osmolar iodinated contrast media in patients at increased risk of CI-AKI (1B) KDIGO. Kidney International Supplements (2012) 2, 8–12

Contrast-induced AKI IV isotonic sodium chloride or sodium bicarbonate solutions in patients at increased risk for CI-AKI (1A) No use oral fluids alone in patients at increased risk of CI-AKI (1C) KDIGO. Kidney International Supplements (2012) 2, 8–12

REPLACEMENT FLUID In the absence of hemorrhagic shock
Using isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume in patients at risk for AKI or with AKI (2B) KDIGO. Kidney International Supplements (2012) 2, 8–12

Vasopressors Insufficient data to conclude that one vasoactive agent is superior to another in preventing AKI Vasoactive agents should not be withheld from patients with vasomotor shock over concern for kidney perfusion Use of vasopressors in conjunction with fluids in patients with vasomotor shock with, or at risk for, AKI (1C) KDIGO. Kidney International Supplements (2012) 2, 8–12

Total energy intake Achieving 20–30 kcal/kg/d in patients with any stage of AKI (2C) Avoid restriction of protein intake (2D) 0.8–1.0 g/kg/d of protein in non-catabolic AKI patients (2D) 1.0–1.5 g/kg/d in patients with AKI on RRT (2D) Up to 1.7 g/kg/d in patients on CRRT and in hypercatabolic patients (2D) Preferentially via the enteral route (2C) KDIGO. Kidney International Supplements (2012) 2, 8–12

Loop Diuretics Decrease the metabolic demand of renal tubular cell  O2 requirement A greater urine flow  may reduce tubular obstruction and back-leak of filtrate Can convert oliguria to non-oliguria, make pt management easier No evidence that conversion of oliguria to non-oliguria is effective in reducing mortality or need for dialysis No use diuretics to prevent AKI (1B) and treat AKI, except in the management of volume overload (2C) KDIGO. Kidney International Supplements (2012) 2, 8–12

Indications for dialysis
A Refractory Acidosis E Refractory hyperkalemia I Intoxication : methanol, ethylene glycol, lithium O Refractory volume Overload U Uremia : uremic pericarditis, encephalopathy or BUN>100, Cr>10 in non-hypaercatabolic state BUN>70,Cr >7 in hypercatabolic state

for renal replacement therapy
:43:20 Common indications for renal replacement therapy Absolute indication Metabolic abnormality BUN> 100 mg/dL Hyperkalemia > 6 mEq/L with ECG abnormalities Hypermagnesemia> 8 mEq/L with anuria and absent DTR Acidosis pH<7.15 Lactic acidosis related to metformin use Fluid overload Diuretic resistant Adapted from Gibney et al, Clin J Am Soc Nephrol 2008 35

Initiate RRT Life-threatening changes in fluid, electrolyte, and acid-base balance exist Consider the broader clinical context, the presence of conditions, and trends of laboratory tests > single BUN and creatinine thresholds alone KDIGO. Kidney International Supplements (2012) 2, 8–12

CRRT Hemodynamically unstable patients (2B) Acute brain injury
Increased intracranial pressure Generalized brain edema (2B) KDIGO. Kidney International Supplements (2012) 2, 8–12

Hypokalemia Plasma [ K+] < 3.5 mEq/L

Spurious (pseudo) hypokalemia
Uptake by metabolically active cells as in AML with marked leukocytosis Prevent by Rapidly separating plasma and cells or Store at 4C True hypokalemia (inappropriate kaliuresis) in leukemia Proximal and distal tubulopathies Paraneoplastic expression of renin in leukemic cells

Cause of a Shift K+ into Cells
Hormones Insulin, beta-agonists (stress/sepsis), aldosterone Acid base disturbances Metabolic alkalosis Gain in ICF anions: anabolism Growth, recovery from DKA, TPN, red cell synthesis Rare factors Hypokalemic periodic paralysis Barium and Chloroquine intoxication Hypothermia Fall in serum K+ < 1 mEq/L

Hypokalemic periodic paralysis
Intermittent acute attacks of muscle weakness, with hypokalemia (often with low phos and Mg) Triggered by large CHO meals, rest post-exercise K+ Shifting Normal acid base balance with low urine K+ Causes Inherited form AD = mutation in alfa 1 subunit of DHP-sensitive CaC (CACNA1S) SCN4A = skeletal Na channel KCNJ2 = Kir2.1 K channel Thyrotoxicosis related = Asians and Mexicans

Hypokalemic periodic paralysis
Treatment Oral mEq K for acute attack then D/C precaution overshoot hyperkalemia Nonpharmacologic prevention Hypokalemic PP include avoiding strenuous exercise and high-carbohydrate loads Carbonic anhydrase inhibitor, either acetazolamide 250 mg twice daily Potassium-sparing diuretics (spironolactone 100 mg daily) B2 blockade and Rx thyroid disease

Cause of hypokalemia Test for diagnosis
Low urine K excretion Low intake Intracellular shift GI loss High urine K excretion Metabolic acidosis Metabolic alkalosis with HT without HT Test for diagnosis

Etiology Low intake Shift K + loss (diarrhea, ostomy, sweating)
TTKG = U K+ x Serum osmolality P K+ x Urine osmolality Low intake Shift K + loss Extra renal loss Renal loss -Urine K < 20 mEq/d (<15 mEq/L) -TTKG < 2 -Urine K/Cr < 15 mEq/g Cr (diarrhea, ostomy, sweating) -Urine K > 20 mEq/d (>15 mEq/L) -TTKG > 2 -Urine K/Cr > 15 mEq/g Cr

Test used to monitor the K+ excretion process
Strengths Weakness Expected value normal renal loss 24 hr urine potassium Valuable Does not indicate pathophysiology <15 >40 Urine K/Urine creatinine Can use random urine Expected rate of Cr excretion <15 mEq/gCr >15 mEq/gCr TTKG Physiologic basis Translates urine to CCD Many unverified assumption <2 >10 Random urine K+ Simple Does not consider MCD water reabsorption Factional excretion of K+ None Expected values depend on GFR <5-7% >5-7%

Urinary electrolytes Extra-renal loss Renal loss K+< 15 mEq/day Na+<100 mEq/day K+< 15 mEq/day K+/Cr < 15 mEq/g K+> 15 mEq/day K+/Cr > 15 mEq/g Repeat after increasing dietary Na+ to >100 mEq/day Diarrhea Cellular Shifting Low K intake Blood pressure High BP Low-Normal BP Metabolic acidosis Metabolic alkalosis Renin Activity Serum Aldosterone RTA DKA Urine Cl- Low (<10 mEq/day) Vomiting Penicillin derivatives Betahydroxybutyrate High (>10 Meq/day) -Gitelman’s syndrome -Bartter’s syndrome -Normotensive 1 aldosterone -Diuretics -Severe K depletion -Mg deficiency

Renal loss with MK and Hypertension
R A Renin secreting tumor Renovascular hypertension Malignant hypertension Vasculitis Primary hyperaldosteronism Adrenal adenoma/carcinoma Bilateral adrenal hyperplasia Glucocorticoid-responsive aldosteronism R A Congenital adrenal hyperplasia 11-beta hydroxylase deficiency 17-alfa hydroxylase deficiency Ectopic ACTH Cushing syndrome/disease Apparent mineralocorticoid excess Liddle’s syndrome 11 beta-hydroxysteroid dehydrogenase deficiency

Hypokalemia Muscular Cardiac muscle: arrhythmias (digitalis, heart disease) Skeletal muscle: weakness, cramps, paralysis, rhabdomyolysis Smooth muscle: constipation, ileus Renal Concentrating defect : polyuria (nephrogenic DI) Medullary interstitial disease Metabolic alkalosis

EKG changes in hypokalemia
A. Lowering & broadening of T wave, slightly prolonged QT interval Low, broad T wave with a double summit Depression of ST segment & slight lengthening of QT interval D. E. F. G. Marked ST deviations, sagging, downward T waves & prominent U waves

Life threatening hypokalemia
Cardiac arrhythmias Respiratory failure Hepatic encephalopathy

High Risk of Arrhythmia
Older patients Heart disease patients Patients on digoxin Patients on antiarrhythmic drugs Cohn JN, et al. Arch Intern Med. 2000:2429.

Approximation of total body K+ deficit
Serum [K+] K+ deficit (mEq/L) (mEq/70 kg body wt) Each decrease in 0.3 mEq/L, K deficit 100 mEq Caution; overestimate & underestimate

Treatment First step; Identify and stop ongoing losses of potassium
Discontinue diuretics/laxatives Use potassium sparing diuretics if diuretic therapy is required Treat diarrhea or vomiting Use H2-blocker to decrease nasogastric suction loss Control hyperglycemia if glycosuria is present

Treatment Second step; Repletion of potassium losses
Oral potassium (KCl) Liquid (KCL elixir, 20 mEq/15 mL ) Tablets (Addi-K 19 mEq/750 mg) Absorbed readily, large doses can be given safely Caution; GI side effect KHCO3 (K citrate): RTA Fruit (K supplement) Ulcerative GI tract K citrate/phosphate

Infusion pump is preferred to prevent overly rapid potassium
IV Potassium Reserved for severe hypokalemia, life threatening hypokalemia or TPN Preparation; Potassium chloride (KCL 2 mEq/mL) Rate infused mEq/hr Peripheral vein < mEq/L High concentration induces phlebitis Avoid glucose containing fluid Infusion pump is preferred to prevent overly rapid potassium Life threatening hypokalemia: K2HPO4 will stay in ICF during anabolism, no increase in serum [K+]

Emergency condition Mini-bag NSS or NSS/2 100 mL with potassium 40 mEq
High concentration = 400 mEq/L Infused into a large central vein (Femoral vein)

Uncontrolled diabetes
Diabeitc ketone acidosis (DKA)/hyperosmolar hyperglycemic state Normal serum K level Marked potassium deficit Acidosis/High osmolality/insulin deficiency Potassium supplementation: serum K <4.5 mEq/L Insulin must not be given in patient with severe hypokalemia (<3.3 mEq/L)

Refractory hypokalemia
Looked for Mg deficiency Preparation; Oral; magnesium hydroxide/magnesium oxide/magnesium gluconate Intravenous; magnesium sulfate 50% MgSO4 inj. 2 ml =1 g /amp = 8.1 mEq/amp 10% MgSO4 inj. 10 ml = 1 g /amp =8.1 mEq/amp 4-6 gm (30-50 mEq) of IV magnesium given slowly over 8-24 hours Caution; Rapidly infusion induces hypotension and paralysis digitalized patient

Hyperkalemia Potassium > mEq/ L

Hyperkalemia Pseudohyperkalemia Excess intake and Tissue necrosis
Hemolysis WBC > 50,000 Platelets > 750,000 Muscle activity during venupuncture Excess intake and Tissue necrosis Hemolysis/rhadomyolysis/tumor lysis syndrome Redistribution Beta-blockers, digoxin, hypertonic saline Reduced renal K excretion AKI/advanced CKD/renal tubular defects Medications

Serum K > 5.5 mEq/L No Pseudohyperkalemia BUN/Cr
(GFR < 20 mL/min)? Yes No ACEI, ARB Aldactone Amiloride Triamterene Trimethoprim Pentamidine NSAID B-blocker Heparin Anti fungal CNI Condition DM HIV AKI CKD High intake +CKD Addison disease Resistant -Obstructive uropathy -Interstitial disease -Pseudohypoaldosteronism Satirapoj B. Royal Thai Army Medical Journal. 2007;60(3-4):

Drug induced hyperkalemia

Clinical approach to Hyperkalemia
Need of emergency treatment Hyperkalemia with any ECG manifestation K > 6.5 mEq/L regarding absence of EKG change

Acute Treatment of hyperkalemia
Blocks effect of hyperkalemia on heart IV calcium Shifts K into cells Glucose and insulin, β2 agonists Removes K from body Kayexalate, dialysis, loop diuretics

Calcium gluconate Mechanism
Raise Action potential threshold to usual 15 mV difference between resting and threshold potential

IV Calcium 10% Calcium gluconate 10 mL IV over 2 – 3 minutes under continuous EKG monitoring Effect start in 1 – 3 minutes Last for 30 – 60 minutes Repeated dose should be given in No improvement in abnormal EKG Abnormal EKG recurs after initial improvement

Insulin Regular insulin 10 unit IV + 50% Dextrose 50 mL
Plasma K drop mEq/L Effect begins in 10 – 20 minutes Peak at 30 – 60 minutes Last for 4 – 6 hours To prevent hypoglycemia, 10% Dextrose at mL/hr with closed monitor blood glucose be used Hyperglycemia (> mg/dL): no need IV glucose

Sodium bicarbonate No role in treatment of acute hyperkalemia especially a single agent Severely acidic patients with hyperkalemia, sodium bicarbonate may be some of benefit Side effect : hypernatremia, volume overload, reduced ionized calcium

Cation-exchange resins
Increase GI tract K excretion Sodium or calcium polystyrene sulfonate Oral gm every 4-6 hours 1 gm bind 1 mEq of K Reduce Plasma K 1 mEq/L in 24 hours Per rectal 50 gm + water 150 mL per rectal at least min 1 gm bind 0.5 mEq of K Reduce Plasma K 0.8 mEq/L in 24 hours Side effects: GI irritation, constipation, bowel necrosis in postoperative patients, and history of bowel obstruction

Treatment Treatment Dose Time frame IV calcium gluconate 10 mL IV push
Seconds to minutes Glucose +Insulin RI 10 U + 50% glucose 50 mL IV 5-10 min (30-60 min) Sodium or calcium polystyrene sulfonate mg + water mL oral -50 mg + water 150 mL rectal retention min 1-4 hr (rectal) >6 hr (oral) Dialysis Immediate Satirapoj B. Royal Thai Army Medical Journal. 2007;60(3-4):

Blumberg A, et al. Am J Med 1988; 85: 507-512.

Hyponatremia Plasma Na+< 135 mEq/L

Hyponatremia Pseudohyponatremia (Posm 280-290 mOsm/kg) Hyperlipidemia
-Hyperproteinemia True Hypotonic hyponatremia (Posm < 280 mOsm/kg) Hypertonic hyponatremia (Posm > 290 mOsm/kg) -Hyperglycemia -Mannitol [ Na+ ] falls 1.6 (if BS <400), 2.4 mEq/L (if BS >400), for every increase of 100 mg/dL in glucose conc. Example1: Na+ 132, BS 400 Na+= {( ) X 1.6} = 136.8 100 Example2: Na+ 125, BS 600 Na+= {( ) X 2.4} = 137 100

PATHOPHYSIOLOGY OF HYPONATREMIA
Decrease Plasma Na+ = Total body Na+ Total body water Excess of total body water relative to total body solute water water water Na Na Na Hypovolemia Euvolemia Hypervolemia

Clinical causes of hyponatremia
Hypertonic hyponatremia (Posm > 295 mOsm/kg) -Hyperglycemia -Mannitol Pseudohyponatremia (Posm mOsm/kg) Hyperlipidemia -Hyperproteinemia Hypotonic hyponatremia (Posm < 280 mOsm/kg) Excess water intake (Uosm < 100 mOsm/kg) -Psychogenic polydipsia -Low solute intake -Chronic kidney disease Non-osmotic ADH release (Uosm > 100 or 300 mOsm/kg) Decreased ECF volume -Renal loss: UNa+>20 mEq/L -Extrarenal loss: UNa+< 20 mEq/L -Vomiting -Diarrhea -Excessive sweating Normal ECF volume : UNa+>20 mEq/L -Hypothyroidism -Adrenal insufficiency -SIADH Increased ECF volume : UNa+<20 mEq/L -CHF -Liver failure -Nephrotic syndrome -Pregnancy Volume depletion Diuretic/salt wasting syndrome Advance CHF Advance cirrhosis SIADH

Assessment of ECFV status
ECFV Depletion Sunken eyes Orthostatic hypotension Flatted neck veins Increased heart rate Decreased urine output Decreased BW

Laboratory investigation
Hypovolemia Euvolemia Hypervolemia Indirect lab Hemoconcentation Increase albumin BUN:Cr > 20:1 Elevate HCO3- Indirect lab (SIADH) Uric <5 BUN:Cr < 10:1 Slight decrease HCO3- Slight decrease AG Indirect lab Hemodilution Iow albumin BUN:Cr > 20:1 Elevate HCO3- Special lab TFT Cortisol level

Euvolemic Hyponatremia SIADH Hypothyroidism 2° Adrenal insufficiency

Syndrome of Inappropriate Antidiuresis (SIADH)
Essential features Effective osmolality <275 mOsm/kg Urinary osmolality >100 mOsm/kg at some level of decreased effective osmolality Clinical euvolemia Urinary sodium >30 mmol/L with normal dietary salt and water intake Absence of adrenal, thyroid, pituitary or renal insufficiency No recent use of diuretic agents European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

Syndrome of Inappropriate Antidiuresis (SIADH)
Supplemental features Plasma uric acid < 4 mg/dL BUN <21.6 mg/dL FE Na >0.5% FE urea >55% FE uric >12% Failure to correct hyponatremia after 0.9% saline infusion Correction of hyponatremia through fluid restriction European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

Major Causes of SIADH Pulmonary diseases Neurologic disorders
Ectopic production ADH Administration of exogenous ADH or oxytocin Symptomatic HIV infection Nausea, Fever, Pain Postoperative state Drugs Idiopathic

Clinical settings Acute Hyponatremia Duration < 48 hrs
Symptomatic patients: nausea, vomiting, headache, hiscough, mental change, convulsion Chronic Hyponatremia Duration > 48 hrs w/ brain adaptation Asymptomatic and Plasma [ Na+] >120 meq/L.

Classification of symptoms of hyponatraemia
Severity Symptom Moderately severe Nausea without vomiting Confusion Headache Severe Vomiting Cardiorespiratory distress Abnormal and deep somnolence Seizures Coma (Glasgow Coma Scale ≤8) European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

Risks factors of CNS symptoms
Pre-menstruant females Elderly females on thiazide diuretics Children Psychogenic polydipsia Hypoxemia

Identification and treatment of reversible etiologies
Symptomatic Asymptomatic Acute Duration < 48 hr Chronic Duration >48 hr or unknown Chronic Rarely < 48 hr Emergency correction needed Hypertonic saline (3%) at 1-2 mL/kg/hr + furosemide No immediate correction needed Some immediate correction needed Hypertonic saline (3%) at 1-2 mL/kg/hr Perform frequent measurement of serum and urine electrolyte Do not exceed 12 mEq/L/day Long-term management Identification and treatment of reversible etiologies

Treatment water water water Na Na Na Hypovolemia Euvolemia
Rehydration : Isotonic Restrict oral fluid Restrict oral fluid Diuretic: furosemide water water water Na Na Na Hypovolemia Euvolemia Hypervolemia

Simple calculation 3%NaCL at rate = 1x kg BW mL/hr will raise serum [Na+] at 1 mEq/L/hr Eg; Pt. BW 70 kgs. Need to increase serum[Na+] 1 mEq/L/hr must infuse 3% NaCl at rate 1x70 =70 mL/hr

Hyponatremia with Severe Symptoms
Prompt IV infusion of 150 ml 3% hypertonic over 20 min (1D) Checking the serum sodium concentration after 20 min while repeating an infusion of 150 ml 3% hypertonic saline for the next 20 min (2D) Repeating therapeutic until a target of 5 mmol/L increase in serum sodium concentration is achieved (2D) European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

Hyponatremia with Moderately Severe Symptoms
Starting prompt diagnostic assessment (1D) Cause-specific treatment (1D) Immediate treatment with a single IV infusion of 150 ml 3% hypertonic saline or equivalent over 20 min (2D) European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

Calculation TBW male = 0.6 X BW TBW female = 0.5 X BW
ในสารน้ำที่ให้ 1 ลิตรจะเพิ่ม Na ได้ = (Na ในสารน้ำที่ใช้ + K ในสารน้ำที่ใช้) – ค่า Na ของผู้ป่วย (TBW + 1) TBW male = 0.6 X BW TBW female = 0.5 X BW

Female BW = 40 , Na 112 mEq/L K= 4 mEq/L RX 0.9% NaCl
(Na K ในสารน้ำที่ใช้) – 112 0.5x = 42/21 = 2 24 ชั่วโมง เราต้องการ เพิ่ม < 8-12 mEq สมมุติเราจะเพิ่ม 6 mEq ต้องใช้สารน้ำทั้งหมด ประมาณ cc (rate 120 cc/hr) Monitor Serum Na 2-6 hr later

Rate serum Na correction
Limiting the increase in serum sodium to 10 mmol/L in the first 24 h 8 mmol/L during every 24 h Rx until a serum sodium concentration of 130 mmol/L (2D) European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

SIADH Moderate or profound hyponatraemia
First-line treatment: restrict fluid intake as (2D) Second line treatments: Increase solute intake with 0.25–0.50 g/kg/day of urea (2D) Combination of low-dose loop diuretics and oral sodium chloride (2D) Against lithium: slow onset toxicity Against demeclocycline (1D): nephrotoxicity European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

Aggressive Rx: rapid correction
Chronic hyponatremia Aggressive Rx: rapid correction Brain Osmotic Demyelination Syndrome Brain adaptation ↑ Na H2O H2O Risk factors Alcoholism, Malnutrition, Burns, Severe potassium depletion Elderly females on thiazide diuretics > 12 mEq/L elevation of Na+ on the first day Hypoxic episodes

Rapid Correction (>20 mEq/L)  Osmotic Demyelination Syndrome
Typically delayed for 2-6 days Often irreversible or only partially reversible: Dysarthria, dysphagia, paraparesis or quadriparesis, lethargy, coma, seizures

Risks for osmotic demyelination
Alcoholism Malnutrition Burns Severe potassium depletion Elderly females on thiazide diuretics More than a 12 meq/L elevation of Na+ on the first day Overcorrection of the Na+ to above 140 meq/L within the first two days Hypoxic episodes

Hyponatraemia is corrected too rapidly
Re-lowering the serum Na >10 mmol/l during the ﬁrst 24 hr or >8 mmol/l in any 24 hr thereafter (1D) Discontinuing the active treatment (1D) Infusion of 10 ml/kg of electrolyte-free water over 1 h under strict monitoring of urine output and ﬂuid balance (1D) Add IV desmopressin 2 mg, with no repeated more frequently than every 8 hr (1D) European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

Phramongkutklao Hospital and College of Medicine
Thank you for your attention Phramongkutklao Hospital and College of Medicine

Emergency in Nephrology

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