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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
diuretics or, in rare circumstances, sodium polystyrene sulfate (SPS),
depending on the cause of hyperkalemia.
Hypokalemia
Hypokalemia is defined as a serum potassium concentration less than
3.5 mEq/L.
Etiology
Hypokalemia is commonly encountered in hospitalized and ambulatory
patients. Figure 4 shows the various causes of hypokalemia.
454
R. K. Medapalli and M. J. Ross
y
Fig. 2. Suggested approach for interpretation of transtubular potassium gradient in
patients with hyperkalemia.
Transtubular potassium gradient (TTKG)
Greater than 7
Serum aldosterone level
Low
Non-anion
gap
metabolic
acidosis and
urine pH > 5.5
Hyperkalemic
type-1 RTA
Normal
Consider :
- Acute transplant rejection
- Lupus nephritis
- Cyclosporine use
(PRA and cortisol levels
will also be normal)
High
Consider:
- Heart failure
- Cirrhosis
- Renal salt wasting
Low
Hypoaldosteronism
Plasma renin activity (PRA)
Increased
Serum cortisol level
Decreased
Primary adrenal
insufficienc
Less than 7c
S
erum aldosterone level
High
Pseudoh
ypoaldosteronism
(PRA will also be high)
Decreased
Hyporenemic
hypoaldosteronism
Normal
Primary hypoaldosteronism, or
congenital adrenal hyperplasia
Decreased intake alone is rarely the culprit, as the kidney is able to
lower potassium excretion to 5–25 mEq/day in the presence of
hypokalemia.
4
However, decreased intake can exacerbate potassium
depletion from another cause.
Hypokalemia is a common finding in alkalosis. This is often because
the underlying disorder (e.g. diuretic treatment, vomiting and hyperaldosteronism) results in concomitant loss of both potassium and hydrogen
ions. Alkalosis also contributes to hypokalemia, as intracellular hydrogen
ions are exchanged for extracellular potassium ions to counteract the alkalosis and maintain electroneutrality.
In addition, alkalosis increases urinary potassium losses by increasing
filtration of bicarbonate, exceeding the reabsorptive capacity of the
proximal nephron, thereby increasing delivery of sodium and water to
455
Disorders of Potassium Homeostasis
Fig. 3. Suggested approach to treatment of patients with hyperkalemia.
Treatment of Hyperkalemia
Pseudohyperkalemia?
No Yes
K>6.5mEq/L or EK
G changes?
No treatment
Yes
Emergent treatment
EKG changes?
Yes N o
IV calcium
IV insulin + glucose
Nebulized albuterol
IV NaHCO
PO/PR SPS and/or IV fur
Consider hemodialysis
(if conservative measures ineffective
or marked or ongoing tissue injury)
(if acidosis)
3
Non
Dietary K restriction
Stop K-sparing diuretics
osemide
No
emergent treatment
Consider SPS
C
onsider diur
etics
456
R. K. Medapalli and M. J. Ross
p
Table 1. Medications Used in the Initial Treatment of Hyperkalemia
Drug Dosage Mechanism Onset/Duration Expected Effect Comments
Calcium IV: 1 amp (1 g; 10 mL Stabilizes cell O: 5–10 min EKG normalization • Do not mix in
Gluconate or of 10% solution) membrane. D: 30–60 min bicarbonate solutions.
Calcium over 2–3 min. • Central venous access
Chloride Can repeat once required for CaCl
2
.
after 5 min. • CaCl
2
has 3 times
more elemental Ca
+ +
.
•↑ in Ca
++
can cause
digitalis toxicity.
Insulin + IV: 10 units regular Drives K
+
O: 15–20 min 0.5–1.5 mEq/L ↓•Use insulin alone in
Glucose insulin + 1 amp into cells. D: 4–6 hr hyperglycemic
D50W (50 mL of patients.
50% glucose solution).
Sodium IV: 1 amp (45 mEq; Drives K into O: 30–60 min Variable • Most effective in
bicarbonate 50 mL of 7.5% cells in D: 4–6 hr patients with acidosis.
solution) over exchange • In patients with ↓Na
+
,
5 min. for H
+
ions. raises plasma Na+and
Can repeat in 30 min. counteracts EKG
effects of ↑K
+
.
Albuterol INH: 10–20 mg in Drives K into O: 20–30 min 0.5–1.5 mEq/L ↓•Can cause tachycardia
4 mL Saline. cells. D: 3–4 hr and angina in CAD
patients.
(Continued)
457
Disorders of Potassium Homeostasis
p
Table 1. (Continued )
Drug Dosage Mechanism Onset/Duration Expected Effect Comments
Furosemide IV: ≥40 mg. ↑ delivery of O: 30 min Variable • Patients with chronic
Na
+
and H2O D: 2 hr hyperkalemia typically
to distal have abnormality in
nephron, renal K excretion and
causing ↑ K
+
may not respond very
secretion much.
• Large doses may be
needed in renal failure.
Sodium PO: 15–30 g in 60–120 mL Binds K and O: 1–2 hr Variable • Avoid in the first week
polystyrene of 20% sorbitol. releases (longer after surgery in postop
sulfate Repeat Q 4–6 Na in gut. when patients and in patients
hourly PRN. given PR) with an illeus (risk
PR: 50 g in 150 mL D: 4–6 hr of colonic necrosis).
of tap water. • Na
+
retention can lead
Retain for at least to exacerbation of
60 min. Repeat edema in susceptible
Q 2–4 hourly PRN. patients.
O: onset of action; D: duration of action; CAD: coronary artery disease; IV: intravenous; INH: inhalation.
458
R. K. Medapalli and M. J. Ross
p
Fig. 4. Etiologies of hypokalemia organized by pathomechanism.
Hypokalemia
Increased urinary losses
(UK > 30mEq/d or
U KC ratio > 25 mEq/gm)
Hypo or normotensive
With acidosis
DKA
Type 1 & 2 RTA
Amphoterecin B
Toulene toxicity
With alkalosis
Diuretics
Vomiting
NGT drainage
Salt wasting nephropathies
- Bartter's syndrome
- Gitelman's syndrome
- Tubulointerstitial disease
- Tulular injury due to
lysozyme in leukemia
- Hypercalcemia
Hypomagnesemia
Polyuria
Primary (often psychogenic)
Central diabetes insipidus
Hypertensive
Primary hyperaldosteronism (low PRA, elevated PAC & PAC/PRA ratio >=30)
Secondary hyperaldosteronism (elevated PAC, elevated PRA & PAC/PRA ratio ~10)
Renovascular disease
Renin secreting tumor
Non-aldosterone minerelocorticoid (low PAC & low PRA)
Cushing's syndrome
Liddle's syndrome
Exogenous minerelocorticoid
Chronic licorice ingestion
Congenital adrenal hyperplasia
Deoxycorticosterone producing tumor
Increased entry in to the cells
(UK : variable
U KC ratio variable)
Metabolic alkalosis
Insulin/glucose administration
Increased beta-adrenergic activity
Epinephrine release during stress
Albuterol & Terbulatine
Dopamine
Hypokalemic periodic paralysis
(calcium channelopathy)
Familial autosomal dominant form
Acquired in pts with thyrotoxicosis
(especially asian males)
Acute rise in hematopoiesis
After administration of
- Vitamin B12
- Folic acid
- GM-CSF
Acute chloroquine intoxication
Increased GI losses
(UK < 25mEq/d or
U KC ratio < 15 mEq/gm)
With alkalosis
Vomiting
NGT drainage
With acidosis
Diarrhea
VIPoma
Villous adenoma
Laxative abuse
Key: UK: urine potassium
U KC ratio: urine potassium-creatinine ra
DKA: diabetic ketoacidosis
RTA: renal tubular acidosis
NGT: nasogastric tube
PRA: plasma renin activity
PAC: plasma aldosterone concentration
GM-CSF: granulocyte macrophage colon
stimulating factor
HD: hemodialysis
PD: peritoneal dialysis
Others
(UK < 25mEq/d or
U KC ratio < 15 mEq/gm)
Increased sweat losses
Hot climates
Cystic fibrosis
Dialysis
HD - usually acute
PD - usually chron
Plasmapheresis
(with albumin use)
Decreased intake
ic
tio
y
the collecting duct, where sodium is reabsorbed in exchange for tubular
secretion of potassium and H
+
.
Hypomagnesemia is present in about 40% of patients with hypokalemia,
often because the underlying disorder (e.g. diuretics, vomiting, diarrhea,
Bartter and Gitelman syndromes) leads to concurrent potassium and magnesium losses.
1
Though the mechanism by which hypomagnesemia increases
urinary potassium excretion is incompletely understood, there is evidence that
reduced intracellular magnesium increases potassium secretion by tubular
cells into the tubular lumen.
5
Correction of hypomagnesemia therefore minimizes urinary potassium losses and is a crucial component of the treatment for
hypokalemia in patients with concomitant hypomagnesemia.
Clinical Manifestations
Signs and Symptoms
Symptoms of hypokalemia are rare until the potassium concentration
drops below 3 mEq/L, unless the plasma potassium falls rapidly or there
is a predisposing factor for arrhythmias (digoxin, hypomagnesemia,
coronary ischemia, drugs that prolong the QT interval and increased β-
adrenergic activity). Symptomatic hypokalemia manifests with cardiac
arrhythmias or muscle weakness, or both. The pattern of muscle weakness
is similar to that found in hyperkalemia.
ECG Manifestations
U waves, which occur following T waves, are characteristic of
hypokalemia and are most frequently seen in the lateral precordial leads
(V4–V6). Hypokalemia is also associated with ST segment depression
and T wave flattening.
Workup
The initial workup should include an assessment of the chronicity of
hypokalemia, an electrocardiogram, arterial blood gas analysis and serum
459
Disorders of Potassium Homeostasis
460
R. K. Medapalli and M. J. Ross
magnesium level. Conditions resulting in enhanced cellular uptake of
potassium should be ruled out. Urinary potassium excretion should be
assessed and, in cases where it is increased, measurement of blood pressure
and acid base status can help identify the underlying cause (see Fig. 4).
Random Urine Potassium–Creatinine Ratio
The random urine potassium–creatinine ratio is usually less than 15 mEq/g
creatinine when hypokalemia is caused by poor dietary intake, increased
cellular uptake, or gastrointestinal losses.
6
Values greater than 25 mEq/g of
creatinine suggest inappropriately high renal potassium excretion.
7
24 hr Urinary Potassium Excretion
In patients with hypokalemia, excretion of greater than 30 mEq/day indicates excessive urinary potassium losses (except in oliguria).
1
In patients
who excrete less than 15 mEq/day, renal losses are not the cause of the
hypokalemia and the patient should be evaluated for extrarenal potassium
losses or low intake.
1
PAC, PRA and PAC/PRA Ratio
These tests aid in differentiating primary hyperaldosteronism, secondary
hyperaldosteronism and other sources of mineralocorticoid excess (see
Fig. 4).
The PAC/PRA ratio is typically calculated by measuring a morning
(preferably 8 A.M.) ambulatory and paired PAC and PRA levels.
8
ACE inhibitors, ARBs and direct renin inhibitors elevate the PRA and
lower the PAC/PRA ratio. So, in a patient taking these drugs, a detectable
PRA or a low PAC/PRA ratio does not exclude the diagnosis of primary
hyperaldosteronism, but an undetectable PRA strongly suggests primary
hyperaldosteronism.
Sprinonolactone and eplerenone should be discontinued for at least
six weeks before prior testing. Amiloride and triamterene do not interfere
461
Disorders of Potassium Homeostasis
p
Table 2. Guide to Potassium Replacement
Medication Usual Dosing* Comments
Oral Potassium chloride If serum K 3.0–3.5 mEq/L: Crystalline form is the cheapest. Solution has
Crystalline form (salt 10–20 mEq 2–4 times/day a very bad taste. Slow-release preparation
substitute): rarely causes ulcerative GI lesions.
50–65 mEq/level tsp If serum K <3.0 mEq/L:
Solution: 20 mEq/15 ml 40–60 mEq 3–4 times/day. KCl preparations preferred in patients with
and 40 mEq/15 ml Continue until K is between metabolic alkalosis.
Slow release tablet: 8 mEq, 3.0 and 3.5 persistently;
10 mEq, 15 mEq and thereafter, reduce dose
20 mEq. and/or frequency.
Potassium citrate Solution: 15–30 mL QAC Potassium citrate or bicarbonate preparations
Solution: potassium citrate and HS preferred for long-term use in patients with
1100 mg per 5 mL Powder: 1 packet dissolved metabolic acidosis.
Powder: 3300 mg per packet in water QAC and HS Equivalent to 2 mEq of K and 2 mEq
HCO
3
per mL.
Adjust dose based on urinary pH.
Potassium bicarbonate
Tablet for oral solution: 25 mEq 25 mEq 2–4 times/day Same as for potassium citrate.
(Continued)
462
R. K. Medapalli and M. J. Ross
p
Table 2. (Continued )
Medication Usual Dosing* Comments
Intravenous Potassium chloride Use in patients who cannot Avoid mixing in dextrose solutions as dextrose
Available premixed solutions: eat or as an adjunct to oral can lead to transient reduction in serum K
+
20 mEq in 1 L of half-isotonic replacement in severe conc. (0.2–1.4 mEq/L) due to redistribution
saline (K <3.0 mEq/L) or into cells.
symptomatic hypokalemia: Avoid mixing in normal saline, as the
Highly concentrated solutions Max concentration through a solution will be hypertonic.
in SWFI (sterile water for peripheral vein: 40 mEq/L; Continuous EKG monitoring in patients
injection): 10 mEq, 20 mEq, Max concentration through a receiving K >10–20 mEq/hr.
30 mEq and 40 mEq central line: 200 mEq/L; Use concentrations >100 mEq/L only in
Max rate: 10–20 mEq/hr. severely symptomatic patients who cannot
Can use higher rates in tolerate a large fluid load.
life-threatening situations.
* Based on the assumption that there are no ongoing losses (e.g. diuretic therapy, GI losses) and that the patient does not have a chronic potassium wasting
condition (e.g. diuretic therapy, primary aldosteronism, Gitelman’s disease). For such patients the rate of replacement must be increased according to the
rate of potassium loss.
unless the patient is on high doses. Most other antihypertensive medications can also be continued.
9
Treatment
The initial treatment of hypokalemia is focused on normalizing the serum
potassium levels, replacing magnesium (if low) and managing cardiac
arrhythmias, (if present). See Table 2 for additional information on potassium replacement. The serum potassium concentration should be monitored periodically to ensure adequate repletion and to avoid hyperkalemia.
Furthermore, the underlying cause of hypokalemia should be treated.
Patients with ongoing losses will need chronic replacement with oral
potassium preparations or the addition of a potassium-sparing diuretic.
References
1. Rose BD, Post TW. (2001) Hypokalemia. In: Clinical Physiology of
Acid-Base and Electrolyte Disorders. McGraw-Hill, Columbus, OH,
pp. 836–887.
2. Rennke HG, Denker BM (2007) Disorders of potassium balance. In:
Disorders of potassium balance. In Renal Pathophysiology: The
essentials. Lippincott Williams & Wilkins, Baltimore, MD, pp. 175–197.
3. Rose BD, Post TW. (2001) Hyperkalemia. In: Clinical Physiology of
Acid-Base and Electrolyte Disorders. McGraw-Hill, Columbus, OH,
pp. 888–930.
4. Rose BD, Post TW. (2001) Introduction to disorders of potassium bal-
ance. In: Clinical Physiology of Acid-Base and Electrolyte Disorders.
McGraw-Hill, Columbus, OH, pp. 822–835.
5. Huang CL, Kuo E. (2007) Mechanism of hypokalemia in magnesium
deficiency. J Am Soc Nephrol 18(10): 2649–2652.
6. Groeneveld JH et al. (2005) An approach to the patient with severe
hypokalaemia: The potassium quiz. QJM 98(4): 305–316.
7. Lin SH et al. (2004) Laboratory tests to determine the cause of
hypokalemia and paralysis. Arch Intern Med 164(14): 1561–1156.
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Disorders of Potassium Homeostasis