Jorge Lamarche, Alfredo Peguero Rivera, Craig Courville, Mohamed Taha, and Marina Antar-Shultz are Academic Nephrology Attending Physicians at the James A. Haley Veterans' Hospital and Assistant Professors at the University of South Florida Department of Nephrology and Hypertension, all in Tampa, Florida. At the time the article was written Andres Reyes was a Medical Fellow at the University of South Florida. Correspondence: Jorge Lamarche (jorge.lamarche@va.gov)
Author disclosures The authors report no actual or potential conflicts of interest with regard to this article.
Disclaimer The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies.
Sonographic inferior vena cava (IVC) luminal diameter and inspiratory collapsibility together serve as a surrogate marker of preload venous return and right side heart function. Such imaging results have been shown to be more accurate than jugular venous distension on physical examination but only modestly helpful as a surrogate for central venous pressure (CVP), with more accuracy in the lower values of the CVP.11 However, this procedure can be repeated often after volume resuscitation to achieve a 1.5- to 2.5-cm diameter dimension of the IVC and < 25% inspiratory collapsibility as a goal.
An IVC with a diameter > 2.5 cm in the context of a suspected prerenal AKI is more likely the consequence of heart failure (HF) rather than hypovolemia. The caveat to this finding is that pulmonary hypertension may induce false-positive results.12,13 Hepatic vein dilation is another sign of HF and/or pulmonary hypertension. Furthermore, sonographic images of the left ventricle either from the parasternal long axis or subxiphoid approach can identify supranormal left ventricular ejection fraction (LVEF) or hyperdynamic heart as an important clue of the absolute or relative decrease of EACF.14 Conversely, a decrease in EACF in patients with low LVEF can be assessed qualitatively at the bedside in patients with systolic HF. Supporting evidence of prerenal azotemia as the result of HF can be suggested by the presence of pleural effusions and bilateral comet/rockets tails or B lines in lung sonography.15
The easily recognizable hypoechoic ascitic fluid in the presence of small, hyperechoic gross changes in the echocardiographic texture of liver may indicate a hepatorenal component as the cause of prerenal failure. A small increase of > 20% in the diameter of the portal vein with deep inspiration indicates portal hypertension, with a sensitivity of 80% and a specificity of 100%.15,16 Other clinical scenarios leading to AKI in association with systemic hypotension may be identified quickly with the aid of POC sonography. These scenarios include cardiac tamponade, tension pneumothorax, right ventricular dysfunction (as a surrogate of pulmonary embolism), or an acute coronary event.16,17 Alternatively, identifying the presence of severe left ventricular hypertrophy through POC ultrasonography in a patient with AKI and normal or low normal blood pressures may alert clinicians to the diagnosis of normotensive renal failure in individuals with previously unrecognized severe hypertension. In this clinical context, keeping mean arterial pressures higher than usual with vasopressors may improve renal function while decreasing dialysis utilization.18-21
Likewise, in clinical scenarios of shock with AKI, POC ultrasonography has proven to be an indispensable tool. For example, rapid exploration of the biliary tree demonstrating anterior gallbladder wall thickening, a stone or sludge, common bile duct dilation, or perigallbladder inflammation suggests acute cholecystitis and/or cholangitis as the cause. The presence of dyspnea in association with hypotension and unilateral signs of a higher proportion of comet tails and/or a lung consolidation suggests pneumonia. Rapid differentiation between acute respiratory distress syndrome (ARDS) and pulmonary edema from HF is possible with ultrasonography. When pleural line abnormalities are seen, ARDS is a common cause.
POC ultrasonography will be key in management of ARDS, as ultrasound results will help avoid the use of excessive diuretics, which can result in renal hypoperfusion and AKI.22 In trauma patients, the ultrasound examination will identify free fluid (bleeding) as the source of the prerenal failure, along with its cause (aortic dissection, hepatic hemorrhage, splenic hemorrhage, ectopic pregnancy, etc).23 Sonographic free air observed in the abdomen can provide the clue of a perforated viscus.24 The sonographic image of an inflamed pancreas can suggest pancreatitis as the cause of the systemic hypotension. Ultimately, intravascular losses in the hypoechoic edematous bowel wall in obstruction, ileus, pseudomembranous, or infectious or autoimmune enterocolitis can lead to significant decreases in the EACF and cause prerenal injury.
