Acute renal colic is a severe form of sudden flank pain that typically originates over the costovertebral angle and extends anteriorly and inferiorly towards the groin or testicle. It is often caused by acute obstruction of the urinary tract by a calculus and is frequently associated with nausea and vomiting. The degree of pain is related to the degree of obstruction and not the size of the stone, although stone size can be a reasonable predictor of the likelihood of spontaneous passage. While kidney stones are not the only cause of flank pain, their frequency, and the severity of the pain they cause makes nephrolithiasis the most likely presumptive diagnosis when sudden flank pain occurs.
Nephrolithiasis, also known as kidney stones, is a common condition affecting 5% to 15% of the population at some point, with a yearly incidence of 0.5% in North America and Europe, and is usually caused by a crystal or crystalline aggregate traveling from the kidney through the genitourinary system and becoming stuck creating an obstruction to urinary flow, typically in the ureter. This obstruction results in proximal ureteral and renal pelvic dilation which is the immediate cause of the intense pain known as renal colic.
While the nature and onset of the pain depends on the underlying cause, its exact location, and severity, for most patients the pain peaks at about 1 to 2 hours after its initial onset.
Renal colic is caused by dilation of the renal pelvis and ureteral segments. While usually colic is from an acute obstruction such as a ureteral calculus, it may also be due to a variety of other problems and disorders such as from ureteral spasms immediately after double J stent removal or ureteroscopy. Similar ureteral blockages from chronic sources (such as ureteropelvic junction obstructions, prostate, cervical or pelvic cancer, scarring and retroperitoneal fibrosis among others), do not generally cause acute pain or colic.
Flank pain can be caused by multiple etiologies. These include:
Ureteral calculi are a common cause of the most acute and severe level of flank pain. The bulk of this review will therefore focus on renal colic from obstruction by a ureteral stone.
Approximately 5% to 15% of the population will be affected by a kidney stone, and of those, 50% will have a recurrent stone within five to seven years of the initial presentation if preventive measures are not taken. Over 70% of stones occur in people 20 to 50 years old, and they are more common in men than women by a factor of about 2:1. Patients with obesity, hypertension, a positive family history of nephrolithiasis, irritable bowel syndrome and/or diabetes are at increased risk for kidney stone formation.
As a stone moves from the renal collecting system, it can significantly affect the genitourinary tract. It can cause constant or intermittent obstruction and hydronephrosis of the ureter, causing urine to back up into the kidney. Intermittent obstruction often causes longer-lasting discomfort and pain than a constant blockage where compensatory mechanisms can offset the increased ureteral intraluminal pressure to some degree. An acute ureteral obstruction causes a decrease in the glomerular filtration rate of the affected kidney and increases urine excretion by the unaffected renal unit as well as very severe, excruciating pain. Complete obstruction of the ureter can lead to the eventual loss of renal function, with damage becoming irreversible, possibly starting at just one to two weeks. Additionally, there is a risk of rupture of a renal calyx with the development of a urinoma. Of even more concern is the possibility that an obstructed renal unit might become infected, causing obstructive pyelonephritis or pyonephrosis. This condition can be life-threatening and requires immediate surgical drainage as antibiotics alone will be ineffective.
Renal calculi can become impacted, most commonly at one of three locations: 1) at the ureteropelvic junction, as the renal pelvis narrows abruptly to meet the ureter, 2) near the pelvic brim, where the ureter takes a posterior turn, or 3) at the ureterovesical junction which is the narrowest portion of the ureter.
Pain is the result of a combination of ureteral muscle spasms, increased proximal peristalsis from activation of intrinsic ureteral pacemakers, stone-induced localized inflammatory changes, renal swelling with capsular stretching, edema, and irritation. These processes stimulate submucosal stretch receptors in the ureter, renal pelvis, and capsule which are a direct cause of pain. Of all the various factors that can contribute to flank pain and renal colic, stimulation of the renal pelvis, peripelvic renal capsule, and calices from stretching most closely mimics typical renal colic.
The immediate effect of a newly obstructing ureteral stone is to increase proximal intraluminal pressure which initially distends the renal pelvis and increases ureteral peristalsis. Peak renal pelvic pressure from a high-grade obstruction is usually obtained within two to five hours of a complete ureteric obstruction. Other changes in the kidneys after a complete ureteral blockage include pyelolymphatic and pyelovenous backflow. Interstitial renal edema develops which significantly increases lymphatic drainage from the affected kidney and stretches the renal capsule leading directly to painful stimuli from capsular stretch receptors.
Often, a state of equilibrium will be achieved as the increasing proximal ureteral dilation allows some urine to pass around the obstruction which is enough, along with the other compensatory measures, to relieve the pain and achieve stability.
Pain fibers are primarily through the preganglionic sympathetic nerves and the ascending spinothalamic tracts. When the stone approaches the intramural ureter, the nervi erigentes can become involved which can cause various bladder symptoms including frequency, urgency, dysuria, hesitancy and difficulty in voiding.
Renal blood flow increases for the first 90 minutes after initial ureteral blockage before diminishing. This is caused by vasodilation of the afferent preglomerular arterial blood supply. By five hours after the ureteral obstruction, renal blood flow and ureteral intraluminal pressures have decreased back to normal or below. Over time, renal blood flow tends to slowly diminish. After three days, renal blood flow has dropped to about half from the normal baseline and this continues to slowly diminish over time. By eight weeks, renal blood flow is only 12% of its prior, normal baseline value. Even then, the dilation and hydroureteronephrosis usually remains but ureteral peristalsis has almost disappeared. Renal blood flow in teh contralateral kidney has increased at this point.
Nausea and vomiting is associated with classic renal colic in about half or more of patients with acute obstructing calculi. This is due to a common innervation pathway between the kidneys and the GI tract embryologically through afferents of the vagus nerve and celiac axis. This effect can be exacerbated by NSAIDs and opioid medications that have GI side effects.
Patients with renal colic typically present with sudden onset of flank pain radiating laterally to the abdomen and/or to the groin. Patients often report a dull constant level of pain with colicky episodes of increased pain. The constant pain is often due to stretching of the renal capsule due to obstruction, whereas colicky pain can be caused by peristalsis of the ureteral smooth muscle. Many patients report associated nausea or vomiting, and some may report gross hematuria. As the stone migrates distally and approaches the bladder, the patient may experience dysuria, urinary frequency, urgency, or difficulty in urination.
Patients experiencing renal colic may present in very severe pain. Classically, these patients are unable to find a comfortable position and are often writhing or constantly pacing around the examination table. The exam may reveal flank pain more commonly than abdominal pain, and the skin may be cool or diaphoretic. There is often a prior personal or family history history of stones, recent ureteroscopic surgery, or just after removal of a double J stent.
In the case of recent ureteroscopy or immediately after removal of a double J stent, the history alone can provide the diagnosis. In these cases, the renal colic is due to ureteral spasm which effectively causes an obstruction with resultant proximal ureteral and renal dilation even without a stone. The pain can be just as intense as from an obstructing ureteral stone.
Diagnosis is made through a combination of history and physical exam, laboratory testing, and imaging studies. Urinalysis shows some degree of microscopic or gross hematuria in 85% of stone patients, but should also be evaluated for signs of infection (e.g., white blood cells, bacteria). Urinary pH greater than 7.5 may be suggestive of a urease producing bacterial infection, while pH values less than 5.5 may indicate the presence of uric acid calculi.
A basic metabolic panel (BMP) should be obtained to assess for renal function, dehydration, acid-base status, and electrolyte balance. Serum calcium should be checked. A complete blood count (CBC) can be considered to evaluate for leukocytosis if there is a concern for infection although a mild elevation of WBCs is common secondary to white blood cell demargination.
Hematuria is present in 85% of acute renal colic cases caused by calculi. While the presence of hematuria is suggestive of a stone, it is not definitive and neither does the absence of hematuria prove that a stone is not present.
Consider obtaining a parathyroid hormone (PTH) level if hypercalcemia is present and therefore primary hyperparathyroidism is suspected. If possible, urine should be strained to capture stones for chemical analysis to help determine optimal preventive prophylactic measures. Further metabolic testing, such as a 24-hour urine collection for volume, pH, calcium, oxalate, uric acid, citrate, sodium, magnesium and potassium concentrations, should be considered in high-risk first-time stone formers, pediatric patients or recurrent stone formers. It is highly recommended in nephrolithiasis patients with solitary kidneys, renal failure, renal transplants, gastrointestinal (GI) bypass, and any patient with high or increased anesthesia risk.
Renal ultrasonography can be used to establish hydronephrosis and measure resistive index and track larger renal stones (especially uric acid), but it will often miss stones smaller than 5 mm in size and is not a reliable imaging modality for visualizing ureteral calculi. The degree of perinephric fluid can be a predictor of the degree of obstruction. Resistive index can be useful in diagnosing ureteral obstructions. It is defined as (peak systolic velocity - end diastolic velocity)/ peak systolic velocity) where normal is typically 0.7 or less. Higher levels indicate either obstruction or intrinsic renal disease. 
Unenhanced (or helical) CT is the gold standard for the initial diagnosis of suspected renal colic; with a sensitivity of 98%, the specificity of 100%, and negative predictive value of 97%. This modality allows rapid identification of stone, provides information as to the location and size of the stone, and any associated hydroureter, hydronephrosis, or ureteral edema, and can give information regarding potential other etiologies of pain (e.g., abdominal aortic aneurysm, malignancy). In those patients with no previous history of nephrolithiasis, CT should be performed to guide management. CT scans may underestimate stone size in comparison with an intravenous pyelogram or abdominal x-ray.
However, CT scans do expose patients to a significant radiation burden and they can be costly. In some patients with a history of renal colic that present with pain similar to previous obstructing urolithiasis, it may be sufficient to perform ultrasonography (US). While US is less sensitive (60% to 76%) than CT for detecting calculi less than 5 mm, it can reliably detect hydronephrosis and evidence of obstruction (increased resistive index in the affected kidney). It is also the modality of choice for evaluating a pregnant patient with concern for renal colic. Studies have shown that using ultrasonography as a primary imaging modality does not lead to an increase in complications in comparison to CT. Ultrasound is also a good way to follow a patient known to have uric acid urinary stones.
An abdominal x-ray (KUB) can identify many stones, but 10% to 20% of renal calculi are radiolucent and provide little information regarding hydronephrosis, obstruction, or the renal anatomy. Additionally, bowel gas, the bony pelvis, and abdominal organs may obstruct stone visualization. The KUB is recommended in kidney stone cases when the CT scan is positive, and the exact location of the stone is known. This helps in clearly identifying those stones that can be tracked by follow-up KUB and those that might be amenable to lithotripsy.
Combining renal ultrasound (which can easily demonstrate hydronephrosis but is less reliable in detecting stones) with a KUB (which has good sensitivity for imaging calculi but not dilation), can be very cost effective as an alternative to CT scans with lower cost and reduced radiation. Symptomatic stones are likely to produce hydronephrosis or obstruction (visible on ultrasound) or will be seen directly on the KUB. The combination of KUB radiography with renal ultrasonography provides a reported diagnostic accuracy for an obstructing stone of 90%, specificity of 93%, and a sensitivity of 88%.
If the stone should pass before imaging can be performed, some evidence of residual inflammation may remain, such as hydronephrosis or pain, even if no stone is specifically or definitively identified.
Treatment includes the following:
Calculus size, location, and patient discomfort predict the likelihood of spontaneous stone passage. Approximately 90% of stones less than 5 mm pass within four weeks. Up to 95% of stones larger than 8 mm can become impacted, requiring intervention to pass.
Indications for hospital admission include a significant renal stone in a solitary kidney, severe kidney injury, an infected renal stone, intractable pain or nausea, urinary extravasation, or hypercalcemic crisis.
Patients with infected stones (e.g., nephrolithiasis plus evidence of urinary tract infection) require special and more urgent treatment. The infected stone acts as a nidus for infection and leads to stasis, decreasing the ability to manage infections. Frequently, these stones need to be removed in their entirety operatively to prevent a repeat infection and the formation of new stones.
Intervention for a stone is recommended by 4 weeks with no changes even if the patient is asymptomatic. This is due to the likelihood of scarring and other complications. It can be difficult to convince an asymptomatic patient to agree to a surgery. We have found the most effective technique is to explain the policy early so patients understand the need for a procedure if a stone or obstruction appears stuck and is not resolving on its own.
24-hour urine tests are the cornerstone of long-term preventive therapy, but they require very high levels of patient dedication and compliance to be successful. Nevertheless, they should be offered to all nephrolithiasis patients; especially those with recurrent stones and a high risk of new stone formation.
The management of renal stones is by an interprofessional team that consists of a nephrologist, emergency department physician, radiologist, urologist, and a primary care provider. The majority of renal stones pass within four weeks, but stones larger than 8 mm may require some intervention before they can pass. Healthcare workers, including nurse practitioners who see patients with kidney stones, should contact the urologist when large stones fail to pass. Urologic nurses are involved in treatment, monitor patients, and update the team on changes in patient status. Pharmacists review prescribed medications for appropriate dosages, interactions, and provide patient education. In some cases of infected stones, surgery may be required. Because the recurrence of kidney stones is common, the patient should be educated on fluid intake and avoidance of certain foods. The prognosis for most patients with kidney stones is good. [Level 5]
|||Ganti S,Sohil P, Renal Colic: A Red Herring for Mucocele of the Appendiceal Stump. Case reports in emergency medicine. 2018; [PubMed PMID: 30631605]|
|||Kutilek S,Plasilova I,Chrobok V, Two Different Causes of Paediatric Hypercalcaemia. Sultan Qaboos University medical journal. 2018 Aug; [PubMed PMID: 30607285]|
|||Nadav G,Eyal K,Noam T,Yeruham K, Evaluation of the clinical significance of sonographic perinephric fluid in patients with renal colic. The American journal of emergency medicine. 2018 Dec 20; [PubMed PMID: 30595428]|
|||Gandhi A,Hashemzehi T,Batura D, The management of acute renal colic. British journal of hospital medicine (London, England : 2005). 2019 Jan 2; [PubMed PMID: 30592663]|
|||Kominsky H,Rose J,Lehman A,Palettas MS,Posid T,Caterino J,Knudsen BE,Sourial MW, Trends in acute pain management for renal colic in the emergency department at a tertiary care academic medical center. Journal of endourology. 2020 Jul 15; [PubMed PMID: 32668985]|
|||Motov S,Drapkin J,Butt M,Thorson A,Likourezos A,Flom P,Marshall J, Analgesic Administration for Patients with Renal Colic in the Emergency Department Before and After Implementation of an Opioid Reduction Initiative. The western journal of emergency medicine. 2018 Nov; [PubMed PMID: 30429938]|
|||Terry RS,Preminger GM, Metabolic evaluation and medical management of staghorn calculi. Asian journal of urology. 2020 Apr [PubMed PMID: 32257805]|
|||Аgenosov MP,Каgan OF,Khеyfets VK, [Features of urolithiasis in patients of advanced and senile age.] Advances in gerontology = Uspekhi gerontologii. 2018; [PubMed PMID: 30584876]|
|||D'Costa MR,Pais VM,Rule AD, Leave no stone unturned: defining recurrence in kidney stone formers. Current opinion in nephrology and hypertension. 2018 Dec 5; [PubMed PMID: 30531469]|
|||Raja AS,Pourjabbar S,Ip IK,Baugh CW,Sodickson AD,O'Leary M,Khorasani R, Impact of a Health Information Technology-Enabled Appropriate Use Criterion on Utilization of Emergency Department CT for Renal Colic. AJR. American journal of roentgenology. 2019 Jan; [PubMed PMID: 30403534]|
|||Piazzese EM,Mazzeo GI,Galipò S,Fiumara F,Canfora C,Angiò LG, The renal resistive index as a predictor of acute hydronephrosis in patients with renal colic. Journal of ultrasound. 2012 Dec [PubMed PMID: 23730388]|
|||Nicolau C,Claudon M,Derchi LE,Adam EJ,Nielsen MB,Mostbeck G,Owens CM,Nyhsen C,Yarmenitis S, Imaging patients with renal colic-consider ultrasound first. Insights into imaging. 2015 Aug [PubMed PMID: 25994497]|
|||Thungkatikajonkit P,Wongwaisayawan S,Wibulpolprasert A,Viseshsindh W,Kaewlai R, Is Combined Ultrasound with Radiography Sufficient for the Diagnosis of Obstructive Ureteric Stone in Patients with Acute Flank Pain? Journal of medical ultrasound. 2020 Apr-Jun [PubMed PMID: 32874866]|
|||Masic D,Liang E,Long C,Sterk EJ,Barbas B,Rech MA, Intravenous Lidocaine for Acute Pain: A Systematic Review. Pharmacotherapy. 2018 Dec; [PubMed PMID: 30303542]|
|||Mulay SR,Shi C,Ma X,Anders HJ, Novel Insights into Crystal-Induced Kidney Injury. Kidney diseases (Basel, Switzerland). 2018 Jun; [PubMed PMID: 29998119]|
|||Rodger F,Roditi G,Aboumarzouk OM, Diagnostic Accuracy of Low and Ultra-Low Dose CT for Identification of Urinary Tract Stones: A Systematic Review. Urologia internationalis. 2018; [PubMed PMID: 29649823]|
|||Maldonado-Avila M,Del Rosario-Santiago M,Rosas-Nava JE,Manzanilla-Garcia HA,Rios-Davila VM,Rodriguez-Nava P,Vela-Mollinedo RA,Garduño-Arteaga ML, Treatment of reno-ureteral colic by twelfth intercostal nerve block with lidocaine versus intramuscular diclofenac. International urology and nephrology. 2017 Mar [PubMed PMID: 27995373]|
|||Nikiforov S,Cronin AJ,Murray WB,Hall VE, Subcutaneous paravertebral block for renal colic. Anesthesiology. 2001 Mar [PubMed PMID: 11374617]|
|||Kapural L,Lee N,Badhey H,McRoberts WP,Jolly S, Splanchnic block at T11 provides a longer relief than celiac plexus block from nonmalignant, chronic abdominal pain. Pain management. 2019 Mar 1 [PubMed PMID: 30681022]|
|||Leslie SW,Sajjad H,Bashir K, 24-Hour Urine Testing for Nephrolithiasis Interpretation . 2020 Jan [PubMed PMID: 29494055]|