Acute Kidney Colic/Acute renal colic is severe pain resulting from the presence of a stone in the urinary system. The stone can be present anywhere along the path between the kidneys and the urethra. Nephrolithiasis refers to kidney stones, or renal calculi, and, in conjunction with ureteral calculi, are the primary cause of acute renal colic. Nephrolithiasis has a lifetime prevalence of five to fifteen percent and an incidence of 0.5% in North America and Europe. This activity reviews the evaluation and management of nephrolithiasis and highlights the role of the interprofessional team in caring for patients affected by this condition.
Renal colic is a type of abdominal pain commonly caused by obstruction of the ureter from dislodged kidney stones. The most frequent site of obstruction is the vesicoureteric junction (VUJ), the narrowest point of the upper urinary tract. Acute obstruction and the resultant urinary stasis (disruption of urine flow) can distend the ureter (hydroureter) and cause a reflexive peristaltic smooth muscle spasm, which leads to a very intense visceral pain transmitted via the ureteric plexus.
An 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 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 make 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.[rx][rx][rx][rx]
Causes of Acute Kidney Colic
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 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
Abdominal Aortic Aneurysm
Costochondritis (rib pain)
Dermatological (skin) disorders (Herpes Zoster)
Double J stent placement or recent removal
Extrinsic ureteral compression (surgical clips, staples, cancers)
Local mass or growth
Neurological disorders and neuropathic pain
Referred pain from back or thoracic pathologies (radiculitis)
Renal abscess, infarction or venous thrombosis
Retroperitoneal pathology (abscess, hematoma)
Subcapsular spontaneous renal hematoma (Wunderlich syndrome)
Ureteropelvic junction obstruction
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.
There are multiple predictors and risk factors for kidney stone formation.
The following are the most common:
Inadequate urinary volume – Patients with extremely low urine volumes (usually less than 1 liter per day) increase the concentration of solutes (indicated by urine with an osmolarity greater than 600 mOsm/kg) and promote urinary stasis, which can cause supersaturation of solutes and lead to stone formation. The optimal daily urine volume for stone formers is 2,500 ml with a minimum acceptable level of 2,000 ml.[rx][rx]
Hypercalciuria – Most often, this is an idiopathic finding. It can be secondary to increased intestinal absorption of calcium, higher circulating serum calcium, reduced renal calcium reabsorption (renal calcium leak), hypervitaminosis D, hyperparathyroidism, high protein load, or systemic acidosis. Hypercalciuria increases the urinary saturation of calcium salts like oxalate and phosphate, causing the formation of crystals and calculi. Calcium-containing stones form approximately 80% of all renal calculi. Hypercalciuria is usually defined as urinary calcium of 250 mg or more per 24 hours. Treatment involves minimizing excessive daily oral calcium intake, correcting phosphate deficiencies that lead to increased Vitamin D activity, and the use of thiazides to increase calcium reabsorption in the nephron.
Hyperoxaluria – Oxalate naturally occurs in plants where it binds tightly to calcium in the plant’s tissue fluid. Ingestion of vegetable material results in intestinal oxalate absorption and urinary excretion. As oxalate has no nutritional or beneficial role in human physiology, it is excreted in the urine where it can form crystals and stones with calcium. Oxalate is considered the strongest chemical promotor of stones. Normal urinary oxalate is up to about 40 mg per day but optimal 24-hour urine levels are generally at 25 mg/day or less. Green leafy vegetables like spinach, rhubarb, and collard greens are particularly high in oxalate.
Hyperuricosuria – High urinary uric acid levels can promote both calcium oxalate and uric acid stone formation. Uric acid stones account for 5% to 10% of all renal calculi. Hyperuricosuria can be secondary to a high animal protein diet or a genetic defect causing increased uric acid excretion. Most pure uric acid stones are caused by high total urinary acid levels and not by elevated urinary uric acid levels. Allopurinol or febuxostat (Uloric) can be used to reduce uric acid production and potassium citrate is used for aciduria.
Infection stones – These are caused by urea-splitting organisms (Proteus or Klebsiella spp but not Escherichia coli) that break down urea in the urine, increasing concentrations of ammonia and pH which promote struvite stone formation and growth. Infection stones are also called struvite or triple (Magnesium, Ammonium, Calcium) phosphate calculi. Treatment includes control of infection with total surgical removal of all stones which are considered infected. A specific urease inhibitor, acetohydroxamic acid, may be useful in selected cases.[rx]
Hypocitraturia – Inadequate urinary citrate levels can contribute to new nephrolithiasis formation. 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 by forming soluble complexes with calcium and magnesium. Optimal levels are approximately 300 mg (or more)/L of urine. Potassium citrate supplements are also recommended to optimize urine pH in cases of uric acid stones and aciduria.
Symptoms of Acute Kidney Colic
Small stones may not cause any symptoms. Larger stones can cause renal colic, especially if they block a ureter. This is the tube urine travels through on its way from your kidney to your bladder.
Symptoms of renal colic include:
- intense pain along the side of your body between your ribs and hip, or in your lower abdomen
- pain that spreads to your back or groin
- nausea or vomiting
- Renal colic pain often comes in waves. These waves can last from 20 to 60 minutes.
- pain when you urinate
- blood in your urine, which may be pink, red, or brown
- cloudy or foul-smelling urine
- gravel — tiny pieces of stones in your urine
- urgent need to urinate
- urinating more or less than usual
- fever and chills (if you have an infection)
Diagnosis of Acute Kidney Colic
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 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 a 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 a 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 exams, 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 commonly secondary to white blood cell emargination.
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 conclusively 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.[rx] 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.[rx][rx]
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 a 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 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 the 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.
A plain 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 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 no 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%.[rx]
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 of Acute Kidney Colic
Most small stones are passed spontaneously and only pain management is required. Above 5 mm (0.20 in) the rate of spontaneous stone passage decreases. NSAIDs (non-steroidal anti-inflammatory drugs), such as diclofenac[rx] or ibuprofen, and antispasmodics like butylscopolamine are used. Although morphine may be administered to assist with emergency pain management, it is often not recommended as morphine is addictive and raises ureteral pressure, worsening the condition. Vomiting is also considered an important adverse effect of opioids, mainly with pethidine.[rx] Oral narcotic medications are also often used.
Treatment includes the following:
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 distension 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 such as ketorolac (15 mg to 30 mg intravenously (IV) or intramuscularly (IM)) or diclofenac (37.5 mg IV) are most commonly used.[rx][rx][rx]
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.[rx]
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.
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 adequate hydration.
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 are 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. Silodosin (Rapaflo) 4 and 8 mg was compared to standard tamsulosin 0.4 mg. The higher dose of silodosin (8 mg) was comparable to the tamsulosin, but the lower dose of 4 mg was clearly inferior with reduced expulsion rates and increased pain reported.[rx]
Definitive management of impacted stones. There are several invasive methods to improve the 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 with definitive stone therapy postponed until the patient is stable.
The optimal timing of intervention for renal colic depends on the underlying etiology. For an obstructing stone, intervention is suggested even in asymptomatic patients after 30 days due to the increased risk of scarring and other complications.
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 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 alkalinize) to a pH of 6.5. Hyperuricosuria 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). [rx][rx][rx]
Nerve blocks can often be helpful, especially in chronic cases of flank pain. An anesthetic injection is typically an injection proximal to the area of the 11th or 12th intercostal nerve. Good efficacy of a nerve block suggests a musculoskeletal or neuropathic etiology. Paravertebral, splanchnic, and intercostal nerve blocks have all shown varying degrees of efficacy in relief from flank pain.[rx][rx][rx]
24-hour urine testing for kidney stone prophylaxis is now recommended for all high-risk and recurrent stone formers. The American Urological Association Guidelines recommend informing even first-time stone formers about 24-hour urine testing and prophylactic therapy. Good guidelines for the interpretation of 24-hour urine tests and optimal treatment selection have been published and are now available for free download.[rx]
There is typically no antalgic position for the patient (lying down on the non-aching side and applying a hot bottle or towel to the area affected may help). Larger stones may require surgical intervention for their removal, such as shockwave lithotripsy, laser lithotripsy, ureteroscopy or percutaneous nephrolithotomy. Patients can also be treated with alpha blockers[rx] in cases where the stone is located in the ureter.
- Ureteroscopy guided stone extraction – This invasive surgical procedure involves a doctor inserting a thin scope with a light and attached camera into the urinary tract. Using this allows them to locate and remove the stone.
- Extracorporeal shock wave lithotripsy (ESWL) – ESWL is a non-invasive treatment. It is the process of aiming small sound waves at the kidneys to break up stones into tiny pieces. A person can then pass these fragments in the urine.
- Percutaneous nephrolithotomy – Doctors typically perform this procedure under general anesthesia. They will make a small incision in the person’s back to access the kidney and will remove the stone using a lighted scope and small surgical instruments.
- Stent placement – Sometimes, doctors place a thin tube into a person’s ureter to help relieve the obstruction and promote the passing of stones.
- Ureteroscopy – Your doctor inserts a thin, lighted scope up through your urethra and bladder to remove the stone.
- Percutaneous nephrolithotomy – This procedure uses tiny instruments inserted through a small cut in your back to remove a stone. You will be asleep during this procedure.
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