38 Evaluation of Flank Pain Joseph G. Barone Objectives 1. To discuss the potential etiologies of flank pain. 2. To discuss the imaging modalities available for the evaluation of flank pain. 3. To discuss the evaluation of a patient with flank pain. 4. To discuss the clinical presentation of a patient with urinary calculi. Case You are asked to examine a 65-year-old woman with left flank pain. The pain is acute, severe, and radiates to the left lower quadrant. The patient complains of nausea, but there is no vomiting or diarrhea. Past medical history is significant only for hypertension. The patient does not smoke and denies alcohol and drug use. On physical examination, the patient is afebrile, and the remaining vital signs also are normal. The only abnormality detected on physical examination is severe left costovertebral angle tenderness on percus- sion. Laboratory evaluations, including a complete blood count and serum chemistries, are normal. Urine Gram stain demonstrates no bac- teria on an unspun specimen. Urinalysis demonstrates the presence of red blood cells and irregular crystals. An abdominal plain film demon- strates a 2-mm calcification at the level of the left pelvic brim. Introduction Flank pain often is due to a urologic etiology, such as renal calculus disease or acute pyelonephritis; however, cardiac, intraabdominal, musculoskeletal, and psychological causes also need to be consid- ered. The quality and severity of the pain may provide a clue to its 670
Evaluation of Flank Pain
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Objectives
1. To discuss the potential etiologies of flank pain. 2. To discuss the imaging modalities available for
the evaluation of flank pain. 3. To discuss the evaluation of a patient with flank
pain. 4. To discuss the clinical presentation of a patient
with urinary calculi.
Case
You are asked to examine a 65-year-old woman with left flank pain. The pain is acute, severe, and radiates to the left lower quadrant. The patient complains of nausea, but there is no vomiting or diarrhea. Past medical history is significant only for hypertension. The patient does not smoke and denies alcohol and drug use.
On physical examination, the patient is afebrile, and the remaining vital signs also are normal. The only abnormality detected on physical examination is severe left costovertebral angle tenderness on percus- sion. Laboratory evaluations, including a complete blood count and serum chemistries, are normal. Urine Gram stain demonstrates no bac- teria on an unspun specimen. Urinalysis demonstrates the presence of red blood cells and irregular crystals. An abdominal plain film demon- strates a 2-mm calcification at the level of the left pelvic brim.
Introduction
Flank pain often is due to a urologic etiology, such as renal calculus disease or acute pyelonephritis; however, cardiac, intraabdominal, musculoskeletal, and psychological causes also need to be consid- ered. The quality and severity of the pain may provide a clue to its
670
38. Evaluation of Flank Pain 671
etiology. Flank pain that is due to infection, such as acute pyelone- phritis, usually is steady and dull, whereas pain that is due to an acutely obstructing calculus can be intense and sharp.
The kidney and its capsule are innervated by sensory fibers travel- ing to the T10-L1 spinal cord. Pain that originates from the kidney often is felt just lateral to the sacrospinalis muscle beneath the 12th rib pos- teriorly. The pain often radiates anteriorly, but it also may be referred to the inguinal, labial, penile, or testicular areas. It is not uncommon for a man with a ureteral calculus to complain of pain at the tip of the penis or for a women with the same problem to experience labial pain.
Flank pain that originates from urinary tract pathology may be caused by obstruction, inflammation, or mass. Hydronephrosis occurs when there is obstruction of the urinary tract that results in dilation of the renal collecting system. Dilation of the renal collecting system leads to distention of the renal capsule, and this distention results in flank pain. In the case presented above, flank pain accompanied by crystals in the urine is suggestive of hydronephrosis due to an obstructing renal calculus.
When evaluating a patient with flank pain, the severity of the pain generally correlates inversely with the duration of the problem. That is, chronic, gradual distention of the renal capsule over a long period of time due to a slowly enlarging ureteral tumor often is associated with mild to moderate flank pain. The pain is mild or dull because it results in gradual but possibly severe distention of the renal collecting system and capsule. In contrast, the acute flank pain that is associated with an obstructing renal calculus often is severe, since it results in sudden distention of the renal collecting system and capsule. In the case presented, it is likely that an obstructing calculi is causing the patient’s symptoms. Severe flank pain caused by an acute urinary tract obstruction is termed renal colic.
It is important for the clinician to determine if the pain represents an emergency or if the problem can be managed in the outpatient setting. In this regard, it is important to determine if there is associated fever, dehydration, nausea, or vomiting. Comorbid medical conditions, such as diabetes, immunocompromise, or pregnancy, also need to be considered. When flank pain presents in association with any one of these factors, hospital admission may be necessary to prevent possible complications, such as pyelonephritis or urosepsis, from developing. In the case presented, none of these factors are present, so this patient can be managed in the outpatient setting.
Since a prime objective for the clinician is to determine if the flank pain represents an emergent medical problem, it is helpful to consider the differential diagnosis of flank pain (see Algorithm 38.1).
Differential Diagnosis of Flank Pain
Urinary Calculi
One of the most common causes of acute, severe flank pain is sudden distention of the renal collecting system and capsule secondary to an
672 J.G. Barone
obstructing urinary calculi. Most urinary calculi cause pain only when they obstruct the flow of urine from the kidney into the bladder. A nonobstructing stone usually does not cause significant flank pain. Since the patient in the case presented has pain, it is prob- able that obstruction is present. Typically, the stone becomes caught in the renal pelvis or ureter and causes obstruction of urine flow. The back pressure results in pain and hydronephrosis.
Types of Urinary Calculi The most common type of urinary tract calculus is composed of calcium oxalate. Oxalate is found in many green leafy vegetables and teas, and it is considered to be an inducer of stone formation. When urine becomes supersaturated with calcium or oxalate, precipitation of crystals can result in stone formation. Causes for supersaturation with calcium or oxalate include excess bone resorption of calcium from immobility, intestinal hyperabsorbtion of calcium from sarcoidosis, and renal leak of calcium seen with renal tubular acidosis. However, most individuals who form calcium oxalate stones do not drink enough fluids, which results in concentrated urine. This facilitates crystal pre- cipitation and stone formation. Even though the patient in the case pre- sented has a family history of calcium oxalate calculi, dehydration is the most likely cause of her stone formation. For this reason, calcium oxalate stones are more common in the summer months and in the
Flank pain
Calculi
Hospitalization Hydration Relieve obstruction Drain abscesses Antibiotics
Cardiology consult Control arrhythmia
Oral analgesics Oral hydration Strain urine
Algorithm 38.1. Algorithm for the clinical evaluation of the patient presenting with acute flank pain. CT, computed tomography; H&P, history and physical examination; IVP, intravenous pyelogram; KUB, kidney and urinary bladder; UA, urinalysis; US, ultrasound.
38. Evaluation of Flank Pain 673
southern United States “stone belt,” where it is hot and where dehy- dration is more likely to occur.
Other common types of stones include magnesium ammonium phosphate and carbonate apatite stones. These stones sometimes are called infection stones, since they form secondary to urinary tract infections with urea splitting bacteria. Urea splitting bacteria raise the pH of the urine, and this facilitates the formation of infection stones by lowering the solubility of magnesium-ammonium and phosphate. Common urea splitting bacteria include Escherichia coli and Proteus mirabilis. Infectious stones can enlarge quickly and sometimes can fill the entire renal collecting system to form a staghorn calculus. The term staghorn calculus indicates that the stone is a large stone, but it does not imply stone composition. All urinary calculi have the potential to form staghorn calculi; however, infection stones result in staghorn formation most often.
Some stones, including uric acid and cystine stones, form sec- ondary to metabolic abnormalities. These stones are seen less com- monly in clinical practice, but they should be suspected in patients with a history of gout or homozygous cystinuria. It is estimated that 25% of patients with uric acid stones have gout. Uric acid is an end product of purine metabolism. Hyperuricosuria may be seen in gout, myelo- proliferative disorders, idiopathic hyperuricosuria, and patients with increased dietary purine. Uric acid stones are clinically unique, since they cannot be seen on a standard abdominal x-ray. They can, however, be visualized on ultrasound or computed tomography (CT) scan. Since the formation of uric acid stones is very dependent on the pH of the urine, they generally form only if the urine pH is consistently below 5.5. Uric acid stones have been dissolved successfully by raising urinary pH to 6.5 or slightly above. Typically, an oral urinary alkalin- izing agent, such as potassium citrate, is used to raise urine pH and dissolve uric acid stones. Cystine stones are uncommon and form only in patients who are homozygous for cystinuria. Cystinuria is an inher- ited defect of the renal tubule causing loss of cystine, ornithine, arginine, and lysine. The loss of cystine is the only clinical problem patients suffer, since they excrete over 250mg of cystine per liter of urine. This high urinary cystine level is problematic, since stone for- mation results in urinary cystine levels of 170mg per liter of urine at pH 5. Patients who are heterozygous for cystinuria excrete less urinary cystine and generally do not suffer from cystine stone formation.
Risk Factors Some of the common risk factors for developing urinary calculi include inadequate fluid intake, excess sodium intake, metabolic abnormalities, inflammatory bowel disease, dehydration, and family history.
Patients with inflammatory bowel disease form stones composed of calcium oxalate by a unique mechanism. Fat malabsorption caused by the inflammatory bowel disease results in excess fats in the gut, which bind to calcium. This creates a situation in the gut in which oxalate, which normally binds to calcium, enters the bloodstream in its ionic
674 J.G. Barone
form. The oxalate then is excreted by the kidneys, and hyperoxaluria results. Since oxalte is a stone inducer, it binds with urinary calcium and facilitates calcium oxalate stone formation.
Other medical conditions increase the risk for stone formation by causing hypercalciuria, which is excess calcium in the urine. These medical problems include renal tubular acidosis, sarcoidosis, hyper- parathyroidism, chronic immobility, and paralysis. In these condi- tions, hypercalciuria results when excess calcium is absorbed from bone or the gut and ultimately is excreted by the kidneys. In renal tubular acidosis, the renal tubule leaks calcium directly into the urine.
Chronic urinary tract infection also can lead to stone formation due to urea splitting bacteria, which lead to an elevated urine pH. Urease catalyzes the hydrolysis of urea into ammonia and carbon dioxide. These end products cause a rise in urinary pH, which facilitates infec- tious stone formation. P. mirabilis and E. coli are the most common urea splitting bacteria that are associated with urinary tract infection and urinary calculi formation. These bacteria raise the pH of the urine, and this allows the precipitation of magnesium-ammonium-phosphate or apatite stones. Patients with infected urine and flank pain due to an obstructing calculi may require hospitalization to prevent urosepsis.
Management As illustrated in the case presented, most patients who present with flank pain secondary to acutely obstructing urinary calculi can be managed on an outpatient basis. Cornerstones of therapy include adequate hydration, pain relief, and control of any associated nausea or vomiting.
If the pain is severe enough to require intravenous morphine sulfate or if there is associated fever or dehydration due to nausea or vomit- ing, hospital admission may be necessary. Again, one of the most important decisions the clinician has to make is to determine if the patient can be treated as an outpatient or if the patient needs hospital admission. There are several indications for hospital admission, and fever is a common indicator for admission (Table 38.1). As Table 38.1 indicates, appropriate blood and urine cultures need to be performed, and other causes of infection need to be considered. Fever in the pres- ence of obstructing urinary calculi can be an ominous clinical find- ing that suggests an accumulation of purulent urine proximal to an obstructing stone. This is an especially serious situation if the patient has comorbid medical conditions, such as diabetes. Emergent intra- venous antibiotics, aggressive intravenous fluid hydration, and per- cutaneous or transureteral drainage of the infected urine usually are necessary in these situations. Patients with fever and obstructing urinary calculi should not be discharged from the emergency room, as urosepsis and septic shock can develop quickly.
Following the acute event, it is suggested that all patients who form urinary stones undergo a metabolic evaluation consisting of a com- plete blood count, urinalysis, serum chemistry profile, and a 24-hour urine collection for calcium, phosphorus, uric acid, creatinine, citrate, and oxalate levels. This evaluation can be done on an outpatient basis.
38. Evaluation of Flank Pain 675
Table 38.1. Evidence-based practice management guideline for the evaluation of fever in critically ill adult patients.a
Temperature measurement Level I: Record the temperature and the site of measurement in the patient’s medical record.
The nosocomial spread of pathogens must be avoided when using temperature measurement devices.
Level II: Temperature is measured most accurately by indwelling vascular or bladder thermistors, but most other sites are acceptable. Axillary measurements should not be used.
Laboratory testing for the evaluation of fever should be individualized for each patient.
Blood cultures Level I: For skin preparation, povidone-iodine should be allowed to dry for 2min, or tincture
of iodine for 30s. Alcohol skin preparation, an acceptable alternative for iodine- allergic patients, need not be allowed to dry.
Level II: Obtain a single pair of blood cultures after appropriate skin disinfection after the initial temperature elevation, and another pair within 24h thereafter from a second peripheral site. Additional cultures should be based on high clinical suspicion of bacteremia or fungemia, and not instituted automatically for each temperature elevation.
If two peripheral sites are not available, one pair of cultures may be drawn through the most recently inserted catheter, but the diagnostic accuracy is reduced.
Draw at least 10–15mL blood/culture.
Suspected intravascular catheter infection Level II: Examine the catheter insertion site for purulence, and distally on the extremity for
signs of vascular compromise or embolization. Any expressed purulence from an insertion site should be collected for culture and
Gram stain. The catheter should be removed and cultured for evidence of a tunnel infection,
embolic phenomena, vascular compromise, or sepsis. Two blood cultures should be drawn peripherally, or one may be drawn from the
most proximal port (if a multilumen catheter). Both the introducer and the catheter itself should be cultured for suspected
pulmonary artery catheter infection. It is not routinely necessary to culture the intravenous fluid infusate.
Suspected ICU-acquired pneumonia Level I: A chest x-ray should be obtained to evaluate for suspected pneumonia.
Posteroanterior and lateral films or computed tomography of the chest can offer more information.
Level II: Lower respiratory tract secretions should be sampled for direct examination and culture. Bronchoscopy may be considered.
Respiratory secretions should be transported to the laboratory within 2h of collection.
Pleural fluid should be obtained for culture and Gram stain if there is an adjacent infiltrate or another reason to suspect infection.
Evaluation of the febrile patient with diarrhea Level II: If more than two diarrheal stools occur, a single stool sample should be sent for
Clostridium difficile evaluation. A second sample should be sent if the first is negative and suspicion remains high.
If illness is severe and rapid testing is unavailable or nondiagnostic, consider flexible sigmoidoscopy.
If illness is severe, consider empiric therapy with metronidazole until the results of studies are available. Empiric therapy (especially with vancomycin) is not recommended if two stool evaluations have been negative for C. difficile, and is discouraged because of the risk of producing resistant pathogens.
Stool cultures are rarely indicated for other enteric pathogens if the patient is HIV- negative or did not present to the hospital with diarrhea.
Continued
676 J.G. Barone
The most common abnormality detected is a low urine volume, usually less than 1L/day, due to inadequate fluid intake. In this situation, the patient should be encouraged to increase fluid intake and to maintain a urine volume of 2 to 3L per day. Water is the best fluid to drink, while teas, cranberry juice, and other drinks that are high in oxalate should be limited. Cranberry juice has been shown to be effective in reducing the risk for recurrent urinary tract infections, but it is high in oxalate and should be limited in patients who form stones. Patients sometimes also are advised to limit the intake of certain foods that are high in calcium and oxalate, such as cheese, spinach, and nuts; however, it is often difficult to maintain these dietary restrictions.
Medications sometimes are necessary to prevent recurrence. Orthophosphates decrease urinary calcium and are used to prevent calcium stone formation. Hydrochlorothiazide prevents reabsorption of sodium and calcium in the loop of Henle; this leads to an increase
Table 38.1. Continued Suspected urinary tract infection
Level II: Obtain urine for culture and to evaluate for pyuria. If the patient has an indwelling Foley catheter, urine should be collected from the urine port and not the drainage bag.
The specimen should be transported rapidly to the laboratory, or refrigerated if transport will exceed 1h.
Suspected sinusitis Level I: Aspirate should be Gram stained and cultured. Level II: Computed tomography of the facial sinuses is the imaging modality of choice for
the diagnosis of sinusitis. Puncture and aspiration of the sinuses should be performed using sterile technique
if mucosal thickening or an air–fluid level is present in the sinus.
Postoperative fever Level II: Examine the surgical wound for erythema, fluctuance, tenderness, or purulent
drainage. Open the wound for suspicion of infection. Culture and Gram stain should be obtained from purulent material if from deep
within the wound.
Suspected central nervous system infection Level II: Gram stain and culture of cerebrospinal fluid should be performed in cases of
suspected infection. Other tests should be predicated on the clinical situation. A computed tomographic study is usually required before lumbar puncture, which
may need to be deferred if a mass lesion is present. Consider lumbar puncture for new fever with unexplained alteration of
consciousness or focal neurologic signs. In febrile patients with an intracranial device, cerebrospial fluid should be sent for
culture and Gram stain.
Noninfectious causes of fever Level II: Reevaluate all recent medications and blood products the patient has received.
Stop all nonessential medications, or substitute medications for treatments that cannot be stopped.
a Summary of clinical recommendations, Society of Critical Care Medicine, 1998; level III guidelines excluded. Source: Adapted from O’Grady NP, Barie PS, Bartlett JG, et al. Practice guidelines for evaluating new fever in criti- cally ill adult patients. Task Force of the Society of Critical Care Medicine and the Infectious Diseases Society of America. Clin Infect Dis 1998;26:1042–1059, with permission. Published by the University of Chicago. Reprinted from Norton JA. History of Endocrine Surgery. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.
38. Evaluation of Flank Pain 677
in proximal tubular reabsorption of sodium and calcium, which decreases total urinary calcium excretion.
Acute Pyelonephritis
Acute pyelonephritis indicates infection of the kidney and renal pelvis accompanied by fever, flank pain, and infected urine. In the case presented, there is no clinical evidence for pyelonephritis. The diagnosis is made clinically. Bacterial pyelonephritis typically involves an infection of the renal interstitium and collecting system. Bacterial invasion of the kidney results in a humoral response that activates the complement cascade. The polymorphonuclear leukocytes release superoxide radicals that damage not only bacteria but also the sur- rounding renal tissue. If the damage is severe, renal scar or loss can occur.
In the United States, the majority of cases of pyelonephritis are due to the Enterobacteriaceae group of bacteria, mainly E. coli. Proteus, Pseudomonas, Enterobacter, Klebsiella, and Staphylococcus also can cause pyelonephritis. The urea splitting bacteria include E. coli, Proteus, and Klebsiella and are important, since they may facilitate the develop- ment of infection stones.
Patients can present with mild gram-negative bacteremia to septic shock. Renal abscess can form if treatment is delayed, with resultant renal parenchyma loss. In the pediatric population, children with vesi- coureteral reflux are at risk for pylonephritis…
1. To discuss the potential etiologies of flank pain. 2. To discuss the imaging modalities available for
the evaluation of flank pain. 3. To discuss the evaluation of a patient with flank
pain. 4. To discuss the clinical presentation of a patient
with urinary calculi.
Case
You are asked to examine a 65-year-old woman with left flank pain. The pain is acute, severe, and radiates to the left lower quadrant. The patient complains of nausea, but there is no vomiting or diarrhea. Past medical history is significant only for hypertension. The patient does not smoke and denies alcohol and drug use.
On physical examination, the patient is afebrile, and the remaining vital signs also are normal. The only abnormality detected on physical examination is severe left costovertebral angle tenderness on percus- sion. Laboratory evaluations, including a complete blood count and serum chemistries, are normal. Urine Gram stain demonstrates no bac- teria on an unspun specimen. Urinalysis demonstrates the presence of red blood cells and irregular crystals. An abdominal plain film demon- strates a 2-mm calcification at the level of the left pelvic brim.
Introduction
Flank pain often is due to a urologic etiology, such as renal calculus disease or acute pyelonephritis; however, cardiac, intraabdominal, musculoskeletal, and psychological causes also need to be consid- ered. The quality and severity of the pain may provide a clue to its
670
38. Evaluation of Flank Pain 671
etiology. Flank pain that is due to infection, such as acute pyelone- phritis, usually is steady and dull, whereas pain that is due to an acutely obstructing calculus can be intense and sharp.
The kidney and its capsule are innervated by sensory fibers travel- ing to the T10-L1 spinal cord. Pain that originates from the kidney often is felt just lateral to the sacrospinalis muscle beneath the 12th rib pos- teriorly. The pain often radiates anteriorly, but it also may be referred to the inguinal, labial, penile, or testicular areas. It is not uncommon for a man with a ureteral calculus to complain of pain at the tip of the penis or for a women with the same problem to experience labial pain.
Flank pain that originates from urinary tract pathology may be caused by obstruction, inflammation, or mass. Hydronephrosis occurs when there is obstruction of the urinary tract that results in dilation of the renal collecting system. Dilation of the renal collecting system leads to distention of the renal capsule, and this distention results in flank pain. In the case presented above, flank pain accompanied by crystals in the urine is suggestive of hydronephrosis due to an obstructing renal calculus.
When evaluating a patient with flank pain, the severity of the pain generally correlates inversely with the duration of the problem. That is, chronic, gradual distention of the renal capsule over a long period of time due to a slowly enlarging ureteral tumor often is associated with mild to moderate flank pain. The pain is mild or dull because it results in gradual but possibly severe distention of the renal collecting system and capsule. In contrast, the acute flank pain that is associated with an obstructing renal calculus often is severe, since it results in sudden distention of the renal collecting system and capsule. In the case presented, it is likely that an obstructing calculi is causing the patient’s symptoms. Severe flank pain caused by an acute urinary tract obstruction is termed renal colic.
It is important for the clinician to determine if the pain represents an emergency or if the problem can be managed in the outpatient setting. In this regard, it is important to determine if there is associated fever, dehydration, nausea, or vomiting. Comorbid medical conditions, such as diabetes, immunocompromise, or pregnancy, also need to be considered. When flank pain presents in association with any one of these factors, hospital admission may be necessary to prevent possible complications, such as pyelonephritis or urosepsis, from developing. In the case presented, none of these factors are present, so this patient can be managed in the outpatient setting.
Since a prime objective for the clinician is to determine if the flank pain represents an emergent medical problem, it is helpful to consider the differential diagnosis of flank pain (see Algorithm 38.1).
Differential Diagnosis of Flank Pain
Urinary Calculi
One of the most common causes of acute, severe flank pain is sudden distention of the renal collecting system and capsule secondary to an
672 J.G. Barone
obstructing urinary calculi. Most urinary calculi cause pain only when they obstruct the flow of urine from the kidney into the bladder. A nonobstructing stone usually does not cause significant flank pain. Since the patient in the case presented has pain, it is prob- able that obstruction is present. Typically, the stone becomes caught in the renal pelvis or ureter and causes obstruction of urine flow. The back pressure results in pain and hydronephrosis.
Types of Urinary Calculi The most common type of urinary tract calculus is composed of calcium oxalate. Oxalate is found in many green leafy vegetables and teas, and it is considered to be an inducer of stone formation. When urine becomes supersaturated with calcium or oxalate, precipitation of crystals can result in stone formation. Causes for supersaturation with calcium or oxalate include excess bone resorption of calcium from immobility, intestinal hyperabsorbtion of calcium from sarcoidosis, and renal leak of calcium seen with renal tubular acidosis. However, most individuals who form calcium oxalate stones do not drink enough fluids, which results in concentrated urine. This facilitates crystal pre- cipitation and stone formation. Even though the patient in the case pre- sented has a family history of calcium oxalate calculi, dehydration is the most likely cause of her stone formation. For this reason, calcium oxalate stones are more common in the summer months and in the
Flank pain
Calculi
Hospitalization Hydration Relieve obstruction Drain abscesses Antibiotics
Cardiology consult Control arrhythmia
Oral analgesics Oral hydration Strain urine
Algorithm 38.1. Algorithm for the clinical evaluation of the patient presenting with acute flank pain. CT, computed tomography; H&P, history and physical examination; IVP, intravenous pyelogram; KUB, kidney and urinary bladder; UA, urinalysis; US, ultrasound.
38. Evaluation of Flank Pain 673
southern United States “stone belt,” where it is hot and where dehy- dration is more likely to occur.
Other common types of stones include magnesium ammonium phosphate and carbonate apatite stones. These stones sometimes are called infection stones, since they form secondary to urinary tract infections with urea splitting bacteria. Urea splitting bacteria raise the pH of the urine, and this facilitates the formation of infection stones by lowering the solubility of magnesium-ammonium and phosphate. Common urea splitting bacteria include Escherichia coli and Proteus mirabilis. Infectious stones can enlarge quickly and sometimes can fill the entire renal collecting system to form a staghorn calculus. The term staghorn calculus indicates that the stone is a large stone, but it does not imply stone composition. All urinary calculi have the potential to form staghorn calculi; however, infection stones result in staghorn formation most often.
Some stones, including uric acid and cystine stones, form sec- ondary to metabolic abnormalities. These stones are seen less com- monly in clinical practice, but they should be suspected in patients with a history of gout or homozygous cystinuria. It is estimated that 25% of patients with uric acid stones have gout. Uric acid is an end product of purine metabolism. Hyperuricosuria may be seen in gout, myelo- proliferative disorders, idiopathic hyperuricosuria, and patients with increased dietary purine. Uric acid stones are clinically unique, since they cannot be seen on a standard abdominal x-ray. They can, however, be visualized on ultrasound or computed tomography (CT) scan. Since the formation of uric acid stones is very dependent on the pH of the urine, they generally form only if the urine pH is consistently below 5.5. Uric acid stones have been dissolved successfully by raising urinary pH to 6.5 or slightly above. Typically, an oral urinary alkalin- izing agent, such as potassium citrate, is used to raise urine pH and dissolve uric acid stones. Cystine stones are uncommon and form only in patients who are homozygous for cystinuria. Cystinuria is an inher- ited defect of the renal tubule causing loss of cystine, ornithine, arginine, and lysine. The loss of cystine is the only clinical problem patients suffer, since they excrete over 250mg of cystine per liter of urine. This high urinary cystine level is problematic, since stone for- mation results in urinary cystine levels of 170mg per liter of urine at pH 5. Patients who are heterozygous for cystinuria excrete less urinary cystine and generally do not suffer from cystine stone formation.
Risk Factors Some of the common risk factors for developing urinary calculi include inadequate fluid intake, excess sodium intake, metabolic abnormalities, inflammatory bowel disease, dehydration, and family history.
Patients with inflammatory bowel disease form stones composed of calcium oxalate by a unique mechanism. Fat malabsorption caused by the inflammatory bowel disease results in excess fats in the gut, which bind to calcium. This creates a situation in the gut in which oxalate, which normally binds to calcium, enters the bloodstream in its ionic
674 J.G. Barone
form. The oxalate then is excreted by the kidneys, and hyperoxaluria results. Since oxalte is a stone inducer, it binds with urinary calcium and facilitates calcium oxalate stone formation.
Other medical conditions increase the risk for stone formation by causing hypercalciuria, which is excess calcium in the urine. These medical problems include renal tubular acidosis, sarcoidosis, hyper- parathyroidism, chronic immobility, and paralysis. In these condi- tions, hypercalciuria results when excess calcium is absorbed from bone or the gut and ultimately is excreted by the kidneys. In renal tubular acidosis, the renal tubule leaks calcium directly into the urine.
Chronic urinary tract infection also can lead to stone formation due to urea splitting bacteria, which lead to an elevated urine pH. Urease catalyzes the hydrolysis of urea into ammonia and carbon dioxide. These end products cause a rise in urinary pH, which facilitates infec- tious stone formation. P. mirabilis and E. coli are the most common urea splitting bacteria that are associated with urinary tract infection and urinary calculi formation. These bacteria raise the pH of the urine, and this allows the precipitation of magnesium-ammonium-phosphate or apatite stones. Patients with infected urine and flank pain due to an obstructing calculi may require hospitalization to prevent urosepsis.
Management As illustrated in the case presented, most patients who present with flank pain secondary to acutely obstructing urinary calculi can be managed on an outpatient basis. Cornerstones of therapy include adequate hydration, pain relief, and control of any associated nausea or vomiting.
If the pain is severe enough to require intravenous morphine sulfate or if there is associated fever or dehydration due to nausea or vomit- ing, hospital admission may be necessary. Again, one of the most important decisions the clinician has to make is to determine if the patient can be treated as an outpatient or if the patient needs hospital admission. There are several indications for hospital admission, and fever is a common indicator for admission (Table 38.1). As Table 38.1 indicates, appropriate blood and urine cultures need to be performed, and other causes of infection need to be considered. Fever in the pres- ence of obstructing urinary calculi can be an ominous clinical find- ing that suggests an accumulation of purulent urine proximal to an obstructing stone. This is an especially serious situation if the patient has comorbid medical conditions, such as diabetes. Emergent intra- venous antibiotics, aggressive intravenous fluid hydration, and per- cutaneous or transureteral drainage of the infected urine usually are necessary in these situations. Patients with fever and obstructing urinary calculi should not be discharged from the emergency room, as urosepsis and septic shock can develop quickly.
Following the acute event, it is suggested that all patients who form urinary stones undergo a metabolic evaluation consisting of a com- plete blood count, urinalysis, serum chemistry profile, and a 24-hour urine collection for calcium, phosphorus, uric acid, creatinine, citrate, and oxalate levels. This evaluation can be done on an outpatient basis.
38. Evaluation of Flank Pain 675
Table 38.1. Evidence-based practice management guideline for the evaluation of fever in critically ill adult patients.a
Temperature measurement Level I: Record the temperature and the site of measurement in the patient’s medical record.
The nosocomial spread of pathogens must be avoided when using temperature measurement devices.
Level II: Temperature is measured most accurately by indwelling vascular or bladder thermistors, but most other sites are acceptable. Axillary measurements should not be used.
Laboratory testing for the evaluation of fever should be individualized for each patient.
Blood cultures Level I: For skin preparation, povidone-iodine should be allowed to dry for 2min, or tincture
of iodine for 30s. Alcohol skin preparation, an acceptable alternative for iodine- allergic patients, need not be allowed to dry.
Level II: Obtain a single pair of blood cultures after appropriate skin disinfection after the initial temperature elevation, and another pair within 24h thereafter from a second peripheral site. Additional cultures should be based on high clinical suspicion of bacteremia or fungemia, and not instituted automatically for each temperature elevation.
If two peripheral sites are not available, one pair of cultures may be drawn through the most recently inserted catheter, but the diagnostic accuracy is reduced.
Draw at least 10–15mL blood/culture.
Suspected intravascular catheter infection Level II: Examine the catheter insertion site for purulence, and distally on the extremity for
signs of vascular compromise or embolization. Any expressed purulence from an insertion site should be collected for culture and
Gram stain. The catheter should be removed and cultured for evidence of a tunnel infection,
embolic phenomena, vascular compromise, or sepsis. Two blood cultures should be drawn peripherally, or one may be drawn from the
most proximal port (if a multilumen catheter). Both the introducer and the catheter itself should be cultured for suspected
pulmonary artery catheter infection. It is not routinely necessary to culture the intravenous fluid infusate.
Suspected ICU-acquired pneumonia Level I: A chest x-ray should be obtained to evaluate for suspected pneumonia.
Posteroanterior and lateral films or computed tomography of the chest can offer more information.
Level II: Lower respiratory tract secretions should be sampled for direct examination and culture. Bronchoscopy may be considered.
Respiratory secretions should be transported to the laboratory within 2h of collection.
Pleural fluid should be obtained for culture and Gram stain if there is an adjacent infiltrate or another reason to suspect infection.
Evaluation of the febrile patient with diarrhea Level II: If more than two diarrheal stools occur, a single stool sample should be sent for
Clostridium difficile evaluation. A second sample should be sent if the first is negative and suspicion remains high.
If illness is severe and rapid testing is unavailable or nondiagnostic, consider flexible sigmoidoscopy.
If illness is severe, consider empiric therapy with metronidazole until the results of studies are available. Empiric therapy (especially with vancomycin) is not recommended if two stool evaluations have been negative for C. difficile, and is discouraged because of the risk of producing resistant pathogens.
Stool cultures are rarely indicated for other enteric pathogens if the patient is HIV- negative or did not present to the hospital with diarrhea.
Continued
676 J.G. Barone
The most common abnormality detected is a low urine volume, usually less than 1L/day, due to inadequate fluid intake. In this situation, the patient should be encouraged to increase fluid intake and to maintain a urine volume of 2 to 3L per day. Water is the best fluid to drink, while teas, cranberry juice, and other drinks that are high in oxalate should be limited. Cranberry juice has been shown to be effective in reducing the risk for recurrent urinary tract infections, but it is high in oxalate and should be limited in patients who form stones. Patients sometimes also are advised to limit the intake of certain foods that are high in calcium and oxalate, such as cheese, spinach, and nuts; however, it is often difficult to maintain these dietary restrictions.
Medications sometimes are necessary to prevent recurrence. Orthophosphates decrease urinary calcium and are used to prevent calcium stone formation. Hydrochlorothiazide prevents reabsorption of sodium and calcium in the loop of Henle; this leads to an increase
Table 38.1. Continued Suspected urinary tract infection
Level II: Obtain urine for culture and to evaluate for pyuria. If the patient has an indwelling Foley catheter, urine should be collected from the urine port and not the drainage bag.
The specimen should be transported rapidly to the laboratory, or refrigerated if transport will exceed 1h.
Suspected sinusitis Level I: Aspirate should be Gram stained and cultured. Level II: Computed tomography of the facial sinuses is the imaging modality of choice for
the diagnosis of sinusitis. Puncture and aspiration of the sinuses should be performed using sterile technique
if mucosal thickening or an air–fluid level is present in the sinus.
Postoperative fever Level II: Examine the surgical wound for erythema, fluctuance, tenderness, or purulent
drainage. Open the wound for suspicion of infection. Culture and Gram stain should be obtained from purulent material if from deep
within the wound.
Suspected central nervous system infection Level II: Gram stain and culture of cerebrospinal fluid should be performed in cases of
suspected infection. Other tests should be predicated on the clinical situation. A computed tomographic study is usually required before lumbar puncture, which
may need to be deferred if a mass lesion is present. Consider lumbar puncture for new fever with unexplained alteration of
consciousness or focal neurologic signs. In febrile patients with an intracranial device, cerebrospial fluid should be sent for
culture and Gram stain.
Noninfectious causes of fever Level II: Reevaluate all recent medications and blood products the patient has received.
Stop all nonessential medications, or substitute medications for treatments that cannot be stopped.
a Summary of clinical recommendations, Society of Critical Care Medicine, 1998; level III guidelines excluded. Source: Adapted from O’Grady NP, Barie PS, Bartlett JG, et al. Practice guidelines for evaluating new fever in criti- cally ill adult patients. Task Force of the Society of Critical Care Medicine and the Infectious Diseases Society of America. Clin Infect Dis 1998;26:1042–1059, with permission. Published by the University of Chicago. Reprinted from Norton JA. History of Endocrine Surgery. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.
38. Evaluation of Flank Pain 677
in proximal tubular reabsorption of sodium and calcium, which decreases total urinary calcium excretion.
Acute Pyelonephritis
Acute pyelonephritis indicates infection of the kidney and renal pelvis accompanied by fever, flank pain, and infected urine. In the case presented, there is no clinical evidence for pyelonephritis. The diagnosis is made clinically. Bacterial pyelonephritis typically involves an infection of the renal interstitium and collecting system. Bacterial invasion of the kidney results in a humoral response that activates the complement cascade. The polymorphonuclear leukocytes release superoxide radicals that damage not only bacteria but also the sur- rounding renal tissue. If the damage is severe, renal scar or loss can occur.
In the United States, the majority of cases of pyelonephritis are due to the Enterobacteriaceae group of bacteria, mainly E. coli. Proteus, Pseudomonas, Enterobacter, Klebsiella, and Staphylococcus also can cause pyelonephritis. The urea splitting bacteria include E. coli, Proteus, and Klebsiella and are important, since they may facilitate the develop- ment of infection stones.
Patients can present with mild gram-negative bacteremia to septic shock. Renal abscess can form if treatment is delayed, with resultant renal parenchyma loss. In the pediatric population, children with vesi- coureteral reflux are at risk for pylonephritis…
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