Hypokalemia

Approach to etiology of Hypokalemia

Dr.M.Emmanuel Bhaskar

Associate Professor in Medicine

Sri Ramachandra Medical College

Chennai,India

Approach……???????

Approach to hypokalemia

All you need to do is to have a CLOSER LOOK!

Learning objectives

1.To understand a concept based clinical approach to diagnose cause of hypokalemia

2.Understand the clinical relevance of common investigations used in the setting of hypokalemia

Plan for Interaction

Brief Introduction

Presentation of scenario

Discussion by audience

Discussion by presentor

Questions by audience

Answers by the faculty ?

How does body maintain a normal serum K?

Gennari et al NEJM 1998;339:451-458

Case-1

36 year old male admitted with pneumonia with septic shock. Admission labs shows Na-142, K-3, Cl-98, Hco3- 19. On Imipemem,nor-epinephrine,dopamine, pantoprazole , enoxaparin, I.V 0.9% Saline at 125cc/hr.

Day 5 develops Na-138,K-2.2,Cl-106,Hco3-17. Urine K- 30 meq/l .ABG- Ph-7.36 , Hco3-15, Pco2-26mmHg.. Mg-1.2 , Ca-9.6

K-improved to 3.2 with 80 meq /dy of i.v Kcl.

Case-1: Issues ?

Approach?

Case-1: Issues

Septic shock on Ionotropes and saline

Hospital acquired hypokalemia

Urinary K-excretion- ?

Metabolic acidosis with resp alkalosis

Marginally low serum Mg with normal Na,Cl,Ca

Diagnostic protocol based on our observation in 76 cases of hypokalemia [ K<2 meq/l]

Study period: May 2005-May 2009

5 Questions to fix the cause of Hypokalemia !

Is there an obvious gastro-intestinal loss

Is it drugs

How is renal handling of K

Unexplainable Metabolic acidosis/alkalosis

How is serum Mg, Na, Cl, Calcium

Case 1


Is it drugs ???

How is renal handling of K- ??loss


How is serum Mg [?low] ,Na,Cl,Calcium

Case 1

Is it drugs ???

Renal loss ???

Hypomagnesemia???

Drugs and Hypokalemia ?

Drugs and Hypokalemia

Insulin

Salbutamol, Theophylline

Diuretics

Drugs and Hypokalemia

Insulin

Salbutamol, Theophylline

Diuretics

Nor-Epinephrine, high dose dopamine

Fludrocortisone, high dose corticosteroids

Amphotericin-B , Beta-lactum antibiotics

Bicarbonate therapy

Case 1

Is it drugs ??? - YES

Renal loss ???

Hypomagnesemia???

How to assess renal handling of K?

Renal loss of K

Intrinsic renal disorders: Inherited/acquired

Hormonal effects : Hyperaldosteronism


Urinary K excretion- spot or 24 hours

Urinary K / Urinary creatinine ratio

TTKG [ Trans-tubular potassium gradient]

Urinary potassium excretion

A normal kidney should retain most of

the potassium in the setting of hypokalemia.

Spot K <10-15meq/l is normal

Spot K >20 meq/l indicates renal loss

Spot Urinary Potassium excretion

Limitations Poor validity in critically ill patients when considered in isolation due to highpreval of secondary hyperaldosteronism

Extra-renal loss may be associated with elevated spot urinary K !

Reimann et al. Nephrol dial transpt 1999;14:2957-2961

Urinary K/Urinary creatinine ratio

More meaningful test.

Excretion rates are similar during ↓K Ratio <1.5 indicates renal conservation of KRatio > 1.5 indicated renal wasting of K

Factors interfering creatinine secretion.Unclear role in critical illness

Groeneveld et al . Q J Med 2005;98:305-316

What is TTKG?

What is TTKG?

Most disliked term in the chapter on hypokalemia !

What is TTKG?

Soriano et al.J Am Soc Nephrol 2002;13:2160-2170

TTKG

Ratio between K concentration in the collecting duct and the peri-tubular cap

Tells about the behaviour of distal nephron during hypokalemia .

TTKG

Based on one time sample

Most useful test

TTKG

Based on one time sample

Most useful test

NOT AVAILABLE IN MOST CENTRES

TEST REQUIRES OSMOMETER


Urinary K excretion



ALL HAVE SIGNIFICANT LIMITATIONS


Urinary K excretion



ALL HAVE SIGNIFICANT LIMITATIONS

Interpretation in isolation may lead to

CONFUSION

Potassium wasting Renal disorders……loose potassium

They often also loose chloride,

sodium,bicarbonate,magnesium,

water and calcium

Potassium wasting renal disorders

Look beyond urinary K !

Case 1

Is it drugs ???- YES

Renal loss ???- ? YES [ ?aldosterone]

Hypomagnesemia???

Case 1

Is it drugs ???- YES

Renal loss ???- ? YES [ ?aldosterone]

Hypomagnesemia???

Secondary hyperaldosteronism produces

↓K much earlier than Met.alkalosis

How to identify clinically significant hypomagnesemia

How to identify clinically significant Hypomagnesemia?

Hypokalemia refractory to therapy

Serum Mg <1 mg/dl

Associated hypocalcemia [ < 7 mg/dl]*

Metabolic alkalosis

*Agus et al J Am Soc Nephrol 1999;10:1616-1622

What is the relation between magnesium and calcium

What is the relation between magnesium and calcium?

Hypomagnesemia causes impaired PTH release and increased PTH resistance.

Impaired PTH leads to renal loss of Mg

Resolution -Case 1

Is it drugs - YES [ Noradrenaline]

Renal loss ??? – ?YES[?aldosterone]

Hypomagnesemia??? - NO

Case 2

A 23 year old female presented with fatigue

for 3 months which worsened over the last

10 days. Clinical exam was unremarkable

except for a power of 4/5 in all limbs. Labs

showed a Na-134 meq/L,K-1.8 meq/l, Cl-110

meq/l and Hco3-15 meq/l. S.Creatinine-1.1

mg/dl, BUN-14 mg/dl, ABG: Ph- 7.31, Pco2-

30 mmHg, Hco3-14 meq/l, S.Mg-1.1mg/dl

Ca-8.8 mg/dl , Spot urine K-60 meq/l . ECG

showed U waves with QRS widening. Urine

Ph-6, Sp-gravity-1.010, sugar-nil,prot-nil, 5-6

pus cells and no casts.

Case 2 issues ?

Approach?

Case 2 issues

Hypokalemia

Partially compensated metabolic acidosis

Elevated spot urine K-80 meq/l

Mild hypomagnesemia, high normal Cl



Is it drugs




Case 2 :Where to begin?


Is it drugs

How is renal handling of K- loss

Metabolic acidosis/alkalosis

How is serum Mg↓, Na, Cl↑, Calcium

Case 2 :Where to begin?


Is it drugs

How is renal handling of K- loss

Metabolic acidosis/alkalosis


Hypokalemia with metabolic acidosis

Possibilities to consider

Hypokalemia with metabolic acidosis

Acute and chronic diarrheal disorder

Recovery phase of acute tubular necrosis

Renal tubular acidosis [distal , proximal]

Acetazolamide therapy

Met acidosis unrelated to hypokalemia

How to evaluate possible RTA?

Evaluation of possible RTA

Early morning first void urine pH

Confirm kidneys ability to acidify urine

Check for glycosuria, hypophosphatemia

Evaluation of urine pH

Good screening test

Urine ph >5.5 : possible distal [type-1] RTA

Urine ph <5.5 : possible proximal

[type-2]RTA

Analyzed Ideally within 30 minutes

Evaluate kidneys ability to acidify urine

Acid load test : ideal but rarely done

Frusemide test

Frusemide test for RTA-1

Principle

Frusemide increases distal delivery of Na

A normal distal nephron secretes H ion in response to this producing acidic urine

Type-1 RTA nephron fails to do this

Frusemide test: Protocol

Test urine pH

Administed 40 mg of frusemide preferably i.v

Repeat urine pH 1 to 2 hour later

Failure to produce acid urine indicates

Distal [type-1] RTA

Soriano et al. J Am Soc Nephrol 2002;13:2160-2170

Proximal[type-2]RTA

Often associated with additional tubular loss of glucose, phosphate and uric acid

Osteomalacia and rickets may occur

Urinary acidification intact

Isolated proximal bicarbonate loss possible

Case 2

Urine ph in routine sample- 6

Urine pH in first void sample-7

Frusemide test was abnormal

DISTAL RENAL TUBULAR ACIDOSIS

Often there is a diagnostic delay in RTA

Metabolic acidosis is often mild

Becomes severe only during intercurrent illness

Case 3

A 45 year old male presented with confusion

And irritablity for 7 days which was not

associated with fever. Patient is a known

diabetic for 8 years on OHAs. Current

alcoholic and smoker.On exam vitals were

stable and marked disorientation was

present. Labs showed a Na-141 meq/L,

K-1.4 meq/l, Cl-78 meq/l and Hco3-32 meq/l.

S.Creatinine-0.9 mg/dl, BUN-18 mg/dl,

ABG: Ph- 7.49, Pco2- 49 mmHg, Hco3-32

meq/l, S.Mg-0.7mg/dl,Ca-6.4 mg/dl , Spot

urine K-80 meq/l . ECG showed ST

depression ,T-U waves with QRS widening.

Urine Ph-5, Sp-gravity-1.010, sugar-nil,prot-

nil, 5-6 pus cells and no casts.

Case 3 issues?

Approach?

Case 3 issues?

Diabetic , alcoholic

Altered mentation

Hypokalemia, Elevated urinary K loss

Metabolic alkalosis

Hypochloremia,hypomagnesemia,

hypocalcemia, normal Na

Case 3 : Where to begin?


Altered mentation


Metabolic alkalosis



Case 3 : Where to begin?


Altered mentation


Metabolic alkalosis



Hypokalemia with metabolic alkalosis

Possibilities to consider


Vomiting

Diuretics

Secondary hyperaldosteronism

Acquired Hypomagnesemia

Barters/Gittelman/Liddle syndrome

Hypokalemia per se


Vomiting

Diuretics

Secondary hyperaldosteronism

Acquired Hypomagnesemia

Barters/Gittelman/Liddle syndrome

Hypokalemia per se

What are the acquired causes of Hypomagnesemia?

Acquired causes of ↓Mg

Alcoholism , Diabetes

Chronic diarrhea , vomiting, diuretic use

Diuretic phase of ATN

Rapid refeeding

Amphotericin B, Aminoglycosides

Vit D deficiency

Late pregnancy

Agus et al. J Am Soc Nephrol 1999;10:1616-1622

Hypomagnesemia:features

Serum value may not reflect real picture

CNS effects

Hypokalemia refractory to therapy

Metabolic alkalosis, hypochloremia

Hypocalcemia

Sodium not affected in acquired causes

Inherited tubular disorders

A birds eye view

NEJM 1999;340:1177-1187

Inherited tubular disorders vs Acquired Hypomagnesemia

Disorder Bp ↓Mg Na ↓Ca U .Ca

Barter N or low Yes-mild low variable

N or High

Gittel man N or low Yes-sev low no Low

Liddle High no N or High no N

↓ Mg N - N yes variable

Scheinmann NEJM 1999;340:1177-1187



Barter N or low Yes-mild low variable N or High

Gittel man N or low Yes-sev low N Low

↓ Mg N - N yes variable



Barter N or low Yes-mild low variable N or High

Gittel man N or low Yes-sev low N Low

Case 3:resolution

Severe Hypomagnesemia [acquired]

1. risk factors- alcoholism, diabetes

2. Hypokalemia which was refractory

3. Hypocalcemia

4. Metabolic alkalosis, normal Na

Case 4

A 25 year old female presented acute

weakness of all extremities .She had 2

similar episodes in the past. On exam vitals

were stable.Power was 1/5 all limbs. Labs

showed a Na-138 meq/L, K-1.6 meq/l, Cl-98

meq/l and Hco3-25 meq/l. S.Creatinine-0.9

mg/dl, BUN-18 mg/dl,ABG: Ph- 7.38, Pco2-

38 mmHg, Hco3-22 meq/l,

S.Mg-1.7mg/dl,Ca-9 mg/dl , Spot

urine K-8 meq/l . ECG showed ST

depression ,T-U waves with QRS widening.

Urine Ph-5, Sp-gravity-1.010, sugar-nil,prot-

nil, 5-6 pus cells and no casts.

Case 4: issues?

Approach?

Case 4: Issues

Hypokalemia

Extremity weakness

Normal renal handling of K

Normal acid-base status

Normal Na,Cl,Mg and Ca

Case 4: Where to begin?

Hypokalemia

Extremity weakness




Case 4: Where to begin?

Hypokalemia

Extremity weakness




Hypokalemic paralysis with normal acid-base status

Possibilities

Two patients with serum K-1.5

One having paralysis and the other having normal power .Is it

possible?

Two patients with serum K-1.5

One having paralysis and the other having normal power .Is it

possible?............yes

The serum K level does not primarily decide occurrence of

weakness!

What decides weakness in hypokalemia?

Ratio of ICF/ ECF

Normal 38/1

Conditions that lower both cellular and extracellular K may not produce weakness

Conditions rapidly shift large amount of K

into the cells ↑ ratio and cause weakness

Severe hypokalemia with paralysis and normal ABG

Periodic paralysis [familial or sporadic]

Thyrotoxic periodic paralysis

Suicidal Insulin over dose

Groeneveld et al . QJM;2005;98:305-316

Case 4

Sporadic periodic paralysis

1. Recurrence

2. Normal renal handing of K

3. Normal acid-base status

4. Normal thyroid function

In summary………



Is it drugs




Conclusion

Do not consider urinary K excretion in isolation

ABG is a desirable starting point while evaluating mod-severe hypokalemia

Look at Na,Cl,Mg and Ca

My guide and mentor…….

Prof.S.Shivakumar M.D

Prof & HOD of Medicine[retd]

Govt.Stanley Medical College

Chennai

Questions?????

Date post:	18-Nov-2014
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Hypokalemia

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