Acute Renal Colic


Article Author:
Laryssa Patti


Article Editor:
Stephen Leslie


Editors In Chief:
Sebastiano Cassaro
Joseph Lee
Tanya Egodage


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes


Updated:
5/18/2019 9:16:51 PM

Introduction

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 caused by a crystal or crystalline aggregate traveling from the kidney through the genitourinary system. [1] [2] [3] [4] 

Etiology

There are multiple predictors and risk factors for stone formation. The following are the most common:

  1. Inadequate urinary volume. Patients with low urine volumes (usually less than 1 L per day) increase the concentration of solutes (indicated by a urine with an osmolarity greater than 600 mOsm/kg) and promote urinary stasis, which can cause supersaturation of solutes and lead to stone formation.
  2. Hypercalciuria. Most often this is an idiopathic finding, although it can be secondary to increased intestinal absorption of calcium, increased circulating calcium, hypervitaminosis D, hyperparathyroidism, high protein load, or systemic acidosis. Hypercalciuria increases the saturation of calcium salts like oxalate and phosphate, causing the formation of crystals. Calcium containing stones form approximately 80% of all renal stones.  Hypercalciuria is usually defined as urinary calcium of 250 mg or more per 24 hours.
  3. Elevated urine levels of uric acid (uric acid stones account for 5% to 10% of all renal calculi), oxalate, sodium urate, or cystine. Often these can be secondary to a high protein diet, high oxalate diet, or a genetic defect causing increased excretion. Most pure uric acid stones are caused by high urinary total acid levels and not by elevated urinary uric acid.
  4. Infection stones. These are caused by urea-splitting organisms (Proteus or Klebsiella spp but not E. coli), that break down urea in the urine, increasing concentrations of ammonia and pH which promote stone formation and growth. Also called struvite or triple phosphate (Magnesium, Ammonium, Calcium) stones.
  5. Inadequate urinary citrate levels. Citrate is the urinary equivalent of serum bicarbonate. It increases urinary pH, but it also acts as a specific inhibitor of crystal aggregation and stone formation. Optimal levels are approximately 250 mg/L to 300 mg/L of urine.

Epidemiology

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 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, and/or diabetes are at increased risk for kidney stone formation.[5][6][7]

Pathophysiology

As a stone moves from the renal collecting system, it can significantly affect the genitourinary tract. A stone can cause obstruction and hydronephrosis of the ureter, decreasing the rate of ureteral peristalsis and causing urine to back up into the kidney. This can cause decreases in the glomerular filtration rate of the affected kidney, and increase renal excretion of the unaffected kidney as well as very severe, excruciating pain. Complete obstruction of the ureter can lead to eventual loss of renal function, with damage becoming irreversible in 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 an obstructive pyelonephritis or pyonephrosis. This condition can be life-threatening and requires immediate surgical drainage as antibiotics alone are ineffective

Renal calculi can become impacted, most commonly at the ureteropelvic junction (the renal pelvis narrows abruptly to meet the ureter), near the pelvic brim, or at the ureterovesical junction.

History and Physical

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 genitourinary tract smooth muscle against the obstruction. 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 on or 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 history of stones or a family history.

Evaluation

Diagnosis is made through a combination of history and physical exam, laboratory 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 less than 5.5 may indicate the presence of uric acid calculi.

Basic metabolic panel (BMP) should be obtained to assess for renal function, dehydration, acid-base status, calcium and electrolyte balance. Complete blood count (CBC) can be considered to evaluate for white blood cell count (mild elevation is commonly secondary to white blood cell demargination) if there is a concern for infection.

Consider obtaining a parathyroid hormone (PTH) level if primary hyperparathyroidism is suspected as a cause of any hypercalcemia. If possible, urine should be strained to capture stones for analysis to help determine if there is a reversible or preventable cause of stone development. Further metabolic testing (24-hour urine collection for volume, pH, calcium, oxalate, uric acid, citrate, sodium, and potassium concentrations) should be considered in high-risk first-time stone formers, pediatric patients or recurrent stone formers. It is highly recommended in kidney stone patients with solitary kidneys, renal failure, renal transplants, gastrointestinal (GI) bypass, and any patient with high or increased anesthesia risk.

Unenhanced (or helical) CT is the gold standard of initial diagnosis, with a sensitivity of 98%, specificity of 100%, and negative predictive value of 97%. This modality allows rapid identification of a 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 scan does expose patients to a radiation burden and it can be costly. In some patients with a history of renal colic that present with pain similar to previous episodes of renal colic, it may be sufficient to perform ultrasonography (US). However, US is less sensitive (60% to 76%) than CT for detecting calculi less than 5 mm, but 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 stones.

An abdominal x-ray (KUB) can identify many stones, but 10% to 20% of renal stones are radiolucent and provide little information regarding hydronephrosis, obstruction or the kidneys. Additionally, bowel gas, the bony pelvis and abdominal organs may obstruct visualization of a stone.  The KUB is recommended in kidney stone cases when the CT can is positive and the exact location of the stone is known.  This helps in clearly identifying those stones that can be tracted by follow-up KUB and those that might be amenable to lithotripsy.

Using both a KUB and a renal US is a reasonable alternative to a CT scan and far cheaper with less radiation exposure. Symptomatic stones are likely to produce hydronephrosis or obstruction (visible on ultrasound) or will be seen directly on the KUB or the ultrasound.

Treatment / Management

Treatment includes the following:

  1. Immediate intervention with analgesia and antiemetics. NSAIDs and opiates are first line therapies for analgesia. NSAIDs work in two ways in renal colic. First, NSAIDs decrease the production of arachidonic acid metabolites, which mediate pain receptors, alleviating pain caused by dissension of the renal capsule. Additionally, they cause contraction of the efferent arterioles to the glomerulus, causing a reduction in glomerular filtration, and reducing hydrostatic pressure across the glomerulus. Because patients are frequently unable to tolerate oral medications, parenteral NSAIDs like ketorolac (15 mg to 30 mg intravenously (IV) or intramuscularly (IM)) or diclofenac (37.5 mg IV) are most commonly used. 
  2. Successful use of intravenous lidocaine for renal colic has been reported. The protocol is to inject lidocaine 120 mg in 100 mL normal saline intravenously over 10 minutes for pain management. It has been quite effective for intractable renal colic unresponsive to standard therapy and typically starts to work in 3-5 minutes. No adverse events have been reported.
  3. Opiate pain medication, such as morphine sulfate (0.1 mg/kg IV or IM) or hydromorphone (0.02 mg/kg IV or IM), can also be used effectively for analgesia, especially when other measures have failed. However, opiates are associated with respiratory depression and sedation, and there is a risk of dependence associated with prolonged opiate use. 
  4. Fluid hydration. Although there is no evidence to support that empiric fluid will help “flush out” a stone, many patients are dehydrated secondary to decreased oral intake or vomiting and can benefit from hydration.
  5. Medical expulsive therapy. Alpha 1 adrenergic receptors exist in increasing concentration in the distal ureter. The use of alpha blockade medications (for example, tamsulosin or nifedipine) is theorized to facilitate stone passage by decreasing intra-ureteral pressure and dilating the distal ureter. However, data from randomized control trials is somewhat mixed as to whether these medications improved stone passage. The consensus opinion is they may be helpful in smaller stones in the lower or distal ureter.  They are probably of little use in larger stones in the proximal ureter.
  6. Definitive management of impacted stones. There are several invasive methods to improve stone passage. These include shock wave lithotripsy, in which high energy shock waves are used to fragment stones, ureteroscopy with either laser or electrohydraulic stone fragmentation, or in rare cases, open surgery.  In the presence of infection, a double J stent or percutaneous nephrostomy may be used to help with urinary drainage of the affected renal unit and definitive stone therapy postponed until the patient is stable.
  7. Behavior modification and preventative management. Increase fluid intake to optimize urine output with a goal of 2 L to 2.5 L of urine daily. Patients with calcium stones and high urine calcium concentrations should limit sodium intake and have a goal of a moderate calcium intake of 1000 mg to 1200 mg dietary calcium daily. Those with calcium stones and low urinary citrate or those with uric acid stones and high urinary uric acid should increase intake of fruits and vegetables and decrease non-dairy animal protein. They may benefit from potassium citrate supplementation. Uric Acid stone formers are usually best treated with potassium citrate (urinary alkalinizer) to a pH of 6.5.  Hyperuricosuric calcium stone formers can benefit from allopurinol. Thiazide diuretics are indicated in those with high urinary calcium and recurrent calcium stones to reduce the amount of urinary calcium. Patients with hyperoxaluria should be encouraged to lower their oxalate intake (spinach, nuts, chocolate, green leafy vegetables). [8][9][10]

Pearls and Other Issues

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 admission include a 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 new stone formations.

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 patients with recurrent stones and a high risk of new stone formation.

Enhancing Healthcare Team Outcomes

The management of renal stones is by a multidisciplinary team that consists of a nephrologist, emergency department physician, radiologist, urologist, and an internist. The majority of renal stones pass within four weeks but stones larger than 8 mm may require some type of 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. In some cases of infected stones, surgery may be required. Because recurrence of kidney stone 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.

 

 

 


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Acute Renal Colic - Questions

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A 33-year-old male presents to the emergency department with severe pain radiating from his left flank to his groin. The pain is colicky in nature. On exam, the patient appears to be in acute distress. He is tachycardic and diaphoretic and has left costovertebral tenderness. Urinalysis shows greater than 180 RBCs and 3+ blood. What is the best way to make the diagnosis?



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A 30-year-old female presents to the emergency department with severe pain in her right groin. She appears pale and diaphoretic, and in wretching into a basin. She reports that she has had similar pain with menses, but this pain is more severe, and usually does not have accompanying nausea or vomiting. She is unable to tolerate a physical examination due to pain and is pacing around the exam room. Her urine pregnancy test is negative, and urine dipstick shows 3+ blood. What is the next best step in the management of this patient?



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A 25-year-old female patient presents to the emergency department complaining of flank pain radiating to the groin consistent with previous episodes of renal colic. She is found to be febrile to 101.3 degrees F, with a heart rate of 125 bpm and respiratory rate 22/min. Her white blood cell count is 16,000 cells/mm3, and her urine analysis shows blood 3+, leukocyte esterase positive, nitrite positive, >182 white blood cells per field, >182 red blood cells per high power field, and many bacteria. What is the next appropriate step in management?



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A patient is being evaluated in the emergency department for renal colic. He has been treated with a 0.1 mg/kg intravenous dose of morphine and 1 L normal saline bolus over 30 minutes. He received the morphine approximately 20 minutes ago but is complaining of worsening pain. What is the best next step?



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A 54-year-old male presents to the emergency department for evaluation of sudden onset right flank pain that radiates to his right groin. It is associated with nausea, vomiting, diaphoresis, and fever. The patient's temperature is 38 C (102 F), urinalysis shows > 180 RBC, > 180 WBC, many bacteria, positive nitrites, and positive leukocyte esterase. Helical CT of the abdomen and pelvis shows an obstructing stone in the right ureteropelvic junction (UPJ) with associated moderate right hydronephrosis and perinephric stranding consistent with pyelonephritis. What is the next appropriate step in managing this patient?



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A 24-year-old male presents to the emergency department for evaluation of renal colic. He is found to have a 7mm obstructing stone in the right mid-ureter with moderate hydronephrosis. His urinalysis shows 3+ RBCs, moderate blood, and many oxalate crystals. His creatinine is 0.9 mg/dL. He has had multiple episodes of vomiting in the emergency department despite treatment with multiple doses of ondansetron, metoclopramide, and analgesics. Which of the following in the patient's history is an indication for admission?



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A 22-year-old male presents to the hospital complaining of acute right flank pain associated with nausea and vomiting. He denies trauma, fever, or chills. He reports mild diaphoresis. He has a history of renal colic in the past and states that this pain is very similar to previous episodes. What is the best initial test to confirm the recurrence of renal colic?



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Acute Renal Colic - References

References

Ganti S,Sohil P, Renal Colic: A Red Herring for Mucocele of the Appendiceal Stump. Case reports in emergency medicine. 2018;     [PubMed]
Kutilek S,Plasilova I,Chrobok V, Two Different Causes of Paediatric Hypercalcaemia. Sultan Qaboos University medical journal. 2018 Aug;     [PubMed]
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]
Gandhi A,Hashemzehi T,Batura D, The management of acute renal colic. British journal of hospital medicine (London, England : 2005). 2019 Jan 2;     [PubMed]
Аgenosov MP,Каgan OF,Khеyfets VK, [Features of urolithiasis in patients of advanced and senile age.] Advances in gerontology = Uspekhi gerontologii. 2018;     [PubMed]
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]
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]
Masic D,Liang E,Long C,Sterk EJ,Barbas B,Rech MA, Intravenous Lidocaine for Acute Pain: A Systematic Review. Pharmacotherapy. 2018 Dec;     [PubMed]
Mulay SR,Shi C,Ma X,Anders HJ, Novel Insights into Crystal-Induced Kidney Injury. Kidney diseases (Basel, Switzerland). 2018 Jun;     [PubMed]
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]

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