E m e r g e n c y De p a r t m e n t

Management of Acute
K i d n e y In j u r y, E l e c t ro l y t e
A b n o r m a l i t i e s , an d R e n a l
R e plac e men t Th er ap y i n th e
Critically Ill
a,b, c,d,e
Ivan Co, MD *, Kyle Gunnerson, MD, FCCM

KEYWORDS
 Acute kidney injury  Acute renal failure  Electrolyte derangement  Acidosis

KEY POINTS
 Acute kidney injury is a common diagnosis with multiple sequelae and consequences.
 Treatment and management rely on astute diagnosis of the cause for acute kidney injury.
 Renal replacement therapy or hemodialysis is the treatment modality when conservative
management fails.

INTRODUCTION AND DEFINITION

Acute kidney injury (AKI), formerly called acute renal failure, is a common diagnosis in
the emergency department (ED) and in the critically ill.1 Numerous studies have found

Disclosures: None.
a
Department of Emergency Medicine, University of Michigan Health System, 1500 East Med-
ical Center Drive SPC 5301, Ann Arbor, MI 48109, USA; b Department of Internal Medicine,
Division of Pulmonary Critical Care, University of Michigan Health System, 1500 East Medical
Center Drive SPC 5301, Ann Arbor, MI 48109, USA; c Department of Emergency Medicine, Di-
vision of Emergency Critical Care, Massey Family Foundation Emergency Critical Center (EC3),
University of Michigan Health System, 1500 East Medical Center Drive, Ann Arbor, MI 48109-
5303, USA; d Department of Anesthesiology, Division of Emergency Critical Care, Massey Family
Foundation Emergency Critical Center (EC3), University of Michigan Health System, 1500 East
Medical Center Drive, Ann Arbor, MI 48109-5303, USA; e Department of Internal Medicine,
Division of Emergency Critical Care, Massey Family Foundation Emergency Critical Center (EC3),
University of Michigan Health System, 1500 East Medical Center Drive, Ann Arbor, MI 48109-
5303, USA
* Corresponding author. Department of Internal Medicine, Division of Pulmonary Critical Care,
University of Michigan Health System, 1500 East Medical Center Drive SPC 5301, Ann Arbor, MI
48109.
E-mail address: coivan@med.umich.edu

Emerg Med Clin N Am - (2019) -–-

https://doi.org/10.1016/j.emc.2019.04.006 emed.theclinics.com
0733-8627/19/ª 2019 Elsevier Inc. All rights reserved.
2 Co & Gunnerson

significant morbidity and mortality regardless of patient characteristics, comorbidities,

and clinical context.2–5 Mortality has been estimated to occur in 15% to 80% of crit-
ically ill patients. Therapeutic interventions often target correcting electrolyte abnor-
malities, preventing secondary injury with hemodynamic support, and initiation of
emergent hemodialysis in patients with advanced metabolic derangements. Patient
outcome varies depending on the provider’s ability to identify the patient’s AKI early
and provide appropriate treatment interventions.
The definition of AKI has undergone multiple revisions over the past few decades.
The RIFLE (risk, injury, failure, loss, end-stage renal disease) criteria were initially pro-
posed in 2004, and later modified in 2007 to include absolute serum creatinine (SCr)
level increase. In addition, in 2012, both definitions were combined into what is
currently used: the KDIGO (Kidney Disease; Improving Global Outcomes) definition
(Box 1).

EVALUATION AND GENERAL MANAGEMENT OF PATIENTS WITH ACUTE KIDNEY

INJURY

Critically ill patients in the ED may have several contributing causes for their acute in-
juries. A careful review of their history, examination, and known comorbidities may
provide early clues toward identifying the cause of their reduced renal function. AKI
cause can be subdivided into 3 broad categories: prerenal, intrinsic, and postrenal
causes.
AKI rarely causes any symptoms. Most clinical symptoms are a result of the primary
underlying disease leading to the development of AKI rather than the kidney injury it-
self. Outside of clinical history, examination, and comorbidities, laboratory testing may
help delineate the 3 categories of AKI: urine osmolarity, urine electrolytes, renal ultra-
sonography, urinalysis with microscopy. Urine electrolyte levels can be obtained to
calculate the fractional excretion of sodium (FENa) or urea (FEUrea) if the patient is
taking diuretic medications. A FENa less than 1% or FEUrea less than 35% suggests
a prerenal cause of AKI, whereas a FENa greater than 2% or FEUrea greater than 35%
is more consistent with an intrinsic disease process. Cutoff values may be less helpful
in patients with chronic kidney disease or mild cases of AKI. Urinalysis with micro-
scopy is another diagnostic test that can help differentiate the AKI cause by the pres-
ence or absence of casts. Keep in mind that no single value is absolute in diagnosing
AKI.

Prerenal Acute Kidney Injury

Prerenal AKI is often a manifestation of decreased renal perfusion caused by intravas-
cular volume depletion or a decreased renal perfusion pressure leading to a reduced
glomerular filtration rate (GFR). Approximately 70% of patients presenting with AKI
have a prerenal cause.6 Sepsis and septic shock continue to be the most important

Box 1
Kidney Disease; Improving Global Outcomes definitions of acute kidney injury

AKI can be diagnosed if the patient has any of the following:

1. Increase in SCr level by at least 0.3 mg/dL within 48 hours
2. Increase in SCr level to greater than 1.5 baseline occurring within 7 days
3. Urine output less than 0.5 mL/kg/h for 6 hours

Data from Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work
Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl 2012;2:1–138.
 Emergency Department Management 3

Table 1
Causes of prerenal acute kidney injury

Causes of Poor Renal Perfusion Leading

to Prerenal Acute Kidney Injury Potential Causes
Volume depletion Diuretics
Diarrhea
Blood loss anemia
Osmotic diuresis
Diuretic overuse
Burns
Vomiting
Decreased arterial Medication: NSAIDs, cyclosporine, tacrolimus,
pressure angiotensin receptor blocker
Cardiorenal syndrome
Hepatorenal syndrome
Intra-abdominal hypertension
Systemic vasodilation: sepsis

Abbreviation: NSAIDs, nonsteroidal antiinflammatory drugs.

Data from Rahman M, Shad F, Smith M. Acute kidney injury: a guide to diagnosis and manage-
ment. Am Fam Physician 2012;86(7):631–639.

causes of AKI in critically ill patients and account for more than 50% of patients with
AKI admitted to the intensive care unit.7
Several pathophysiologic derangements that can cause a prerenal AKI are not a
result of volume depletion. AKI as a result of decreased arterial pressure secondary
to intravascular fluid overload can be found in patients with congestive heart failure
resulting in cardiorenal syndrome. This kind of prerenal AKI can be treated with
diuretic therapy. Patients with hepatorenal syndrome can manifest as having prerenal
disease; however, intervention with volume expansion or diuretics may be necessary
depending on their clinical state and laboratory findings. Common causes of prerenal
AKI are noted in Table 1.

Intrinsic (Renal) Acute Kidney Injury

Intrinsic renal injury develops when the primary cause of AKI is parenchymal injury,
often caused by medications, toxins, or ischemia. Components of the kidney that
are affected include the tubules, glomerulus, vascular, and the interstitium. Common
causes of intrinsic AKI are listed in Table 2.
Acute tubular necrosis (ATN) is the most common intrinsic cause of AKI, often the
result of prolonged hypotension resulting in ischemic renal tubular injury. There is
no specific intervention to reverse ATN once it develops. Prevention of additional sec-
ondary insults is important for renal recovery. Acute interstitial nephritis is the second
most common cause of intrinsic AKI, often a consequence of certain medications or
infections. Prolonged prerenal disease, if not promptly identified and intervened on,
will eventually progress to intrinsic disease.

Postrenal Acute Kidney Injury

Postrenal AKI is a result of renal congestion caused by a blockage of urinary flow.
Common causes include prostatic hypertrophy, renal calculi, and an external mass
compressing the ureter or the urethra. Postrenal AKI is almost always associated
with some form of hydronephrosis. Despite being the rarest of the 3 causes of AKI,
4 Co & Gunnerson

Table 2
Common causes of intrinsic acute kidney injury

Common Types of Intrinsic AKI Potential Causes

Tubular Ischemia
Nephrotoxins: endogenous toxins such as
calcium, uric acid, hemolysis, rhabdomyolysis,
contrast media, chemotoxic agents
Interstitial Medications: aminoglycosides, cephalosporin, penicillin
Infection: Streptococcus, Epstein-Barr virus
Systemic disease: lupus, sarcoidosis
Glomerular Postinfection
Glomerulonephritis
Vascular Renal thrombosis
Malignant hypertension

Data from Rahman M, Shad F, Smith M. Acute kidney injury: a guide to diagnosis and management.
Am Fam Physician. 2012;86(7):631–639.

diagnosis can often be made with a thorough clinical examination and diagnostic ul-
trasonography to identify the location of the anatomic obstruction.

ACID-BASE DERANGEMENT IN THE CRITICALLY ILL

Before treatment initiation, a solid understanding of the patient’s acid-base derange-

ment is paramount. Patients with AKI may present with a metabolic acidosis, often
classified as either an anion-gap or non-anion gap metabolic acidosis.8
Acid-base homeostasis is normally achieved by the kidney’s ability to excrete acid
load, through the Na1/H1 transporter, which excretes approximately 1 mEq of H1 ions
per kilogram per day in the urine.9 Metabolic acidosis occurs once the mechanism to
excrete H1 is overwhelmed by excessive acid production, inability to reabsorb a bicar-
bonate buffer, or decreased H1 excretion.9
AKI associated non–anion-gap metabolic acidosis (NAGMA) occurs purely from a
loss of bicarbonate without concomitant increase in exogenous acid production.
This condition occurs most commonly in patients with severe hypovolemia secondary
to diarrhea where the large bowel has impaired ability to reabsorb bicarbonate. Wors-
ening chronic renal dysfunction can also cause NAGMA, as well as renal tubular
acidosis (RTA). Patients with an acute RTA have impaired bicarbonate reabsorption
secondary to ion transporter dysfunction.
Anion-gap metabolic acidosis (AGMA) often occurs because of an increased acid
production that the kidneys are unable to excrete because of an acute decrease in
GFR. Bicarbonate in the body is used to buffer the excess ion to no avail, resulting
in a worsening metabolic acidosis.9 Most common causes of AGMA in the critically
ill include lactic acidosis and ketoacidosis. Other causes of AGMA are listed in
Table 3.
The most common AGMA encountered in critically ill patients is lactic acidosis.
Lactate production often occurs as a result of poor tissue perfusion and inadequate
oxygen delivery. Malperfused tissues transition from aerobic to anaerobic glycolysis
metabolism to supplement inefficient ATP production to match the patient’s metabolic
demand.10 Lactate generation results in a metabolic acidosis that can cause myocar-
dial depression, catecholamine resistance, and progressive vasodilatory shock. Vaso-
dilatory shock occurs when vascular wall smooth muscle is unable to constrict despite
a maximum level of plasma catecholamines (released in response to hypoperfusion)
 Emergency Department Management 5

Table 3
Common causes of anion-gap metabolic acidosis

AGMA Mnemonic Causes

M Methanol
U Uremia
D Diabetic, alcohol, starvation ketoacidosis
P Paracetamol/acetaminophen
I Isoniazid, iron ingestion, inborn error of metabolism
L Lactic acidosis
E Ethanol, ethylene glycol
S Salicylates

and inappropriate activation of other vasodilatory mechanisms.11 Transient correction

of the acidic environment with sodium bicarbonate or dialysis can help mitigate the pa-
tient’s vasodilatory shock, but effective treatment should be focused on reversing the
inciting event.11

MEDICAL MANAGEMENT OF ACUTE KIDNEY INJURY

Therapy targeted to improve a patient’s AKI should focus on supportive interventions

that include optimizing hemodynamics, intravascular fluid status, correcting electro-
lyte abnormalities, improving severe pH derangements, and minimizing interventions
that could further reduce the patient’s GFR. In addition to supportive measures, iden-
tifying potential nephrotoxic agents and appropriate pharmacologic dosing adjust-
ments to the patient’s GFR are of utmost importance.12
Fluid Resuscitation
In patients with a prerenal AKI caused by severe hypovolemia, intravenous crystalloid
resuscitation is often the initial and primary therapy. Fluid resuscitation improves car-
diac output and ultimately improves renal perfusion and GFR. There is increasing ev-
idence to suggest that resuscitation using high-chloride-load fluids may be harmful,
causing a worsening NAGMA, renal acidosis, and renal function.13–15 In patients
with prerenal, hypovolemic AKI, lactated Ringer or a balanced crystalloid solution is
currently the resuscitative fluid of choice.16
Hemodynamic Optimization with Vasopressor Therapy
In patients who continue to have hemodynamic instability with a low mean arterial
pressure (MAP) despite fluid resuscitation (or diuresis), vasopressor administration
may be necessary to achieve adequate renal perfusion.17 Vasopressor administration
should be initiated to target an initial MAP of greater than or equal to 65 mm Hg, poten-
tially titrating up to a higher MAP target in patients with a history of hypertension and
clinical improvement with higher blood pressure target.10
No specific vasopressor has been proved to be more effective for the treatment
and/or prevention of AKI in patients with shock. Vasopressor choice should be catered
toward the patient’s primary clinical pathophysiology. Norepinephrine (NE) has been
found to improve creatinine clearance in patients with distributive shock.18 In a
comparative study comparing NE with dopamine, there was no significant difference
between renal function or mortality outcome.19 Dopamine was found to have an
increased incidence of tachydysrhythmias and adverse events.19 Administration of,
renal-dose dopamine to achieve renal vasodilation has not been found to reduce
6 Co & Gunnerson

the incidence of AKI, need for renal replacement therapy, or patient mortality.20 In fact,
dopamine may worsen both renal perfusion and GFR.21–23 As a result, KDIGO has pro-
vided a 1A recommendation against using low-dose dopamine in patients with AKI.16

Management of Electrolyte Derangements

Hyperkalemia is the most common life-threatening electrolyte derangement as a
sequela of AKI. Breakdown in potassium homeostasis, whether a result of reduced
renal excretion (secondary to decreased GFR), excessive intake, worsening acidosis,
or leakage of potassium into the extracellular compartment can rapidly increase serum
potassium levels.24
Hyperkalemia is diagnosed by any serum potassium level greater than 5.5 mEq/L.
There are no specific physical examination findings or clinical symptoms that correlate
with the degree of hyperkalemia. Cardiac rhythm disturbances, most commonly
nonspecific repolarization abnormalities, peaked T waves, widening of the QRS com-
plex, and ST depression, are common sequelae of hyperkalemia.24 The degree of car-
diac rhythm disturbances does not correlate with the degree of hyperkalemia (Fig. 1).
Hyperkalemia therapy should not be solely guided by the potassium level but by
additional clinical symptoms such as cardiac arrhythmias, nausea, vomiting, degree
of metabolic acidosis, and the ability for respiratory compensation.25 Medical therapy
for hyperkalemia involves transient cardiac membrane stabilization and intracellular
shift of potassium until the kidney is able to provide adequate elimination.26 Treatment
options include:
 Calcium gluconate: stabilizes cardiac membrane potential in hyperkalemia-
induced conduction abnormalities.
 Intravenous insulin with dextrose: insulin stimulates the Na1/K1 ATPase pump to
shift excess K1 to the intracellular compartment, whereas dextrose prevents
hypoglycemia.

Fig. 1. Hyperkalemia in patient with K of 6.5 mEq/L manifesting as ST depression and

peaked T waves.
 Emergency Department Management 7

 Beta-adrenergic agonists: stimulate K1 shift from extracellular to intracellular

space via Na1/K1 ATPase pump.
Increased potassium excretion can be considered in outpatients with hyperkalemia;
however, caution should be exercised in critically ill patients because sequelae from
therapy may result in significant clinical complications. These include:
 Loop diuretics: inhibit Na/K/Cl channel, allowing more K to be excreted from the
kidneys. Patients with hypovolemic, prerenal AKI may develop hemodynamic
compromise and reduced GFR.
 Ion-exchange resins: prevent enteral reabsorption of potassium by binding po-
tassium into the resin. In patient with shock and decreased gut perfusion, ion-
exchange resin administration may precipitate gut ischemia and necrosis.27
Increasing potassium excretion is often challenging in critically ill patients with
concomitant renal impairment, and emergent renal replacement therapy may be
required.
Calcium derangement is common, often a result of the increased serum phosphorus
levels that can occur with a decreased GFR. Therapeutic intervention in patients with
hypocalcemia usually involves correction of hyperphosphatemia with oral phosphate
binders. In patients with symptomatic hypocalcemia, the lowest possible dose of
intravenous calcium should be administered to relieve symptoms to avoid excessive
supplementation, which can lead to calcium phosphate crystal formation.
Tumor lysis syndrome (TLS) is an oncologic emergency that often presents with sig-
nificant hypocalcemia, hyperphosphatemia, hyperkalemia, and hyperuricemia. Pa-
tients with recent initiation of chemotherapy to treat hematologic malignancies are
particularly at risk for TLS, because of a massive lysis of tumor cells resulting in a large
release of potassium and phosphorus into the circulatory system. Hyperphosphate-
mia often precipitates with extracellular calcium to form calcium phosphate crystals
that can impair end-organ blood flow.28 Patients with TLS should be initially treated
with intravenous crystalloids to further prevent calcium phosphate crystal formation.
Early hemodialysis should be considered in oliguric patients with severe hyperphos-
phatemia and symptomatic hypocalcemia.

Sodium Bicarbonate Therapy

Administration of sodium bicarbonate in patients with AKI has been controversial,
particularly in those patients with concomitant AGMA.29–31 Treatment goals for pa-
tients with AGMA should be focused on treating the underlying cause. Administration
of sodium bicarbonate alone improves acidemia and serum pH without reversing the
cause of acid production.
Sodium bicarbonate therapy may be warranted in patients with severe metabolic
acidosis as a temporizing measure while the clinician attempts to reverse the under-
lying cause. In patients with a pH less than 7.1, bicarbonate therapy may help tempo-
rize profound hemodynamic instability and improve vasopressor sensitivity.32
The recently published BICAR-ICU (Sodium Bicarbonate Therapy for Patients with
Severe Metabolic Acidaemia in the Intensive Care Unit) trial, randomized 389 critically
ill patients with mean serum bicarbonate level less than 13 mmol/L and acidemia
(mean pH of 7.15) to receive bicarbonate versus placebo to maintain serum pH greater
than 7.3. The study found no difference between 28-day mortality or organ failure at
7 days between treatment and control groups. However, patients with severe AKI
who received bicarbonate therapy did show a trend toward decreased need for renal
replacement therapy.33
8 Co & Gunnerson

Clinicians should be aware of some clinically significant side effects of sodium bi-
carbonate therapy. Sodium bicarbonate ultimately gets metabolized to CO2, causing
a transient increase in arterial PCO2, which may be detrimental for patients with an
already extreme minute ventilation.34
Diuretic Therapy
Loop and thiazide diuretic therapy should be administered only to patients who have
renal injury as a result of fluid overload causing renal congestion and reduced GFR.
Diuretic therapy may stimulate urine output and shift fluid overloaded patients’ volume
status in a favorable direction, but diuretics do not seem to reduce mortality or future
need for renal replacement therapy.35 Diuretics should be avoided in patients with a
hypovolemic, prerenal AKI because this may further reduce renal perfusion.16 Despite
the renoprotective properties of loop diuretics, KDIGO does not recommend the use
of loop diuretics to prevent the worsening of renal function.16,36
In patients with intrinsic or prerenal AKI from cardiorenal syndrome, complicated by
volume overload and hypoxic respiratory failure, the use of diuretics has been shown
to help facilitate fluid removal and improve oxygenation and the tolerance of lung pro-
tective ventilation. Despite the increase in urine output with the assistance of diuretics
in these patients, there were no clinical outcome benefits noted in terms of expedited
recovery from AKI or shorter duration of renal replacement therapy (RRT).37

RENAL REPLACEMENT THERAPY

A small subgroup of patients who present with a severe AKI fail medical management
and require emergent hemodialysis to correct their acid-base disturbances or electro-
lyte abnormalities (hyperkalemia). The timing for initiation of RRT is highly debated.
KDIGO recommends initiating RRT for life-threatening changes in fluid balance, elec-
trolytes, and acid-base levels but provides no specific objective criteria.16 Life-
threatening indications for emergent hemodialysis are listed in Table 4.
Initiation of Renal Replacement Therapy
Initiation of RRT in critically ill patients often requires nephrology consultation as well
as temporary vascular access. Current guideline recommendations suggest the use of
a 10-French or 12-French, double-lumen, central venous dialysis catheter to facilitate
emergent RRT. Emergently placed temporary hemodialysis catheters can be placed
with ultrasonography guidance, in a nontunneled fashion, preferentially in the right

Table 4
Mnemonic for emergent hemodialysis indications

A Acidemia: severe metabolic acidosis despite adequate medical optimization

(pH<7.1)
E Electrolytes: particularly hyperkalemia refractory to medical therapy
I Ingestion: poisoning by drugs that are able to be eliminated with RRT
O Overload: volume overload resulting in hypoxic respiratory failure
necessitating mechanical ventilation
U Uremia: complications secondary to increased BUN (bleeding, pericarditis,
encephalopathy)

Abbreviation: BUN, blood urea nitrogen level.

Data from Nee P, Bailey D, Todd V, et al. Critical care in the emergency department: acute kidney
injury. Emerg Med J 2016;33:361–365.
 Emergency Department Management 9

internal jugular vein (Fig. 2). If the right internal jugular vein is unable to be accessed,
femoral vein access is preferred to left internal jugular vein cannulation. Subclavian
vein access should be avoided, because temporary hemodialysis catheters are asso-
ciated with higher rates of central vein stenosis, which may prevent the use of the ipsi-
lateral arm as a site for long-term hemodialysis access (arteriovenous graft or fistula) in
the future.38

Fig. 2. Difference between temporary hemodialysis catheter (right) and central venous cath-
eter (left).
10 Co & Gunnerson

In order to optimize catheter blood flow, the temporary hemodialysis catheter’s

distal tip must be located within a large central vessel. Catheter length is an important
consideration, and in general should be 12 to 15 cm for right internal jugular, 15 to
20 cm for left internal jugular, and 19 to 24 cm for femoral vein access. Optimal cath-
eter placement is important for establishing an effective venovenous hemodialysis cir-
cuit to provide adequate extracorporeal blood flow for fluid and/or solute removal.39

Mode of Renal Replacement Therapy

Once appropriate vascular access has been obtained and confirmed in the right loca-
tion, delivering RRT via intermittent or continuous hemodialysis should be decided.
This delivery requires an understanding of the indication for initiation of hemodialysis,
hemodynamics, as well as the logistics needed to initiate either mode (Table 5).
Intermittent hemodialysis (iHD) can provide external blood filtration at blood flow
rates of 300 to 500 mL/min, and is often the preferred mode for RRT for rapid removal
of toxins (poisoning), electrolytes (hyperkalemia), and intravascular fluid volume. A sin-
gle hemodialysis session can often be completed in 2 to 4 hours. Hemodynamic sta-
bility is generally required before initiation of iHD. Critically ill patients with hypotension
or vasopressor dependence are often unable to increase cardiac output to compen-
sate for the volume of blood that is being filtered by the extracorporeal circuit. iHD
also has a higher resource demand, because these machines often require an addi-
tional technician if hemodialysis is being performed at the bedside.40,41
Continuous RRT (CRRT) is run at a much slower blood flow rate (usually 20–40 mL/
kg/h) to achieve the same effects of iHD, but over a 24-hour period. It is the preferred
mode of RRT in patients who have unstable hemodynamics or require vasoactive sup-
port. Fluid balance is able to be controlled by intensivists and individualized to each
patient’s needs. The negatives of CRRT are its inability to rapidly clear toxins second-
ary to its low blood flow rate, the need for anticoagulation to prevent circuit clot forma-
tion, and prolonged limitations to patient mobility. There is also an increased nursing

Table 5
Comparison between the 2 common hemodialysis modalities in critically ill patients

Intermittent (iHD) Continuous (CRRT)

Indication Ambulatory, hemodynamically Critically ill,
stable, electrolyte and nonambulatory
poison clearance
Solute Transport Diffusion Convection
Blood Flow (mL/min) 300–400 150–200
Dialysate (L/min) 30 1
Efficiency High Low
Hemodynamic Poor Good
Stability
Duration Average 3 h Continuous 24 h
until discontinued
Anticoagulation Not required secondary to Required (within
high blood flow rate CRRT filter)
Logistics Need tap water supply, technically High workload,
difficult to initiate immobility, costly

Abbreviations: CRRT, continuous RRT; iHD; intermittent hemodialysis.

Data from Alvarez G, Chrusch C, Hulme T, et al. Renal replacement therapy: a practical update.
Can J Anesth 2019;66:593–604.
 Emergency Department Management 11

resource burden, which includes frequently changing the CRRT machine’s dialysate
bath and laboratory draws.40

SUMMARY

Effective treatment of critically ill patients with AKI requires astute clinicians who can
rapidly obtain a detailed history, perform a thorough physical examination, and identify
high-risk elements contributing to the patient’s decreased renal function. Most pa-
tients improve with conservative therapy, including normalizing fluid status, hemody-
namic support, removal of offending agents, and addressing the patient’s underlying
disorder. The utility of sodium bicarbonate administration remains unclear. Sodium bi-
carbonate therapy may be useful in patients with a severe metabolic acidosis (arterial
pH <7.1) as a temporizing intervention until the underlying disorder can be treated and
reversed.
Despite aggressive medical intervention, a subgroup of patients with AKI require
initiation of emergent RRT. Important considerations include RRT mode, appropriate
temporary dialysis catheter equipment, and insertion site. Timely interventions that
address these needs in critically ill patients with AKI are imperative to ensure the
best long-term chances of recovery.

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