bancha satirapoj, md division of nephrology department of medicine phramongkutklao hospital and...

Bancha Satirapoj, MD

Division of Nephrology

Department of Medicine

Phramongkutklao Hospital and College of Medicine

Emergency in Nephrology

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

Stage Serum creatinine Urine output

1 ≥ 0.3 mg/dL OR ≥ 1.5-1.9 times baseline

< 0.5 ml/kg/hr for 6-12 hrs

2 2.0-2.9 times baseline < 0.5 ml/kg/hr for ≥ 12 hrs

33.0 times baselineOR ≥ 4 mg/dLOR initiation of RRT OR in patient<18 yrs, decrease in eGFR<35 mL/min/1.73 m3

< 0.3 ml/kg/hr for ≥ 24 hrsOR Anuria for ≥ 12 hrs

Staging of AKI

Only after volume status had been optimizedUrinary tract obstruction needed to be excluded

Approach to AKI

Azotemia

Pseudoazotemia

CKD

Postrenal AKI

Intrinsic AKI

Prerenal vs ATN

Yes Correct cause

No

Yes

Yes

Yes No

No

No

Yes

INTERPRETING BUN & Cr

CREATININE

Raised Reduced GFR Larged muscle bulk Rhabdomyolysis Reduced tubular secretion

(trimethoprim, cimetidine, probenecid)

Reduced Small muscle mass Pregnancy

BUN

Raised

Reduced GFR

Dehydration

UGI bleeding

Corticosteroid

Hypercatabolic state

High-protein diet

Reduced

Liver disease

Starvation/Anabolic state

Approach to AKI

Azotemia

Pseudoazotemia

CKD

Postrenal AKI

Intrinsic AKI

Prerenal vs ATN

Yes Correct cause

Treatment

No

Yes

Yes

Yes No

No

No

Yes

Differentiating AKI and CKD

Previous Serum Cr

Chronic uremic symptoms/signs :fatigue, cramps, nocturia, hypertension

Broad casts

Differentiating AKI and CKD

Renal Ultrasound

Small shrunken kidneys (usually < 7-8 cm in length)

Thin cortex

Increase renal echogenicity

Differentiating AKI and CKD

X-ray Bone: Rugger-jersey spine Subperiosteal erosions on radial

site of 2nd and 3rd fingers Resorption of the distal clavicles

Approach to AKI

Azotemia

Pseudoazotemia

CKD

Postrenal AKI

Intrinsic AKI

Prerenal vs ATN

Yes Correct cause

Treatment

No

Yes Retain foley’s catheter and Ultrasound kidney

Yes

Yes No

No

No

Yes

Normal

ModerateHydronephrosis

SevereHydronephrosis

Obstructive Uropathy

SevereHydronephrosis

Approach to AKI

Azotemia

Pseudoazotemia

CKD

Postrenal AKI

Intrinsic AKI

Prerenal vs ATN

Yes Correct cause

Treatment

No

Yes

Yes

Yes

Treatment

No

No

No

Yes

Retain foley’s catheter and Ultrasound kidney

Acute Kidney Injury (AKI)

Prerenal (55%)

Intrinsic renal40%

Post renal cause

5%

ATN (85%)AIN 10% AGN 5%

Ischemic ATN (50%) Nephrotoxic ATN (35%)

Urinalysis in Acute Kidney Injury

PrerenalPostrenalOncotic AKI

GlomerulopathyVasculitisThrombotic MA

PyelonephritisInterstitial nephritis

AINAtheroembolic AKI

ATNMyoglobinHemoglobin

Uric acidToxinsDrugs

Plasma cell dyscrasia

HematuriaRBC castsproteinuria

WBCWBC casts

Eosinophils RTE cellsPigmented

casts

Crystalluria Non-albumin

proteinuria

Abnormal sedimentNormal/bland

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

Approach to AKI

Azotemia

Pseudoazotemia

CKD

Postrenal AKI

Intrinsic AKI

Clinical findings urinary indices

Prerenal vs ATN

Yes Correct cause

Treatment

No

Yes Ultrasound kidney

Yes

Yes

Treatment

No

No

No

Yes

Acute Kidney Injury (AKI)

Prerenal (55%)

Intrinsic renal40%

Post renal cause

5%

ATN (85%)AIN 10% AGN 5%

Ischemic ATN (50%) Nephrotoxic ATN (35%)

Acute Tubular Necrosis

SepsisDrugPigment Injury-Myoglobinuria, HemoglobinuriaCrystal Induced Injury-Uric acid nephropathy, -Oxalate nephropathyMetabolic Causes-Hypercalcemia, Myeloma protein, -Light-chain nephropathy

Toxic ATN Ischemic ATN

Prolong prerenal/ischemiaShock

Prerenal azotemia VS ATNPrerenal ATN

1. BUN/Cr >20:1 10:1

2. Urine Sp. Gr >1.018 1.010

3. Uosm > 500 250-300

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 24-72 hr No respond or delay

Prerenal azotemia VS ATNPrerenal ATN

1. BUN/Cr >20:1 10:1

2. Urine Sp. Gr >1.018 1.010

3. Uosm > 500 250-300

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 24-72 hr No respond or delay

FE Na

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

FE Na <1% FE Na >1%

Urinalysis in Acute Kidney Injury

PrerenalPostrenalOncotic AKI

GlomerulopathyVasculitisThrombotic MA

PyelonephritisInterstitial nephritis

AINAtheroembolic AKI

ATNMyoglobinHemoglobin

Uric acidToxinsDrugs

Plasma cell dyscrasia

HematuriaRBC castsproteinuria

WBCWBC casts

Eosinophils RTE cellsPigmented

casts

Crystalluria Non-albumin

proteinuria

Abnormal sedimentNormal/bland

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

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

High risk 1 2 3

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

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

Outlines

Acute kidney injury

Hypokalemia

Hyperkalemia

Hyponatremia

Hypokalemia

Plasma [ K+] < 3.5 mEq/L

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

Treatment Oral 60-120 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

Hypokalemic periodic paralysis

Cause of hypokalemia

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

Extra renal loss

Renal loss

-Urine K < 20 mEq/d (<15 mEq/L)-TTKG < 2 -Urine K/Cr < 15 mEq/g Cr

TTKG = U K+ x Serum osmolality P K+ x Urine osmolality

(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

Test Strengths Weakness Expected value

normal renalloss

24 hr urine potassium

Valuable Does not indicate pathophysiology

<15 >40

Urine K/Urine creatinine

Can userandom urine

Expected rate of Cr excretion

<15 mEq/gCr

>15 mEq/gCr

TTKG Physiologic basisTranslates urine to CCD

Many unverified assumption

<2 >10

Random urine K+

Simple Does not consider MCD water reabsorption

<15 >40

Factional excretion of K+

None Expected values depend on GFR

<5-7% >5-7%

Urinary electrolytes

K+< 15 mEq/dayK+/Cr < 15 mEq/g

DiarrheaCellular ShiftingLow K intake

K+< 15 mEq/dayNa+<100 mEq/day

Repeat after increasing dietary Na+ to >100 mEq/day

Extra-renal loss Renal loss

K+> 15 mEq/dayK+/Cr > 15 mEq/g

Blood pressure

Renin ActivitySerum Aldosterone

Metabolic acidosis Metabolic alkalosis

RTADKA Urine Cl-

High (>10 Meq/day)-Gitelman’s syndrome-Bartter’s syndrome-Normotensive 1 aldosterone-Diuretics-Severe K depletion-Mg deficiency

Low (<10 mEq/day)- Vomiting- Penicillin derivatives- Betahydroxybutyrate

Low-Normal BPHigh BP

Renal loss with MK and HypertensionR A

Renin secreting tumor

Renovascular hypertension

Malignant hypertension

Vasculitis

R A

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. A. Lowering & broadening of T wave, slightly prolonged QT interval

B. Low, broad T wave with a double summit

C. 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

drugsCohn 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)

3.5 125-250

3.0 150-400

2.5 300-600

2.0 500-750

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

TreatmentSecond 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

IV Potassium Reserved for severe hypokalemia, life threatening

hypokalemia or TPN Preparation;

Potassium chloride (KCL 2 mEq/mL) Rate infused 10-20 mEq/hr Peripheral vein < 40-60 mEq/L

High concentration induces phlebitis Avoid glucose containing fluid

Life threatening hypokalemia:• K2HPO4 will stay in ICF during anabolism, no increase in serum

[K+]

Infusion pump is preferred to prevent

overly rapid potassium

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 levelMarked potassium deficitAcidosis/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

Outlines

Acute kidney injury

Hypokalemia

Hyperkalemia

Hyponatremia

POTASSIUM > 5.0-5.5 MEQ/ L

Hyperkalemia

Hyperkalemia

• Pseudohyperkalemia• 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/LPseudohyperkalemia

BUN/Cr (GFR < 20 mL/min)?

Yes No

• AKI• CKD• High

intake+CKD

• ACEI, ARB• Aldactone• Amiloride • Triamterene • Trimethoprim• Pentamidine• NSAID• B-blocker • Heparin• Anti fungal• CNI

Addison disease

ConditionDMHIV

Resistant-Obstructive uropathy-Interstitial disease-Pseudohypoaldosteronism

Satirapoj B. Royal Thai Army Medical Journal. 2007;60(3-4):119-128.

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 0.5-1.2 mEq/L Effect begins in 10 – 20 minutes Peak at 30 – 60 minutes Last for 4 – 6 hours

To prevent hypoglycemia, 10% Dextrose at 50-75 mL/hr with closed monitor blood glucose be used

Hyperglycemia (>200-250 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 15-30 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 30-60 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

TreatmentTreatment Dose Time frame

IV calcium gluconate

10 mL IV pushSeconds to minutes

Glucose +InsulinRI 10 U + 50% glucose 50 mL IV 5-10 min (30-60

min)

Sodium or calcium polystyrene sulfonate

-15-50 mg + water 150-200 mL oral-50 mg + water 150 mL rectal retention 30-60 min

1-4 hr (rectal)>6 hr (oral)

Dialysis Immediate

Satirapoj B. Royal Thai Army Medical Journal. 2007;60(3-4):119-128.

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

Outlines

Acute kidney injury

Hypokalemia

Hyperkalemia

Hyponatremia

Hyponatremia

Plasma Na+< 135 mEq/L

Hyponatremia

Pseudohyponatremia

(Posm 280-290 mOsm/kg)

- Hyperlipidemia-Hyperproteinemia

Hypertonic hyponatremia

(Posm > 290 mOsm/kg)

-Hyperglycemia-Mannitol

True Hypotonic hyponatremia

(Posm < 280 mOsm/kg)

[ 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 400Na+= 132 + {(400-100) X 1.6} = 136.8

100

Example2: Na+ 125, BS 600 Na+= 125 + {(600-100) X 2.4} = 137

100

PATHOPHYSIOLOGY OF HYPONATREMIA

Decrease Plasma Na+ = Total body Na+

Total body water

water water water

Hypovolemia

Na Na Na

Euvolemia Hypervolemia

Excess of total body water relative to total body solute

Clinical causes of hyponatremia

Pseudohyponatremia (Posm 280-295 mOsm/kg)- Hyperlipidemia-Hyperproteinemia

Hypertonic hyponatremia(Posm > 295 mOsm/kg)-Hyperglycemia-Mannitol

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

Excess water intake (Uosm < 100 mOsm/kg)-Psychogenic polydipsia-Low solute intake-Chronic kidney disease

Hypotonic hyponatremia(Posm < 280 mOsm/kg)

Volume depletionDiuretic/salt wasting syndrome

SIADH Advance CHFAdvance cirrhosis

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

- Hemodilution- Iow albumin- BUN:Cr > 20:1- Elevate HCO3-

Indirect lab(SIADH)- Uric <5- BUN:Cr < 10:1- Slight decrease

HCO3-- Slight decrease AG

Special lab- TFT- Cortisol level

Euvolemic Hyponatremia

SIADHHypothyroidism

2° Adrenal insufficiency

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

Syndrome of Inappropriate Antidiuresis (SIADH)

European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

Supplemental featuresPlasma uric acid < 4 mg/dLBUN <21.6 mg/dLFE Na >0.5%FE urea >55%FE uric >12%Failure to correct hyponatremia after 0.9%

saline infusionCorrection of hyponatremia through fluid

restriction

Syndrome of Inappropriate Antidiuresis (SIADH)

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 vomitingConfusionHeadache

Severe VomitingCardiorespiratory distressAbnormal and deep somnolenceSeizuresComa (Glasgow Coma Scale ≤8)

European Renal Best Practice, European Journal of Endocrinology, 2014; 170, G1–G47

Risks factorsof CNS symptomsRisks factorsof CNS symptoms

Pre-menstruant femalesElderly females on thiazide

diureticsChildrenPsychogenic polydipsiaHypoxemia

Symptomatic

AcuteDuration < 48 hr

Chronic Duration >48 hr or unknown

Emergency correction needed• Hypertonic saline (3%) at 1-2

mL/kg/hr+ furosemide

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

Asymptomatic

Chronic Rarely < 48 hr

No immediate correction needed

Long-term management • Identification and treatment of reversible etiologies

water water water

Hypovolemia

Na Na Na

Euvolemia Hypervolemia

Treatment

Restrict oral fluidRehydration : Isotonic

Restrict oral fluidDiuretic: furosemide

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

ในสารน��าที่ให้� 1 ลิ�ตรจะเพิ่�ม Na ได้� =

(Na ในสารน��าที่ใช้� + K ในสารน��าที่ใช้�) – ค่�า Na ของผู้��ป่ วย (TBW + 1)

TBW male = 0.6 X BWTBW female = 0.5 X BW

Female BW = 40 , Na 112 mEq/L K= 4 mEq/LRX 0.9% NaCl

ในสารน��าที่ให้� 1 ลิ�ตรจะ เพิ่�ม Na ได้� =

(Na 154 + K ในสารน��าที่ใช้�) – 112 0.5x40 + 1

= 42/21 = 2

24 ช้#วโมง เราต�องการ เพิ่�ม < 8-12 mEq สมม&ต�เราจะเพิ่�ม 6 mEq ต�องใช้�สารน��าที่#�งห้มด้ ป่ระมาณ 3000 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 h8 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

↑ Na

Brain adaptation

H2O

BrainOsmotic Demyelination Syndrome

Chronic hyponatremia

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

THANK YOU FOR YOUR ATTENTION

Phramongkutklao Hospital and College of Medicine