PoCUS can detect signs of kidney disease and urinary tract obstruction (UTO) and is indicated in patients with unexplained kidney dysfunction, hypertension, or suspected urinary tract obstruction. CT or MRI imaging is indicated if a renal mass, abscess, or stone is suspected or unexplained hydronephrosis is detected. Renal and urinary tract PoCUS should include views of both kidneys and the bladder using a curvilinear transducer in abdominal mode. A phased-array transducer can work if a curvilinear transducer isn’t available.
Chronic kidney disease (CKD), defined as persistent proteinuria or reduced estimated glomerular filtration rate, is often associated with chronic viral infections, obesity, hypertension, and diabetes, which increase glomerular filtration on individual nephrons. CKD is usually asymptomatic but may present with fluid retention, hyperkalemia, chronic metabolic acidosis, hypertension, chronic anemia, and cardiovascular disease. In addition, severely uremic patients (end-stage kidney disease) can also develop nausea, vomiting, anorexia, pericarditis, confusion, lethargy, and unresponsiveness.
Assessing renal cortical echogenicity can help identify chronic kidney disease. The renal cortex is typically darker (hypoechoic) than the liver or spleen and is considered hyperechoic when it’s as bright or brighter than the adjacent liver or spleen. This comparison is subjective, technique-dependent, and complicated in patients with an abnormal liver or spleen. Therefore, consider subtle differences less specific and do not rule out intrinsic kidney disease simply because the kidneys do not appear hyperechoic. However, finding hyperechoic renal cortices is correlated with renal histopathologic changes.1
Finding hyperechoic kidneys should prompt measurement of serum creatinine, urea, electrolytes, urinalysis with sediment exam, and consultative renal ultrasound. Also, evaluate for and treat chronic viral infections, obesity, diabetes, cardiovascular disease, and hypertension. Hypertension associated with proteinuria should be treated with an ACE inhibitor or angiotensin II-receptor blocker, as long as the patient does not develop hyperkalemia or more than a 30% increase in serum creatinine. SGLT2 inhibitors, which induce glucosuria, can prevent kidney disease progression and should also be considered in patients with diabetes and chronic kidney disease. Impaired renal function should prompt specific medication changes, such as adjusting doses of renally cleared drugs and avoiding aminoglycosides, NSAIDs, or tenofovir-based antiretroviral therapy. Treat dehydration or volume overload to achieve euvolemia, noting that diuresis may require higher doses or combinations of diuretics. Recommend smoking cessation and a mostly whole-food plant-based diet not too high in salt, protein, or phosphorus. The most significant dietary sources of phosphorus are dairy, meat, poultry, and processed foods and beverages, which often contain hidden phosphorus-rich additives. Oral sodium bicarbonate may improve outcomes as a treatment for CKD-associated metabolic acidosis, and phosphate binders and vitamin-D analogs may be necessary if there is secondary hyperparathyroidism. If the hemoglobin is low, look for other causes and consider treating CKD-associated anemia with an erythropoiesis-stimulating drug. Be aware that uremia-associated platelet dysfunction can elevate bleeding risk. If available, consider early referral to nephrology, especially if there is severe or rapidly progressive renal dysfunction, severe proteinuria, or red-blood-cell casts in the urine. A nephrologist can help initiate and continue the above treatments, identify unusual conditions, and prepare patients who may eventually need dialysis.
PoCUS can easily detect urinary tract obstruction (UTO). This problem is also treatable and relatively common, especially in the elderly and pelvic-cancer-prone populations, such as where schistosomiasis is endemic, and bladder and cervical cancer are more prevalent. Therefore, have a low threshold to assess for UTO in patients with unexplained kidney dysfunction, hypertension, or suspected urinary tract obstruction.
Causes of Urinary Tract Obstruction
Gradual-onset UTO is often asymptomatic with or without a change in urine output. Such patients may complain about a small urine stream, difficulty initiating the stream, urinary frequency, or overflow incontinence. In contrast, rapid-onset obstruction, such as from a kidney stone or blood clot, is often associated with severe pain. Urinary retention increases the probability and severity of urinary tract infections and should be considered in anyone with sepsis and urinary tract symptoms. In addition, obstructive nephropathy (harm to the kidneys) can cause hypertension, hyperkalemic non-gap metabolic acidosis, and acute kidney injury, especially if the obstruction affects both kidneys or the adjacent kidney cannot compensate.
The bladder lies below the bowel, behind the pubic bone, and between the iliac vessels. To estimate bladder volume, obtain longitudinal and transverse views and identify the longest measurements in 3 dimensions. The product of these measurements in centimeters multiplied by 0.7 can give a rough estimate for volume in milliliters. For example, a patient with a 10cm transverse measurement, 10cm longitudinal measurement, and 10cm anteroposterior measurement would have an estimated bladder volume of 700 mL (10cm height x 10cm depth x 10cm width x 0.7 = 700 mL). This estimation will underestimate volume if the bladder shape is more cuboidal and overestimate volume if the shape is more spherical.2 Always encourage the patient to void before performing PoCUS to diagnose obstruction/retention. Normal post-void residual bladder volume is less than 150 mL, and borderline measurements are not specific for obstruction.
Sometimes, the bladder is completely collapsed and challenging to identify. Abdominal free fluid in ascites displaces the bladder anteriorly, lying just behind the pubic bone. Avoid confusing ascites fluid with a distended bladder. PoCUS should be able to identify a bladder catheter and confirm whether it has drained the bladder. Sometimes, PoCUS of the bladder will identify ultrasound artifacts (usually from excess gain), blood clots, pus, stones, other echogenic debris, or wall-based masses of various shapes and sizes. The bladder wall is thicker when the bladder is collapsed, infected/inflamed, hypertrophic from chronic obstruction, or due to a bladder-wall mass. If a mass or significant debris is suspected, prompt surgical or urological referral for possible cystoscopy is indicated.
Transabdominal PoCUS can also be used to make crude measurements of the prostate,3 which is usually considered enlarged if greater than 30mL in volume calculated as width x height x depth x 0.523. However, PoCUS alone cannot reliably distinguish the causes of prostatomegaly, which include benign prostatic hyperplasia (BPH), prostate cancer, and prostatitis/prostatic abscess. More so than absolute size, the extent to which the prostate protrudes into the bladder may be a better predictor of bladder outlet obstruction. Protrusion >1cm has a positive likelihood ratio of 2.4 for having an unsuccessful trial without a catheter.4
PoCUS views of the kidneys can identify hydronephrosis, which is abnormal renal pelvis dilation where hypoechoic areas (fluid) displace the echogenic fat in the center of the kidney extending from the proximal ureter and into the minor calyces. The renal pelvis and proximal ureter should be differentiated from blood vessels using color Doppler mode. Significant hydronephrosis is unlikely to be normal, and a thinning of the renal parenchyma suggests longstanding obstruction and permanent obstructive nephropathy. Mild hydronephrosis may signify urinary tract obstruction but may also be normal, especially with diuresis or pregnancy.5 Therefore, the clinical significance of low-grade hydronephrosis depends directly on the pretest probability of urinary tract obstruction. Thus, if the pretest probability is low, a negative exam means UTO is unlikely. However, if the pretest probability is high, negative or subtle findings should be followed with repeat testing.
Hydronephrosis may be present in the absence of bladder dilation. In that case, the patient should receive CT scanning to identify the obstruction and determine if ureteral or percutaneous nephrostomy or other procedures are necessary. Treat bladder outlet obstruction or urinary retention with catheter drainage, employing surgical or urology assistance if needed. If bladder distention is not obviously mechanical, consider medical interventions that promote bladder emptying, such as starting an alpha-adrenergic antagonist like tamsulosin, treating constipation, and stopping/reducing drugs associated with urinary retention such as opioids, alpha-adrenergic agonists (amphetamines, decongestants), non-steroidal anti-inflammatory drugs, calcium-channel blockers, anticholinergic drugs like chlorpromazine (CPZ), amitriptyline, antispasmodics (hyoscine butylbromide, cyclobenzaprine), antiparkinsons drugs, first-generation antihistamines (chlorpheniramine, promethazine, diphenhydramine, prochlorperazine), and over-active bladder treatments like oxybutynin.6
When severe UTO is relieved, patients may develop sustained polyuria for hours to days. This is termed post-obstructive diuresis and can lead to dehydration and hyponatremia. Cerebral edema may occur if serum sodium and BUN drop rapidly. These patients need close monitoring and isotonic fluid, potassium, and magnesium replacement as needed. However, excess IV fluid administration may prolong the problem, and permitting mild to moderate hypovolemia may help promote compensatory fluid and salt retention.