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
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Phramongkutklao Hospital and College of Medicine