Electrolyte Disturbance

Electrolyte Disturbance

Lee, Dong Won, MD, PhD

Division of Nephrology

Department of Internal Medicine

Pusan National University School of Medicine

50 세 남자가 의식이 저하되어 왔다 . 피부긴장도는 정상이었다 . 10 년 전부터 정신분열병으로 치료 중이었다 . 진단은 ?

혈액 : glucose 87 mg/dL, BUN/Cr 15/0.9 mg/dL, Na/K 112/3.8 mEq/L, Osm 235 mOsm/L

소변 : Protein (-), RBC 0~2/HPF, WBC 0~2/HPF, Na/K 25/10 mEq/L, Osm 45 mOsm/L

① Primary polydipsia

② Adrenal insufficiency

③ Cushing syndrome

④ Central diabetes insipidus

⑤ Syndrome of inappropriate antidiuresis (SIAD)

Case 1

50 세 남자가 의식이 저하되어 왔다 . 피부긴장도는 정상이었다 . 수개월 전부 터 기침이 심했다 . 진단은 ?

혈액 : glucose 82 mg/dL, Na/K 112/3.5 mEq/L

Osm 240 mOsm/kg H₂O

Cortisol 12.3μg/dL ( 참고치 ; 5~25) TSH 0.9 mIU/L ( 참고치 ; 0.34~4.25) 소변 : Na 82 mEq/L, Osm 430 mOsm/kg H₂O

Case 2

① Primary polydipsia

② Adrenal insufficiency

③ Cushing syndrome

④ Central diabetes insipidus

⑤ Syndrome of inappropriate antidiuresis (SIAD)

Underfilled arterial circulation

AVP ↑

Urine Osm ↑

Water excretion ↓

Overfilled

Upregulated release of AVP

RAS, SNS

Renal tubular Na⁺ reabsorption

Urine Na⁺

Water intake

Natriuresis

Hemodynamic stimuli for ADH(AVP)

50 세 남자가 의식이 저하되어 왔다 . 피부긴장도는 감소해 있었다 . 5 년 전부 터 고혈압과 당뇨병으로 치료 중이었다 . 원인은 ?

① Thiazide

② β-blocker

③ Spironolactone

④ Calcium channel blocker

⑤ Angiotensin II receptor blocker

혈액 : BUN/Cr 28.0/1.1 mg/dL, Na/K/Cl 112/4.0/98 mEq/L, Osm 230 mOsm/L 소변 : SG 1.040, protein (1+), RBC 6-10/HPF, Na 120 mEq/L, Osm 340 mOsm/L

Case 3

High

Decreased Normal

Increased

Low Normal

Na+ wasting nephropathy Hypoaldosteronism

Diuretics Vomiting

Na+ wasting nephropathy Hypoaldosteronism

Diuretics Vomiting Extrarenal Na+ loss

Remote diuretic use Remote vomiting Extrarenal Na+ loss Remote diuretic use Remote vomiting

Maximal volume of maximally dilute urine Hyperproteinemia

Hyperlipidemia Bladder irrigation Hyperproteinemia Hyperlipidemia Bladder irrigation Hyperglycemia

Mannitol

Hyperglycemia Mannitol

SIADH

R/O Hypothyroidism

R/O Adrenal insufficiency

SIADH

R/O Hypothyroidism

R/O Adrenal insufficiency Heart failure

Liver cirrhosis

Nephrotic syndrome Renal insufficiency Heart failure

Liver cirrhosis

Nephrotic syndrome Renal insufficiency

ECF volume

ECF volume Primary polydipsiaPrimary polydipsia

Urine Na+

Urine Na+

< 10 mmol/L > 20 mmol/L

Plasma osmolality Plasma osmolality

No Yes

Pseudo-hyponatremia Pseudo-hyponatremia

Primary Na+ gain exceeded by

Secondary water gain Primary Na+ gain

exceeded by

Secondary water gain

Primary water gain With

Secondary Na+ loss Primary water gain

With

Secondary Na+ loss

Primary Na+ loss Renal or Extrarenal (GI)

Primary Na+ loss Renal or Extrarenal (GI)

Diagnostic approach to hyponatremia

50 세 남자가 의식이 저하되어 왔다 . 오전 8 시부터 고농도 (3%) 식염수를 투여 한 후 의식이 회복되었으나 저녁 8 시경 다시 의식이 저하되었다 . 진단은 ?

① Adrenal adenoma

② Pheochromocytoma

③ Acute cerebral edema

④ Subarachnoid hemorrhage

⑤ Central pontine myelinolysis (Osmotic demyelination syndrome) 오전 8 시 혈액 :

Na/K/Cl 102/3.9/92 mEq/L, Osm 216 mOsm/L

저녁 8 시 혈액 :

Na/K/Cl 138/4.2/105 mEq/L, Osm 290 mOsm/L

Case 4

Complication due to rapid correction of…

Hyponatremia Hypernatremia

CPM (ODS) Cerebral edema

Management of Hyponatremia

Water restriction

- mainstay of therapy in asymptomatic hypoNa and in chronic SIADH - Complications

: volume depletion, hypotension – cerebral vasospasm - SAH

Salt administration

- initial correction rate – neurologic Sx, onset rapidity, magnitude - quantity of Na

required to increase P

= (target Na

– Pt’s Na

) x TBW (50~60% of lean body wt.)

- normal saline or hypertonic saline < 8-10 mmol/L/ first 24hrs

< 18 mmol/L/ first 48hrs

- monitoring of serum Na – fluid Osm > urine Osm

50 세 남자가 의식이 저하되어 왔다 . 피부긴장도는 감소해 있었다 . 혈압

70/45 mmHg, 맥박 90 회 / 분 , 호흡 20 회 / 분 , 체온 36.5℃ 였다 . 치료 는 ?

① 5% D/W

② 0.9% saline (N/S)

③ 3% saline

④ 10% albumin

⑤ Furosemide

혈액 : BUN/Cr 54/2.0 mg/dL, Na/K 148/3.5 mEq/L 소변 : SG 1.030, protein (+), RBC 1-2/HPF

Case 5

50 세 남자가 의식이 저하되어 왔다 . 피부긴장도는 정상이었다 . 혈압

110/70 mmHg, 맥박 72 회 / 분 , 호흡 20 회 / 분 , 체온 36.5℃ 였다 . 치 료는 ?

① 5% D/W

② 0.9% saline (N/S)

③ 3% saline

④ 10% albumin

⑤ Furosemide

혈액 : BUN/Cr 18/0.8 mg/dL, Na/K 158/4.0 mEq/L 소변 : SG 1.030, protein (+), RBC 1-2/HPF

Case 6

Fluid (1L) Distribution Intravascular Interstitial Intracellular

5% D/W ECF/ICF 85 (1) 250 (3) 665 (8)

0.9% N/S ECF 250 (1) 750 (3) 0

0.45% saline 500mL water

500mL saline 40 (1)

+ 125 (1) 125 (3)

+ 375 (3) 335 (8) + 0

Fluid 1 liter ?

- free water, saline, or half saline ?

ECF ICF

Re-distribution of fluid administered

ICF

Blood volume

volumeRBC

ECF

Intravascular volume

Interstitial volume

5% D/W, 1,000 mL

665 85 250

Re-distribution of fluid administered

ICF

Blood volume

volumeRBC

ECF

Intravascular volume

Interstitial volume

0.9% N/S, 1,000 mL

250 750

50 세 남자가 근육통이 심해서 왔다 . 헬스클럽에서 열심히 운동한 후

친구들과 소맥 을 여러 잔 마셨고 집에 돌아와 낮잠 을 자고 일어나니 몸이 천근만근이었다 . 진단은 ?

① 담

② 숙취

③ 고칼륨혈증

④ 저칼륨혈증

⑤ 횡문근융해증

70kg x 60% = 42L ECF (1/3) = 14L ICF (2/3) = 28L

Case 7

Healthy adults

Exercise

- Intracellular K

- β2-stimulation

Diet (Hyperglycemia) - Intracellular water - Cell shrinkage - Insulin release

Interstitial accumulation

Intracellular K uptake

Extracellular movement Intracellular K

concentrated Intracellular K uptake

Limiting muscle contraction, fatigue Rapid vasodilation,

increasing blood supply to exercising muscle Decreasing serum K

K efflux (solvent drag) K efflux

(favorable gradient) Decreasing serum K Decreasing glucose

Diet Serum glucose↓

Exercise

Vasodilation – perfusion↑

Dietary K uptake

Muscular K

uptake

RAPID muscular uptake SLOW renal excretion

Potassium intake

Reabsorption

Secretion Lumen Blood

(Bumetanide) NKCC2

(Thiazide) NCC

KCC

Solvent drag

Paracellular diffusion

Transcellular absorption Paracellular diffusion

recycling ROMK

ROMK KCC

ENaC ROMK

(Amiloride) ENaC (Aldosterone) ROMK

Maxi-K KCC

KCC

KCC

Initial K secretion

Main K secretion

PCT

TALH

DCT

CCD ^ASDN/c MLR, 11βHSD-2 Type I Bartter’s ---

Type II Bartter’s ---

Gitelman’s ---

Liddle’s ---

LUMEN Principal Cell INTERSTITIUM

Na

K

Na

3Na

3Na

K

2K

2K

ATP

Mineralocorticoid (Aldosterone)

ROMK

Maxi-K ENaC

Lumen (-)

potential difference Distal Na⁺- water

delivery

Cortical Collecting Duct

ROMK – low-conductance, major K channel in basal (physiologic) condition Maxi-K – large-conductance, flow-sensitive K channel in high flow condition

65 세 남자가 손발이 저리고 마비되어 왔다 .

약 20 년간 당뇨병을 앓고 있었고 만성신질환 5 기 (eGFR<10 mL/min) 로 치료 중이었다 .

약 1 시간 전 건포도 한 컵을 먹었다고 한다 . 원인은 ? 건포도 ? 고칼륨혈증 ?

건포도 한 컵 ?

- including K

28 mEq - K

28 mEq/14L ECF

- K

2 mEq/L increased ???

70kg x 60% = 42L ECF (1/3) = 14L ICF (2/3) = 28L

Case 8

Healthy adults

K 28 mEq intake

Rapid intracellular uptake (K redistributed into ICF) Na⁺-K⁺-ATPase activated by insulin, β2-adrenergics

Hyperglycemia

 Insulin release

 Intracellular K uptake

 Decrease serum K

Aldosterone

 Renal K excretion ↑

β- > α-adrenergic activity

 Intracellular K uptake

Diabetics

K 28 mEq intake

Rapid intracellular uptake (K redistributed into ICF) Na⁺-K⁺-ATPase activated by insulin, β2-adrenergics

Insulin release ↓

 Hyperglycemia

 Extracellular K release

 Increase serum K

Hypo-Aldosteronism

 Renal K excretion ↓ α- > β-adrenergic activity

 Intracellular K uptake masked

50 세 남자가 의식이 저하되어 왔다 . 피부긴장도는 증가해 있었다 . 10 년 전부 터당뇨병과 고혈압으로 치료 중이었다 . 치료는 ?

① 혈액 투석을 시행한다 .

② 칼륨 제제를 경구로 투여한다 .

③ 인 결합제를 정맥으로 투여한다 .

④ 고농도 식염수 (3%) 를 정맥으로 투여한다 .

⑤ 자연 회복되므로 24 시간 심전도를 측정하면서 관찰한다 . 혈액 : BUN/Cr 50/8.7 mg/dL, Hb 7.4

g/dL,

Na/K 130/7.2 mEq/L, Ca/P 7.2/9.4 mg/dL

Case 9

TTKG (Trans-tubular K gradient)

net K secretion by distal nephron before the effect of ADH correcting for Urine Osm changes (water reabsorption)

(Urine K / Plasma K) (Urine Osm / Plasma Osm)  

Normal

HyperK

HypoK Non-renal

Distal flow (Na delivery)↑

Renal

K secretion (RAS)↑

5~10

Non-renal

Distal flow (Na delivery)↓

Renal

K secretion (RAS)↓

8~10

2~3

Diagnostic approach to hyperkalemia

Managements of hyperkalemia

Mechanism Therapy Onset/duration Dose

Membrane sta-

bilization Calcium 1-3min/30-60min Calcium gluconate 10% 10ml iv

K⁺ shift

Insulin 20min/4-6hr 10U RI iv

+ 50ml 50% glucose

₂-adrenergic agonist 20min/2-4hr Albuterol 0.5mg iv over 15min, 10mg nebulize

K⁺ removal

Calcium or sodium

polystyrene sulphone 1-2hr/4-6hr 15g every 6hrs orally

or 30-60g by retention enema

Dialysis Immediate

/dialysis duration 2-3hr hemodialysis

50 세 남자가 손발이 마비되어 왔다 . 피부긴장도는 정상이었다 . 혈압 140/90 mmHg, 맥박 96 회 / 분 , 호흡 20 회 / 분 , 체온 37℃ 였다 . 치료는 ?

① Furosemide

② Spironolactone

③ K-binding resin

④ Calcium gluconate

⑤ Sodium bicarbonate

혈액 : BUN/Cr 18/0.8 mg/dL, Na/K/Cl 146/2.8/103 meq/L

Renin 0.1 ng ( 참고치 ; 0.3~3.0), Aldosteron 20 ng/dL ( 참고치 ; 8 미만 )

Case 10

Diagnostic approach to hypokalemia

Furosemide (TALH)

Hypokalemia

Thiazide (DCT)

Hypokalemia

CD

Ca²⁺

Ca²⁺Ca²⁺

Ca²⁺

Ca²⁺

Defects in multiple renal tubular transport pathways

Bartter’s syndrome

Gitelman’s syndrome

Liddle’s syndrome

CORTISOL

equal affinity for MLR

CORTISONE

minimal affinity for MLR

11β-hydroxysteroid dehydrogenase-2

(11βHSD-2)

CORTISOL-dependent MLR activation

SAME (Syndrome of Apparent Mineralocorticoid Excess)

- Hypertension - Hypokalemia - Hypercalciuria - Metabolic alkalosis - Suppressed PRA. Aldo

Glucocorticoid

Cushing’s syndrome

- Hypertension

- Hypokalemia (10%)

Systemic glucocorticoids↑

by pituitary ACTH

Systemic glucocorticoids↑

by ectopic ACTH

- Hypertension

- Hypokalemia (60-100%)

Mg deficiency

RAPID muscular uptake SLOW renal excretion

K excretion /

ROMK Na⁺-K⁺-ATPase

Reducing Mg-dependent ROMK block

secretion

Potassium supplement

Supplemental K

– TMC cause of hyperkalemia

Serum K

start to increase within 72h after administration

If, insufficient serum K

increase within 96h – combined Mg depletion

Prescription

1. Peripheral iv route – K < 60mEq/L

2. with Crystalloid solution, without Dextrose solution 3. Infusion rate < 40mEq/h

4. EKG monitoring

5. Check serum [K

] every 4-6 h