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Multi-Organ Point-Of-Care Ultrasound in Acute Kidney Injury: Editorial
Multi-Organ Point-Of-Care Ultrasound in Acute Kidney Injury: Editorial
aDivision
of Nephrology, Medical College of Wisconsin, Milwaukee, WI, USA; bDepartment of
Nephrology, International Renal Research Institute of Vicenza (IRRIV), San Bortolo Hospital, Vicenza, Italy;
cDepartment of Medicine, University of Padova, Padova, Italy; dDivision of Nephrology, Hypertension and
Abstract
Acute kidney injury (AKI) is a clinical syndrome caused by a Point-of-care ultrasonography (POCUS) is a limited
multitude of hemodynamic, toxic, and structural insults to bedside ultrasound (US) examination performed by the
the kidney, and portends worse patient outcomes. Despite clinician to answer focused clinical questions and guide
careful history taking, physical examination, and analysis of patient management. Once confined to procedural guid-
laboratory data, a void is evident in the diagnostic process ance, the utility of diagnostic POCUS is being increas-
and clinical monitoring of AKI. Point-of-care ultrasonogra- ingly recognized in the field of nephrology as an adjunct
phy (POCUS) is a limited ultrasound study performed by the to physical examination [1, 2]. In fact, some institutions
clinician at bedside as an adjunct to physical examination. have formally integrated POCUS training into their ne-
Growing body of evidence points to POCUS as a powerful phrology fellowship curricula [3]. While the role of PO-
tool in a variety of clinical settings. Herein, we discuss how CUS has been discussed in a variety of clinical settings, its
nephrologist-performed POCUS has the potential to provide role in acute kidney injury (AKI) remains less well ex-
answers to focused questions that we encounter in diagno- plored.
sis and management of patients with AKI. From excluding AKI is frequently encountered in hospitalized patients
hydronephrosis to providing real-time insights into hemo- and is a clinical manifestation of several pathophysiolog-
dynamics, incorporation of POCUS helps integrate all the ic processes that acutely affect the renal function [4]. It is
pieces of patient data and formulate individualized treat- associated with high mortality rates ranging from 16 to
ment plans. Future studies are needed to evaluate the im- 50% depending on the severity, etiology, comorbidity
pact of multi-organ POCUS on AKI-related pragmatic patient burden, as well as socioeconomic factors [5, 6], which un-
Pneumonia
Heart
Left and right ventricular systolic function
Stroke volume
Pericardial effusion
Venous Doppler
HEPATIC V. Left ventricular filling pressures
Hepatic vein
PORTAL V. Right ventricular sydtolic pressure
Portal vein
Renal parenchymal vein Right atrial pressure by IVC/IJV US
ELEVATED RIGHT
Kidney
HEART PRESSURE Size and echogenicity
Hydronephrosis
Peri-nephric collections
Urinary bladder Resistive index
Fig. 1. Common sonographic parameters and findings assessed using POCUS in AKI. Red and blue arrows indi-
cate blood blow; yellow arrows indicate backward transmission of cardiac pressures. Illustration made using Bio-
render®. IVC, inferior vena cava; IJV, internal jugular vein; US, ultrasound.
derscores the importance of timely diagnosis and appro- The utility of POCUS in discerning the cause of intrin-
priate treatment. The etiology of AKI can be broadly di- sic AKI is limited. Parameters such as cortical echogenici-
vided into hemodynamic causes (i.e., impaired renal per- ty, kidney size, and arterial resistive index (RI) are useful
fusion), obstruction of the urinary tract, and intrinsic when interpreted in the right clinical context but are non-
renal diseases including glomerulonephritis and tubu- specific [11]. For example, enlarged kidneys with pre-
lointerstitial pathology. This classification is rather sim- served parenchymal thickness and altered cortical echo-
plistic; in clinical practice, multiple pathologies can coex- genicity may prompt the nephrologist to pursue work up
ist, and syndrome-based nomenclature might be more for infiltrative diseases such as amyloidosis and malig-
suitable such as cardiorenal, hepatorenal, hepatocardio- nancy although these findings are not diagnostic per se
renal, and sepsis-associated AKI depending on the con- [10, 12]. On the other hand, in instances where baseline
text [7, 8]. In patients presenting with AKI, urinary tract serum creatinine is not available, the likelihood of treat-
obstruction must be excluded as a readily treatable etiol- able disease can be deemed low if the kidney size is small
ogy. As such, a renal sonogram is often obtained as a part and cortical echogenicity is increased [13].
of initial diagnostic work up to rule out hydronephrosis. In our opinion, hemodynamic AKI is where nephrol-
POCUS allows this binary yes-or-no question to be an- ogist-performed POCUS could prove the most helpful.
swered within minutes. Moreover, having first-hand This type of AKI encompasses various insults that result
knowledge of the patient’s history and clinical course is in renal hypoperfusion (e.g., hypovolemia, systemic vaso-
an added advantage for the clinician compared to a radi- dilatation, and increased intra-abdominal pressure) and
ologist. In one study, general internist-performed PO- renal venous congestion. It must be noted that renal per-
CUS had a sensitivity of 90% and specificity of 96% for fusion is determined by the difference between forward
detection of hydronephrosis [9]. Similarly, bladder-relat- flow/mean arterial pressure and venous outflow/right
ed causes of obstruction such as blocked Foley catheter, atrial pressure (RAP). However, clinical assessment had
stone, mass, and prostatomegaly can be identified at the traditionally revolved around the adequacy of forward
bedside by nephrologist using ultrasonography [10]. flow, ignoring the deleterious effect of venous conges-
Na 127 mmol/L Creatinine 2.6 mg/dL AP: Severe congestion, start IV diuretic
Continuous (Normal)
Na 135 mmol/L Creatinine 1.7 mg/dL AP: Improving congestion, transition to oral diuretic
Continuous (Normal)
Na 137 mmol/L Creatinine 1.5 mg/dL (baseline) AP: Improving congestion, discharge with follow up
Fig. 2. Doppler venous waveforms demonstrating improvement influences diuretic absorption. Renal parenchymal vein is normal-
(from top to bottom) in a patient with AKI and hyponatremia. In ly continuous (similar to portal but below-the-baseline) and with
physiologic state, hepatic vein Doppler resembles central venous increasing RAP, becomes pulsatile with distinct S- and D-waves,
trace, and S-wave is larger than the D-wave. As the RAP increases, with S-reversal ultimately like that of hepatic vein. Generally, im-
S-wave reduces in amplitude and finally reverses leaving only D- provement in portal vein precedes that of hepatic and renal veins
wave below the baseline. Portal vein is normally continuous (<30% as seen above. Renal interstitial edema may delay the recovery of
pulsatile) and the pulsatility increases with increasing RAP eventu- venous waveform. Na, serum sodium; AP, assessment and plan;
ally with late-systolic flow reversal (below-the-baseline flow). Pul- S-wave, systolic wave; D-wave, diastolic wave.
satile portal vein might indicate gut congestion, which potentially
tion/iatrogenic fluid overload on the kidney. Accumulat- minister intravenous albumin if the lung US demon-
ing data, however, suggests that fluid overload portends strates congestion, RAP is elevated, or FoCUS reveals
worse outcomes [14]. Adding to the problem, the diag- high cardiac output indicating a vasodilatory state rather
nostic accuracy of conventional physical examination than volume depletion [16]. FoCUS also allows detection
findings is often limited for detecting clinically significant of abnormalities such as cardiac chamber enlargement,
aberrations in fluid status [1]. Multi-organ POCUS aids gross valvular dysfunction, and pericardial effusion
in the objective volume status assessment by facilitating prompting appropriate intervention and/or specialist
comprehensive evaluation of the hemodynamic circuit at consultation. Further, POCUS may provide clues to
the bedside. This involves Pump, Pipes, and Leaks ap- raised intra-abdominal pressure by revealing large asci-
proach where pump represents focused cardiac US (Fo- tes, bowel obstruction or gaseous distension, small IVC
CUS), pipes represent inferior vena cava (IVC) US and discordant with internal jugular vein, and diminished he-
Doppler evaluation of the systemic veins, and the leaks patic vein flow. Figure 1 illustrates the common sono-
indicate assessment of extravascular lung water and asci- graphic findings and parameters used in the evaluation of
tes [15]. In other words, one can assess the forward arte- AKI.
rial inflow, venous outflow, as well as tissue congestion, In addition, serial POCUS examinations can aid in as-
and instantaneously integrate this data with overall clini- sessing the efficacy and adequacy of therapy. For exam-
cal picture to formulate an individualized management ple, in a patient with hypovolemic AKI and/or hypona-
plan for the patient. For instance, in a patient suspected tremia, bedside stroke volume assessment can be used to
to have hepatorenal syndrome, there is no reason to ad- monitor improvement in hemodynamics along with lab-
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