that warrant providers’ attention:
1. Volume overload: In the most basic generalizations, AKI represents an ineffective ability
of the kidneys to clear excess water from the
body. This is quite problematic, since most critical care patients have a positive volume status.
This is especially true with septic patients, due
to the volume expansion that occurs during
the initial resuscitation, as well as the constant
obligate fluid intake due to antibiotic therapies, electrolyte management, intravenous
medication administration, blood products
and enteral/parenteral nutrition.
Hypervolemia presents a host of unique
challenges. Patients with known heart disease
can become susceptible to systolic dysfunction,
worsening the volume status and AKI by way
of cardiorenal syndrome. Pulmonary congestion from hypervolemia can also cause acute
lung injury, another life-threatening complication of critical care patients. 8, 9
Volume overload can pose not only an
immediate threat to a patient’s life, but it can
also have long-lasting effects on post-recovery
morbidities. Aggressive treatment and planning must be undertaken at the first indication
that an AKI is developing in the presence of
volume overload. Therapy should center on
loop diuretics. An initial load of furosemide
40–80 mg IV can be given. If urine output
doesn’t respond after an hour, a second dose
of furosemide is given at twice the strength
of the first.
If the urine output doesn’t respond to furosemide alone, the addition of a thiazide diuretic
has been shown to achieve sufficient diuresis
in some patients. However, if diuresis proves
futile, RRT should be emergently arranged. 10
2. Hyperkalemia. Along with hypervolemia,
derangements in serum potassium are a common and serious complication of AKI. For
patients with serum potassium levels of 5.0–
5. 4 mEq/L (i.e., mild hyperkalemia), medical
management can be attempted to lower the
extracellular potassium levels. However, medical management should only be attempted
if the known cause of the AKI is established
and easily reversible (i.e., true hypovolemia).
In patients with potassium values greater
than 5. 4 mEq/L, intractable/progressively
worsening AKI, or conditions causing cell
breakdown (i.e., rhabdomyolysis), emergent
RRT must be arranged. An attempt at medical management can be done as a bridge to
RRT, but dialyzing these patients is the primary goal. 10
3. Metabolic acidosis. Acid/base balance
within the kidneys is achieved by two mechanisms: 1) excretion of hydrogen ions; and 2)
production of bicarbonate. When a patient
is suffering from AKI, both mechanisms are
impaired and metabolic acidosis ensues.
However, the metabolic acidosis that occurs
because of AKI is a product of the buildup
from the body’s daily metabolic processes. It’s
important to remember that patients suffering
from AKI are usually critically ill from other
disease processes that greatly exacerbate the
hydrogen ion burden of normal metabolism
(e.g., lactic acidosis from sepsis, ketoacidosis
from hyperglycemic crisis, etc.).
Like hyperkalemia, the treatments for
AKI-induced metabolic acidosis are medical
management or RRT. Any patient with scant
urine production and severe acidosis (pH <
7. 1) should be considered for emergent RRT.
In severely acidotic states, the body’s normal
physiology is extremely altered.
For instance, moderate to severe acidosis
can lead to ventricular systolic dysfunction,
lowered threshold for cardiac automaticity/
arrhythmia, arterial dilation, venous constriction,
impairment of antibiotic efficacy and decreased
responsiveness to adrenergic antihypertensives.
For patients with moderate to severe aci-
dosis who aren’t hypervolemic, IV bicarbonate
can be administered with caution. Bicarbon-
ate administration can come with some seri-
ous risks and should only be administered
with expert consultation. Bicarbonate admin-
istration in patients who are already volume
overloaded should be avoided with the plan
to seek emergent RRT.
Due to the large sodium burden of IV bicarbonate, a patient’s hypervolemia can be exacerbated; even euvolemic patients can become
volume overloaded from bicarbonate, especially
when oliguric. Patients with worsening acidosis and oliguria from an AKI that’s unlikely
to be quickly reversed, should be referred for
emergent RRT. This is especially true in cases
where the pH is expected to progress to < 7. 1.
4. Uremia. The clearance of metabolic waste
is the primary function of the kidneys. When
these waste products build up within the body
as a result of AKI, they can become toxic and
interfere with a host of normal physiologic
The most common results of high uremic toxin burden are uremic encephalopathy,
neuropathy, pericarditis and uremic bleeding.
Collectively, these conditions are known as
uremia or uremic syndrome.
Although the physiologic processes for most
of these complications aren’t fully understood,
it’s well accepted that all are direct results of
the increased load of these toxins within the
body. In uremic encephalopathy, the toxins
interfere with the actions of neurotransmitters.
For neuropathies, the toxins can degrade
myelin. These toxins also impede the actions of
both platelets and the clotting factors needed
The mechanism that leads to inflammation of the pericardial sack is poorly understood, though there appears to be a relationship
Critically ill patients who develop an AKI are some of the most challenging and resource-intensive patients
in the ICU. Photo A.J. Heightman