Page 84 - JSOM Summer 2022

compared to only about 2% of total body stores found in concentrations greater than 40mEq/L generally requires cen-
ECF. 27–29 Along with sodium, potassium helps to maintain tral venous access due to its vesicant effect in smaller vessels
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electrical membrane stability, and altering ECF sodium con- which can cause loss of IV access. Serum levels can be re-
centrations (as in cases of IV saline administration), can im- checked every 2–4 hours, although there is no firm consensus
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pact potassium levels. Potassium homeostasis is controlled on frequency. Resuscitation should proceed slowly to avoid
partly by the kidneys, and despite its relatively low levels in the overcorrection and risk of rebound hyperkalemia (below). 30,36
circulating ECF, shifts in potassium concentrations can have
significant effects on muscle, specifically cardiac tissue. 27–30 Hyperkalemia (High Potassium)
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The normal range for potassium is generally 3.5–5mEq/L, Hyperkalemia (K > 5mEq/L) has numerous causes, most com-
with hypokalemia defined below 3.5mEq/L and hyperkalemia monly from pseudohyperkalemia, or a false elevation due to
as above 5mEq/L. 27,28,30 cell lysis during blood collection. 30,40 Despite this, findings of
hyperkalemia should not be lightly dismissed. Rhabdomyoly-
Hypokalemia (Low Potassium) sis is the most common cause of hyperkalemia in the setting
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Hypokalemia (K < 3.5mEq/L) commonly results from im- of extreme exertion. This diagnosis is associated with diffuse
paired renal regulation and retention of potassium, with much muscle aches, as well as dark urine (myoglobinuria). Military
rarer instances of insufficient intake. 27,29–31 Given pervasive trauma patients who have sustained battlefield injuries such
hypertension diagnoses, and treatment to include the use of as crush and burn injuries, should be evaluated for hyperkale-
diuretics (such as hydrochlorothiazide), a brief medical his- mia, as high levels of ICF potassium are released into the ECF
tory is important in suspected or diagnosed hypokalemia. during tissue destruction. 30,41,42 Specifically, prolonged field
However, in an otherwise healthy servicemember, more acute care of trauma patients are at risk of acute kidney injury (AKI)
losses through vomiting and/or diarrhea are the most com- which may worsen hyperkalemia. 41
mon causes of hypokalemia. 27,30 Additionally, hypokalemia
has been documented in military cases of environmental hy- Hyperkalemia assessment focuses on cardiac manifestations
pothermia and hyperthermia, the latter both with and without with complaints of symptomatic palpitations, best evaluated
significant exertion. 32–34 through ECG and cardiac monitoring. Although not always
present, peaked T waves are pathognomonic for hyperkale-
Hypokalemia is often asymptomatic, but beyond vague elec- mia; however, ECG manifestations may also show PR interval
trolyte derangement symptoms, patients may present with prolongation, loss of p waves, and widening QRS as severity
numbness, tingling, and palpitations, with decreased deep progresses. 30,35,41,43 Conversely, ECGs may appear largely unre-
tendon reflexes on exam. 30,35,36 If electrocardiogram (ECG) is markable despite the presence of significant hyperkalemia. 35,42
used, hypokalemia can manifest with decreased or flattened
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T waves and the growth of a subsequent U wave. 27,30,35,37 As Regardless of mild (K = 5.5–6.5mEq/L) or moderate-severe
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severity progresses, sinus bradycardia, ventricular tachycar- (K > 6.5mEq/L) hyperkalemia classification, the initial evalu-
dia or fibrillation and torsades de pointes can develop. 30,35,37,38 ation of hyperkalemia in the mild or asymptomatic atraumatic
Cardiac monitoring should be used to monitor treatment ef- patient should include consideration of repeat sampling to
fects when an abnormal ECG is present. Additionally, all pa- confirm initial findings and exclude pseudohyperkalemia. 30,40
tients with hypokalemia should be evaluated for magnesium Once this is done, treatment should be initiated with concerns
levels, if available, as refractory hypokalemia can result from for short progression of severity and possibly fatal dysrhythmia
hypomagnesemia. 30 manifestations from cardiac effects. 29,30,42 A largely two-prong
approach for treatment focuses on cellular membrane stabili-
Hypokalemia treatments are dependent on level of severity, zation and transcellular shifting therapies (from ECF to ICF).
with a focus on identifying and treating underlying causes as Calcium, generally given in the form of calcium gluconate (1g
well as direct electrolyte replacement. Severe hypokalemia can ampule via slow IV push), aids cardiac membrane stabiliza-
be defined as a serum level less than 2.5mEq/L; however, ECG tion and should be administered as a temporizing measure in
or other abnormal exam findings supersede laboratory values the presence of ECG changes. 30,41,44 Alternatively 1g of calcium
in making the diagnosis. 30,36 Conversely, nonsevere hypoka- chloride can be given via IV push or diluted in a 50mL mini-
lemia can then be defined in patients with potassium above bag and given over 10 minutes. The use of calcium gluconate
2.5mEq/L without symptoms or ECG findings. to treat trauma-induced coagulopathy may make this interven-
tion readily available, although calcium chloride can be given
In stable, alert patients, oral potassium supplementation is (via central line access only given its caustic nature and risk
preferred, although caution is warranted for gastric irritation of tissue necrosis). 30,41 Medics should be mindful that calcium
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and possible ulceration. Low dosages (20–40mEq tablets) supplementation is strictly for membrane stabilization, and
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should be diluted in other oral fluids to reduce this risk. IV will not significantly lower serum potassium levels. 30,45 Cal-
potassium replenishment in more severe or otherwise unstable cium administration can be repeated after 5 minutes if there is
patients is given as a “piggyback” fluid with saline or LR due no significant ECG changes. 30,45
to its caustic nature on vasculature, but should not be given
in dextrose-containing fluids as this can prolong hypokale- Concurrent treatment to shift excess potassium from the ECF
mia due to triggered endogenous insulin release. For every to ICF should be considered for continued patient manage-
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1mEq/L deficit, approximately 200–400mEq of potassium is ment. These include the use of β-agonist medications, such as
required for correction. 27,29,39 In non-severe hypokalemia, oral albuterol (20mg in 4mL of saline nebulized over 10 minutes),
potassium tablets or IV doses of 10–20mEq/L can be given given to alert patients with positive airway control. 30,41,44 In-
hourly, with no more than four doses in a 24-hour period. sulin (10–20 units IV) is highly recommended to drive potas-
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More severe cases require repeat up to 40mEq/L adminis- sium back into the ICF, but should be given concurrently with
tered three to four times a day. 27,29,39 Replacement with IV one ampule of D W per 10U of regular insulin) to prevent
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82 | JSOM Volume 22, Edition 2 / Summer 2022