Acute Renal Failure
Acute renal failure occurs in 5 percent of hospitalized patients. Etiologically, this common condition can be categorized as prerenal, intrinsic or postrenal.
Most patients have prerenal acute renal failure or acute tubular necrosis (a type of intrinsic acute renal failure that is usually caused by ischemia or toxins). Using a systematic approach, physicians can determine the cause of acute renal failure in most patients. This approach includes a thorough history and physical examination, blood tests, urine studies and a renal ultrasound examination. In certain situations, such as when a patient has glomerular disease, microvascular disease or obstructive disease, rapid diagnosis and treatment are necessary to prevent permanent renal damage. By maintaining euvolemia, recognizing patients who are at increased risk and minimizing exposure to nephrotoxins, physicians can decrease the incidence of acute renal failure. Once acute renal failure develops, supportive therapy is critical to maintain fluid and electrolyte balances, minimize nitrogenous waste production and sustain nutrition. Death is most often caused by infection or cardiorespiratory complications
Oliguria literally means "reduced" urine volume— less than that necessary to remove endogenous solute loads that are the end products of metabolism. As long as the patient's kidney can usually concentrate urine in a normal fashion to a specific gravity of 1.035, oliguria (for that person) is present at urine volumes under 400 mL/d, or approximately 6 mL/kg body weight. On the other hand, if the kidney concentration is impaired and the patient can achieve a specific gravity of only 1.010, oliguria is present at urine volumes under 1000-1500 mL/d.
Acute renal failure is a condition in which the glomerular filtration rate is abruptly reduced, causing a sudden retention of endogenous and exogenous metabolites (urea, potassium, phosphate, sulfate, creatinine, administered drugs) that are normally cleared by the kidneys. The urine volume is usually low (under 400 mL/d). However, if renal concentrating mechanisms are impaired during acute renal failure, the daily urine volume may be normal or even high (high-output or nonoliguric renal failure). Rarely, there is no urine output at all (anuria) in acute renal failure.
Prompt differentiation of the cause is important in determining appropriate therapy. Prerenal renal failure is reversible if treated promptly, but a delay in therapy may allow it to progress to a fixed, nonspecific form of intrinsic renal failure (eg, acute tubular necrosis). The other causes of acute renal failure are classified on the basis of their involvement with vascular lesions, intrarenal disorders, or postrenal disorders.
PRERENAL RENAL FAILURE
The term prerenal denotes inadequate renal perfusion because of reduced intravascular volume or lowered effective arterial circulation. The most common cause of this form of acute renal failure is dehydration due to renal or extrarenal fluid losses from diarrhea, vomiting, excessive use of diuretics, and so on.
Less common causes are septic shock, "third spacing" with extravascular fluid pooling (eg, pancreatitis), and excessive use of antihypertensive drugs, which causes relative or absolute depletion of intravascular fluid volume. Heart failure with reduced cardiac output also can reduce effective renal blood flow. Careful clinical assessment may identify the primary condition responsible for prerenal renal failure, but many times several conditions can coexist. In the hospital setting, these circulatory abnormalities often lead to more fixed, acute renal failure (acute tubular necrosis), since these patients often have multiple comorbid conditions.
Acute reductions in glomerular filtration rate may also be noted in patients with cirrhosis (hepatorenal failure) or in patients taking cyclosporine, tacrolimus, nonsteroidal antiinflammatory drugs, or angiotensin-converting enzyme inhibitors. It is felt that these conditions represent significant intrarenal hemodynamic functional derangements mediated by prostaglandins and renin-angiotensin such that the glomerular capillary pressure suddenly falls. In these clinical circumstances, the urinary findings may mimic prerenal renal failure, but the patient's clinical assessment does not demonstrate the extrarenal findings seen in common prerenal conditions, as noted in the following section. Improvements in glomerular filtration rate are usually noted after drug discontinuance or, in cases of hepatorenal renal failure, with management of the liver disease or liver transplantation.
A. Symptoms and Signs: Except for rare cases with associated cardiac or "pump" failure, patients usually complain of thirst or of dizziness in the upright posture (orthostatic dizziness). There may be a history of overt fluid loss. Weight losses over hours to days quantitatively reflect the degree of dehydration.
Physical examination frequently reveals decreased skin turgor, collapsed neck veins, dry mucous membranes and axillas, and, most important, orthostatic or postural changes in blood pressure and pulse.
Table 1 Causes of acute renal failure.
I. Prerenal renal failure:
2. Vascular collapse due to sepsis, antihypertensive drug therapy, "third spacing"
3. Reduced cardiac output
1. Angiotensin-converting enzyme inhibitor drugs
2. Nonsteroidal anti-inflammatory drugs
3. Cyclosporine; tacrolimus
4. Hepatorenal syndrome
2. Dissecting arterial aneurysms
3. Malignant hypertension
IV. Parenchymal (intrarenal):
b. Interstitial nephritis
c. Toxin, dye-induced
d. Hemolytic uremic syndrome
a. Acute tubular necrosis
b. Acute cortical necrosis
1. Calculus in patients with solitary kidney
2. Bilateral ureteral obstruction
3. Outlet obstruction
4. Leak, post-traumatic
B. Laboratory Findings:
1. Urine The urine volume is usually low. Accurate assessment may require bladder catheteriza-tion followed by hourly output measurements (which will also rule out lower urinary tract obstruction; see discussion following). High urine specific gravity (> 1.025) and urine osmolality (> 600 mOsm/kg) also are noted in this form of acute apparent renal failure. Routine urinalysis usually shows no abnormalities.
2. Urine and blood chemistries-The blood urea nitrogen-creatinine ratio, normally 10:1, is usually increased with prerenal renal failure. Because mannitol, radiocontrast dyes, and diuretics affect the delivery and tubular handling of urea, sodium, and creatinine, urine and blood chemistry tests performed after these agents have been given produce misleading results.
3. Central venous pressure-A low central venous pressure indicates hypovolemia, which may be due to blood loss or dehydration. If severe cardiac failure is the principal cause of prerenal renal failure (it is rarely the sole cause), reduced cardiac output and high central venous pressure are apparent.
4. Fluid challenge-An increase in urine output in response to a carefully administered fluid challenge is both diagnostic and therapeutic in cases of prerenal renal failure. Rapid intravenous administration of 300-500 mL of physiologic saline or 125 mL of 20% mannitol (25 g/125 mL) is the usual initial treatment. Urine output is measured over the subsequent 1-3 h. A urine volume increase of more than 50 mL/h is considered a favorable response that warrants continued intravenous infusion with physiologic solutions to restore plasma volume and correct dehydration. If the urine volume does not increase, the physician should carefully review the results of blood and urine chemistry tests, reassess the patient's fluid status, and repeat the physical examination to determine whether an additional fluid challenge (with or without furosemide) might be worthwhile.
In states of dehydration, measured and estimated fluid losses must be rapidly corrected to treat oliguria of prerenal origin. Inadequate fluid management may cause further renal hemodynamic deterioration and eventual renal tubular ischemia (with fixed acute tubular necrosis; see discussion following). If oliguria persists in a well-hydrated patient, vasopressor drugs are indicated in an effort to correct the hypotension associated with sepsis or cardiogenic shock. Pressor agents that restore systemic blood pressure while maintaining renal blood flow and renal function are most useful. Dopamine, 1-5 µg/kg/min, gives "renal-dose" levels providing an increase in renal blood flow without systemic pressor responses. Higher doses of 5-20 µg/kg may be necessary if systemic hypotension persists after volume correction. Discontinuance of antihypertensive medications or diuretics can, by itself, cure the apparent acute renal failure resulting from prerenal conditions.
VASCULAR RENAL FAILURE
Common causes of acute renal failure due to vascular disease include atheroembolic disease, dissecting arterial aneurysms, and malignant hypertension. Atheroembolic disease is rare before age 60 and in patients who have not undergone vascular procedures or angiographic studies. Dissecting arterial aneurysms and malignant hypertension are usually clinically evident. Acute renal venous thrombosis, unless it affects both kidneys, has no deleterious effect on renal clearance function.
Rapid assessment of the arterial blood supply to the kidney requires arteriography or other renal blood flow studies (eg, magnetic resonance imaging or Doppler ultrasound). The cause of malignant hypertension may be identified on physical examination (eg, scleroderma). Primary management of the vascular process is necessary to affect the course of these forms of acute renal failure.
Diseases in this category can be divided into specific and nonspecific parenchymal processes.
1. SPECIFIC INTRARENAL DISEASE STATES
The most common causes of intrarenal acute renal failure are acute or rapidly progressive glomerulonephritis, acute interstitial nephritis, toxic nephropathies, and hemolytic uremic syndrome.
A. Symptoms and Signs: Usually the history shows some salient data such as sore throat or upper respiratory infection, diarrheal illness (occasionally as epidemic), use of antibiotics, or intravenous use of drags (often illicit types).
Oedema of the lung
Bilateral back pain, at times severe, is occasionally noted. Gross hematuria may be present. It is unusual for pyelonephritis to present as acute renal failure unless there is (1) associated sepsis or dehydration, (2) obstruction, or (3) involvement of a solitary kidney. Systemic diseases in which acute renal failure occurs include Henoch-Schonlein purpura, systemic lupus erythematosus, and scleroderma. Human immunodeficiency virus (HIV) infection may present with acute renal failure from HIV nephropathy. The prognosis is quite poor with this condition.
B. Laboratory Findings:
1. Urine-Urinalysis discloses variably active sediments: many red and white cells and multiple types of cellular and granular casts (telescopic urine). Phase contrast microscopy usually reveals dysmorphic red cells in the urine. In allergic interstitial nephritis, eosinophils may be noted. The urine sodium concentration may range from 10 to 40 mEq/L.
2. Blood test- Components of serum complement are often diminished during deposition of immune complexes. In a few conditions, circulating immune complexes can be identified. Other tests may disclose systemic diseases such as lupus erythematosus. Thrombocytopenia and altered red cell morphologic structure are noted in peripheral blood smears in the hemolytic uremic syndrome (HUS).
3. Renal biopsy- Biopsy examination shows characteristic changes of glomerulonephritis, acute interstitial nephritis, or glomerular capillary thrombi (in HUS). There may be extensive crescents involving Bowman's space.
C. X-Ray Findings: Poor visualization on intravenous urography or radionuclide renal scans is characteristic. Routine intravenous urography should be avoided because of the risk of dyeinduced renal injury.
For this reason, sonography is preferable to rule out obstruction.
Therapy is directed toward eradication of infection, removal of antigen, elimination of toxic materials and drugs, suppression of autoimmune mechanisms, removal of autoimmune antibodies, or a reduction in effector-inflammatory responses. Immunotherapy may involve drugs, anticoagulants, or the temporary use of plasmapheresis. Initiation of supportive dialysis may be required.
2. NONSPECIFIC INTRARENAL STATES
Nonspecific intrarenal causes of acute renal failure include acute tubular necrosis and acute cortical necrosis. The latter presents with anuria and associated intrarenal intravascular coagulation and generally has a poorer prognosis than the former. These forms of acute renal failure usually occur in hospital settings. Various morbid conditions leading to septic syndrome-like physiologic disturbances are often present.
Acute tubular necrosis was initially described by Liicke during World War II in patients suffering crush injuries and shock. Degenerative changes of the distal tubules (lower nephron nephrosis) were believed to be due to ischemia. When dialysis became available, most of these patients recovered—sometimes completely—provided intrarenal intravascular coagulation and cortical necrosis had not occurred.
Elderly patients are more prone to develop this form of oliguric acute renal failure following hypotensive episodes. It appears that exposure to some drugs (eg, prostaglandin inhibitors such as nonsteroidal antiinflammatory agents) may increase the risk of acute tubular necrosis. Although the classic picture of lower nephron nephrosis may not develop, a similar nonspecific acute renal failure is noted in some cases of mercury (especially mercuric chloride) poisoning and following exposure to radiocontrast agents, especially in patients with diabetes mellitus or myeloma.
A. Symptoms and Signs: Usually the clinical picture is that of the associated clinical state. Dehydration and shock may be present concurrently, but the urine output and acute renal failure fail to improve following administration of intravenous fluids, in contrast to the situation in patients who have pre-renal renal failure (see preceding discussion). On the other hand, there may be signs of excessive fluid retention in patients with acute renal failure following radiocontrast exposure. Symptoms of uremia per se (eg, altered mentation or gastrointestinal symptoms) are unusual in acute renal failure (in contrast to chronic renal failure).
Cardiovascular. Hypertension, pulmonary edema, peripheral edema, and arrhythmias are among the cardiovascular effects of ARF. As decreased urine output causes fluid retention, the patient develops hypertension. If his heart can’t pump the additional volume, heart failure ensues. Renin overproduction also causes hypertension.
Edema results when extra fluid moves from his blood vessels into the interstitial space or into his tissues. Because blood albumin is essential to regulate the passage of water and solutes through the capillaries and to prevent fluid from shifting into the interstitial spaces, a low serum albumin level can lead to edema.
Hyperkalemia occurs when the kidneys fail to excrete excess potassium. Be on guard for signs and symptoms such as muscle weakness, loss of muscle tone, and neuromuscular irritability, including tingling in the lips or fingertips. Changes in the electrocardiogram, such as a flattened p wave, prolonged QRS complex, and tall, tented T waves, also signal hyperkalemia. Often, though, hyperkalemia doesn’t cause symptoms, so monitoring the patient’s serum potassium level is critical. A level above 6 mEq/liter could trigger bradycardia, heart block, asystole, or another arrhythmia.
Glomerular filtration rate—the key to kidney function
Glomerular filtration rate (GFR), the amount of blood filtered through the glomeruli of the kidneys, is the driving force of urine production. Normally 120 to 125 ml/minute, GFR decreases when renal insult occurs. Increased blood urea nitrogen and creatinine levels are indirect indicators of reduced GFR.
Respiratory. If fluid overload continues, your patient may develop dyspnea, indicating pulmonary edema. Assess him for dyspnea at rest or on exertion and auscultate his lungs for crackles.
Neurologic. Metabolic wastes building up in his blood can affect your patient’s mental status. Look for changes in his level of consciousness, which could progress to coma. Sensory changes and weakness in the extremities signal uremic neuropathy.
Hematologic. Anemia is the main hematologic effect of ARF. Contributing factors include impaired red blood cell (RBC) production, hemolysis, bleeding, hemodilution, and reduced RBC survival. The normal life span of RBCs, about 120 days, is shortened to about 60 days in ARF. And because the damaged kidneys produce less and less erythropoietin to stimulate RBC production, the lost RBCs aren’t replaced. Monitor your patient for decreased hemoglobin and hematocrit levels and dyspnea due to insufficient oxygenation.
Gastrointestinal (GI). Uremia causes anorexia, nausea, and vomiting, which lead to poor nutrition and loss of body mass and muscle. Because uremia also can trigger colitis and gastric ulcers, your patient is at risk for GI bleeding. His breath may take on a foul urine odor caused by an increase in urea.
To confirm ARF, the primary care provider will perform a thorough history and physical examination, blood and urine tests, and possibly a renal ultrasound. If testing confirms ARF, prepare to intervene rapidly to prevent permanent renal damage.
Eliminating the cause
In most cases of ARF, normal kidney function returns naturally within weeks. The treatment goals are to eliminate the cause of ARF and support the patient’s kidney function and other affected body systems. This means reestablishing blood flow to the kidneys for a prerenal condition, treating intrinsic renal disease such as acute glomerulonephritis, or removing a postrenal obstruction. Regardless of the type of ARF affecting your patient, provide the following supportive measures:
Maintain fluid and electrolyte balance. Accurately assessing fluid balance is critical, so strictly monitor your patient’s weight along with his fluid intake and output. Be sure to include vomitus and liquid stools in output measurements.
Assess him for edema, which is often dependent (in the legs and feet if he’s sitting or in the sacral region if he’s supine) but also may appear around his eyes. Document the color and clarity of his urine.
A patient with ARF has an increased risk of hyperkalemia, hyponatremia, and volume overload, so closely monitor his fluid and electrolyte levels. A trial of diuretic therapy may remove excess fluid and electrolytes.
B. Laboratory Findings:
1. Urine-Although the specific gravity may be high immediately after the acute event, it usually becomes low or fixed in the 1.005-1.015 range. Urine osmolality is also low (< 450 mOsm/kg and U/P os-molal ratio < 1.5:1). Urinalysis often discloses tubular cells and granular casts; the urine may be muddy brown. If the test for occult blood is positive, one must be concerned about the presence of myoglobin as well as hemoglobin. Tests for differentiating myoglobin pigment are available.
2. Central venous pressure-This is usually normal to slightly elevated.
3. Fluid challenges-There is no increase in urine volume following intravenous administration of mannitol or physiologic saline. Occasionally following the use of furosemide or "renal doses" of dopamine (1-5 µg/kg/min), a low urine output is converted to a high fixed urine output (low-output renal failure to high-output renal failure), but there is usually no change in the rate of increase of blood urea nitrogen or creatinine.
If there is no response to the initial fluid or mannitol challenge, the volume of administered fluid must be sharply curtailed and the amount given related to measured fluid losses (eg, urine and gastrointestinal) and estimated insensible fluid losses. An early assessment of the rate of rise of serum creatinine and blood urea nitrogen and of the concentrations of electrolytes is necessary to predict the possible use of dialysis therapy. There is some evidence that early use of hyperalimentation might be beneficial in reducing both the need for dialysis and the morbidity and mortality. With appropriate regulation of the volume of fluid administered, solutions of glucose and essential amino acids to provide 30-35 kcal/kg are used to correct or reduce the severity of the catabolic state accompanying acute tubular necrosis.
Serum or plasma potassium must be closely monitored and serial ECGs done to ensure early-recognition of hyperkalemia. This condition can be treated with (1) intravenous sodium bicarbonate administration, (2) Kayexalate, 25-50 g (with sorbitol) orally or by enema, (3) intravenous glucose and insulin, and (4) intravenous calcium preparations to prevent cardiac irritability.
Peritoneal dialysis or hemodialysis should be used as necessary to avoid or correct uremia, hypokalemia, or fluid overload. Hemodialysis in patients with acute renal failure can be either intermittent or continuous (with arteriovenous or venovenous hemofiltration techniques). Vascular access is obtained with percutaneous catheters. The continuous dialysis techniques allow for easier management in many hemodynami-cally unstable patients in intensive care units.
Most cases are reversible within 7-14 days. Residual renal damage may be noted, particularly in elderly patients.
POSTRENAL ACUTE RENAL FAILURE
The conditions listed in Table 1 involve primarily the need for urologic diagnostic and therapeutic interventions. Following lower abdominal surgery, urethral or ureteral obstruction should be considered as a cause of acute renal failure. The causes of bilateral ureteral obstruction are (1) peritoneal or retroperitoneal neoplastic involvement, with masses or nodes; (2) retroperitoneal fibrosis; (3) calculous disease; and (4) postsurgical or traumatic interruption. With a solitary kidney, ureteral stones can produce total urinary tract obstruction and acute renal failure. Urethral or bladder neck obstruction is a frequent cause of renal failure, especially in elderly men.
A number of things can cause kidney failure, but postrenal acute renal failure in particular is caused by anything that interferes with the flow of urine out of your kidneys. All of the blood in your body goes through the kidneys, where waste is usually filtered out and excreted from the body as urine. However, in people with postrenal acute renal failure, something interrupts the urine flow from the kidneys, which means waste can't be filtered or disposed of correctly and waste builds up in the blood. Usually, postrenal acute renal failure is caused by some kind of obstruction in the bladder or its related passageways. Kidney stones or tumors in the ureters (the tubes connecting your kidneys to your bladder) can block waste from passing into the bladder. Also, anything that causes an obstruction in the bladder itself, such as an enlarged prostate, a bladder stone, or a blood clot, may stop urine from properly passing out of the kidneys and through the bladder.
A. Symptoms and Signs: Renal pain and renal tenderness often are present. If there has been an operative ureteral injury with associated urine extravasation, urine may leak through a wound. Edema from overhydration may be noted. Ileus is often present along with associated abdominal distention and vomiting.
B. Laboratory Findings: Urinalysis is usually not helpful. A large volume of urine obtained by catheterization may be both diagnostic and therapeutic for lower tract obstruction.
C. X-Ray Findings: Poor visualization on intravenous urography is characteristic. Radionuclide renal scans may show a urine leak or, in cases of obstruction, retention of the isotope in the renal pelvis. Renal scans are helpful in acute but not in chronic obstruction.
KUB (coral stoun in the right kidney)
Ultrasound examination often reveals a dilated upper collecting system with deformities characteristic of hydronephrosis.
D. Instrumental Examination: Cystoscopy and retrograde ureteral catheterization demonstrate ureteral obstruction.
Treatment options for postrenal acute renal failure may vary depending on the cause of the condition. In instances where the cause of kidney failure is something that can be treated or removed, such as bladder obstruction or kidney stones, it's important to treat that condition first. Once any underlying cause or obstruction has been treated, the kidneys may be able to heal themselves. To promote kidney healing, it's important to replace fluids and minerals that may have been lost. It's also important to maintain a balanced diet that's high in carbohydrates and low in potassium. If levels of certain minerals are too high, doctors may recommend calcium salts or sodium polystyrene sulfonate to be taken, usually by mouth. Doctors may also put you on short-term dialysis, which involves pumping your blood through a machine that filters the blood and removes waste.
Treatment for end-stage kidney disease
If your kidneys can't keep up with waste and fluid clearance on their own and you develop complete or near-complete kidney failure, you have end-stage kidney disease. At that point, dialysis or a kidney transplant is needed.
Dialysis artificially removes waste products and extra fluid from your blood when your kidneys aren't able to perform these functions. In hemodialysis, a machine filters waste and excess fluids from your blood. In peritoneal dialysis, you use a catheter to fill your abdominal cavity with a dialysis solution that absorbs waste and excess fluids — then this solution drains out of your body and is replaced with fresh solution.
If you have no life-threatening medical conditions other than kidney failure, a kidney transplant may be an option for you. Kidney transplant involves surgically placing a healthy kidney from a donor into your body. Transplanted kidneys can come from deceased donors or from living donors.
Some urological conditions have serious or life-threatening consequences and require immediate medical attention. These medical emergencies include
· acute urinary retention,
· Fournier’s gangrene,
· priapism, and
· testicular torsion.
While these conditions are unrelated and have different symptoms, they all require urgent care. Delaying treatment in some cases can result in surgical removal of testicles (orchiectomy), permanent inability to achieve an erection (impotence), or death.
Acute urinary retention is the sudden inability to urinate and is usually symptomatic of another condition that needs treatment.
Incidence and Prevalence
Anyone can experience acute urinary retention. The causes and rate of occurrence varies greatly between genders until about age 60, when men are more often affected as a result of benign prostatic hyperplasia (BPH).
Benign prostatic hyperplasia (BPH).
Kidney stones, prostate cancer, prostatitis, and BPH are risk factors in men. Women with a history of kidney stones or urinary tract infections (UTIs), pregnant women, and those who have had recent gynecological surgery are at higher risk.
Acute urinary retention is caused by obstruction in the bladder or the tube that carries urine from the bladder outside the body (urethra), a disruption of sensory information in the nervous system (e.g., spinal cord or nerve damage), or a situation or event that causes the bladder to become distended.
Factors associated with acute urinary retention include the following:
· Alcohol consumption
· Allergy or cold medications containing decongestants or antihistamines
· Certain prescription drugs (e.g., ipratropium bromide, albuterol, epinephrine) that cause the urethra to become narrow
· Delaying urination for a long time
· Long period of inactivity or bed rest
· Prolonged exposure to cold temperatures
· Spinal cord injury/nerve damage
· Surgery (e.g., complication of anesthesia)
· Urinary system obstruction (e.g., benign prostatic hyperplasia (BPH), kidney stones)
· urinary tract infection
Signs and Symptoms
Acute urinary retention produces severe lower abdominal pain, a distended abdomen, and/or the sudden inability to pass urine.
Complications that may develop with untreated urinary retention include bladder damage and chronic kidney failure.
Diagnosis is based on a sudden lack of urinary output and bladder swelling
(distention) observed during a physical examination.
Treatment should be obtained within 5 hours of the onset of symptoms to avoid the development of complications. The underlying cause of urinary retention (e.g., kidney stones) must be diagnosed and treated as well.
Catheterization of the bladder
A small tube (catheter) is inserted into the bladder through the urethra to drain the urine. Catheterization relieves pain and distention.
Depending on the underlying cause, the recurrence rate can be up to 70% within a week after initial treatment. BPH is responsible for most recurrences.
Fournier’s gangrene, sometimes called Fournier’s disease, is a bacterial infection of the skin that affects the genitals and perineum (i.e., area between the scrotum and anus in men and in women between the vulva and anus). The disease develops after a wound or abrasion becomes infected. A combination of anaerobic (living without oxygen) microorganisms (e.g., staphylococcal) and fungi (e.g., yeast) causes an infection that spreads quickly and causes destruction (necrosis) of skin, tissue under the skin (subcutaneous tissue), and muscle. Staphylococcal bacteria clot the blood, depriving surrounding tissue of oxygen. The anaerobic bacteria thrive in this oxygen-depleted environment and produce molecules that instigate chemical reactions (enzymes) that further the spread of the infection. Fournier’s gangrene can be fatal if the infection enters the bloodstream.
Incidence and Prevalence
Men are ten times more likely than women to develop Fournier’s gangrene. Men aged 60-80 with a predisposing condition are most susceptible.
Women who have had a pus-producing bacterial infection (abscess) in the vaginal area, a surgical incision in the vagina and perineum to prevent tearing of skin during delivery of a child (episiotomy), an abortion resulting in fever and an infection of the lining of the uterus (septic abortion), or surgical removal of the uterus (hysterectomy) are susceptible.
Rarely, children may develop Fournier’s gangrene as a complication in wounds that result from a burn, circumcision, or insect bite.
Men with alcoholism, diabetes mellitus, leukemia, morbid obesity, and immune system disorders (e.g., HIV, Crohn’s disease), and intravenous drug users are at increased risk for developing Fournier’s gangrene. Surgery is also a risk factor.
Fournier’s gangrene develops when multiple bacteria infect the body through a wound, usually in the perineum, tube that carries urine outside the body from the bladder (urethra), or colorectal area. Existing immune system deficiencies help infection to spread quickly, producing a disease that destroys the skin and superficial and deep fascia (membranes that separate muscles and protect nerves and vessels) of the genital area. The chambers in the penis that fill with blood to create an erection (corpora cavernosa), testicles, and urethra are not usually affected.
Signs and Symptoms
The early physical symptoms of Fournier’s gangrene do not always indicate the severity of the condition. Pain sometimes diminishes as the disease progresses. Symptoms are progressive and include the following:
· Crepitant ("spongy" to the touch) skin
· Dead and discolored (gray-black) tissue; pus weeping from injury
· Fever and drowsiness (lethargy)
· Increasing genital pain and redness (erythema)
· Severe genital pain accompanied by tenderness and swelling of the penis and scrotum
Physical examination and blood tests are necessary. A diagnosis is made on finding gangrenous (i.e., spongy, weeping, discolored) skin.
Microscopic examination of a tissue specimen (biopsy) may be taken if visible symptoms are insufficient to distinguish between Fournier’s and other bacterial infections.
Antibiotics (often double or triple drug therapy) along with aggressive surgical removal of all of the diseased tissue is required immediately for an optimal outcome.
Without early treatment, bacterial infection enters the bloodstream and can cause delirium, heart attack, respiratory failure, and death.
Incomplete debridement (surgical removal of dead tissue) allows wound infection to continue to spread. In this event, follow-up surgery is performed.
Paraphimosis occurs when the fold of skin that covers the head (glans) of an uncircumcised penis (i.e., the foreskin) has been retracted and narrows below the glans, constricting the lymphatic drainage and causing the glans to swell. If not corrected, blood flow in the penis becomes impeded by the increasingly constricting band of foreskin, which causes further swelling of the glans. Because lack of oxygen from the reduced blood flow can cause tissue death (necrosis), paraphimosis is considered a medical emergency and requires immediate treatment.
Incidence and Prevalence
Uncircumcised males are at risk. Piercing the penis increases the risk if the penile ring interferes with foreskin retraction or replacement over the glans, and if infection results from the piercing.
Causes include the following:
· Bacterial infection (e.g., balanoposthitis)
· Catheterization (i.e., if the foreskin is not returned to its original position after a urethral catheter is inserted, the glans may become swollen, which can initiate paraphimosis)
· Poor hygiene
· Swelling-producing injury
· Vigorous sexual intercourse
Signs and Symptoms
Symptoms include the following:
· Band of retracted foreskin tissue beneath the glans
· Black tissue on the glans (indicates necrosis)
· Inability to urinate (urinary retention)
· Penile pain
· Redness (erythema)
· Swollen glans (the shaft of the penis is not swollen)
Tissue death caused by loss of blood supply (gangrene) and spontaneous detachment of diseased tissue (autoamputation) of the glans are possible complications of paraphimosis.
Paraphimosis is diagnosed during a physical examination.
Because paraphimosis can be severely painful, a pain reliever is administered before treatment. The first method of treatment after diagnosis involves manual manipulation of the penis to reduce swelling and to replace the foreskin over the glans.
Manual manipulation of the penis
An ice pack may be applied to the penis (after the penis has been wrapped in plastic) to help reduce swelling.
If manual treatment is unsuccessful, the puncture technique uses a needle to drain excess watery fluid in the swollen tissue (edematous fluid) from the glans to reduce swelling.
A third option is to make a small incision in the foreskin to alleviate constriction and allow the swelling to subside. With this procedure, local anesthesia is administered to minimize discomfort.
After reduction of swelling is achieved, antibiotics are prescribed for any underlying infection.
Full recovery from paraphimosis is expected with prompt treatment.
Circumcision is recommended after treatment to prevent a recurring episode.
Priapism is a prolonged, painful penile erection that occurs when blood in the penis is "trapped," or unable to drain. The stagnant blood causes an erection that can last from hours to days. A painful erection lasting for more than 4 hours indicates priapism. If not treated promptly, scarring and permanent inability to achieve an erection (impotence) can result.
Veno-occlusive (low flow)
Veno-occlusive (blocked vein) priapism develops when circulation in the penis becomes sluggish due to obstructed veins. This type usually occurs without a known cause in men who are otherwise healthy.
Arterial (high flow)
This rare, less painful type of priapism results from an injury to the penis or area between scrotum and anus (perineum) that prevents blood in the penis from circulating normally. It indicates a ruptured artery in the penis. There may be a lapse between the time of injury and onset of priapism. Incidence and Prevalence Priapism can affect men of any age. Most venoocclusive priapism in men with sickle cell disease occurs between ages 19-21. The rate of venoocclusive priapism is higher in men who have malaria, leukemia, and Fabry disease.
Diseases that affect blood circulation may predispose men to developing the condition. Forty-two percent of men with sickle cell disease develop veno-occlusive priapism at least once.
Recreational or "party" drug use (e.g., cocaine, ecstasy, marijuana) is a risk factor. An overdose of injectable medication such as papaverine and phentolamine (Regitine®) for erectile dysfunction is also a risk factor. Men with sickle cell disease, leukemia, malaria, and Fabry disease are predisposed to priapism.
Alcohol consumption, androgenic steroids (used to increase muscle size), anticoagulants (Coumadin®, Warfilone®), and antihypertensives (Prazosin®) increase risk. Prolonged sexual activity is also a risk factor.
Priapism may develop as a result of prolonged sexual activity. Other causes include the following:
· Black widow spider bites
· Carbon monoxide poisoning
· Erectile dysfunction injection therapy (if amount of medication injected exceeds prescribed dose)
· Penile or perineal injury (e.g., perineal trauma against the top tube of a bicycle)
· Prescription antidepressive drugs trazodone (Desyrel®) and chlorpromazine (Compazine®, Serentil®)
· Spinal cord trauma
Signs and Symptoms
A painful penile erection that lasts 4 hours or more, and a soft head (glans) with a hard shaft are signs of priapism.
Diagnosis includes a patient history and a physical examination to detect an injury or underlying problem.
In veno-occlusive priapism, angiography may be used to help locate blocked veins. Angiography uses a special dye injected into the bloodstream to enable the physician to see blockages on x-ray.
Doppler sonogram (i.e., digital images of ultrasound echos that detect poor blood flow) may be used to diagnose high- or low-flow priapism.
There are several forms of treatment. Ice packs are applied to the penis and perineum to reduce swelling. Walking up a flight of stairs is sometimes effective, because mild exercise may divert blood flow to other areas of the body. The underlying injury (i.e., ruptured artery) causing arterial priapism is treated by tying off the artery (surgical ligation) to restore normal blood flow.
Low-flow priapism is treated with vasoconstrictive medications injected into the chambers in the penis that fill with blood to create an erection (corpora cavernosa) to narrow the veins and cause swelling to subside. Alpha agonists terbutaline (Adrenalin®, Alupent®) and phenylephrine (Neo-Synephrine®) are commonly used.
After numbing the area, a needle is used to drain the blood from the corpora cavernosa to allow the swelling to subside.
For veno-occlusive priapism, a passageway (shunt) may be surgically inserted to divert blood flow and reestablish circulation.
The underlying cause is treated when disease is present (e.g., leukemia, sickle cell disease).
The prognosis is good for both types of priapism when the condition is resolved quickly. When treatment is delayed, penile scarring and permanent impotence can result.
Testicular torsion is a disorder in which the testicles rotate (twist) and strangle the spermatic cord, which consists of blood vessels, lymphatic vessels, nerves, and the duct that carries sperm from the body (vas deferens), cutting off the blood supply to the testicles. Torsion can cause shrinkage (atrophy) and tissue death (necrosis), and may require surgical removal of the testicles (orchiectomy) if not treated promptly. Torsion often occurs during sleep.
Incidence and Prevalence
Testicular torsion primarily affects infants in the first year of life and adolescent boys age 12-18, although it can occur at any age. Males with one or both testicles not descended into scrotum (cryptorchidism) develop testicular torsion more often than the general population.
Injury to the scrotum or groin and vigorous physical activity are risk factors.
Injury to the scrotum can initiate a muscle spasm that cause the testicles to twist. Some cases result from inadequate connective tissue that "anchors" the testicle within the scrotum. Many cases are idiopathic (i.e., have no known cause).
Signs and Symptoms
Symptoms include the following:
· Blood in semen
· Lower abdominal pain
· Lump in testicle
· Nausea and vomiting
· Sudden, severe testicular pain, followed by diminishing pain after several hours (after necrosis begins to set in)
· Redness of scrotum
· Swelling of one testicle
A patient history and physical examination is usually sufficient to diagnose testicular torsion. Testicular torsion may cause symptoms (e.g., testicular pain and swelling) similar to epididymitis (i.e., inflammation of the tubule where sperm is stored) and diagnostic tests may be necessary.
Color Doppler sonography (color printout of an ultrasound echo test) is used to identify the absence of blood flow typically found in a twisted testicle, which distinguishes the condition from epididymitis.
Urinalysis (analyzing chemical composition of urine) can be used to rule out bacterial infections.
Surgical exploration may be necessary if diagnosis cannot be made using other methods.
Treatment involves untwisting (detorsion), manually if possible and surgically if necessary. Surgical detorsion requires anesthesia followed by an incision in the scrotum.
The testicles are untwisted and evaluated for necrosis. Dead tissue is removed; removal of one or both testicles may be necessary. If necrosis has not occurred, the healthy testicle(s) are then sutured (stitched) to the scrotal wall to avoid recurrence.
If torsion is diagnosed and treated within 5-6 hours, the prognosis is good. The more time that elapses before resolution worsens the prognosis. After 18-24 hours, necrosis usually develops and indicates removal of the affected testicle
INJURIES TO THE BLADDER
Bladder injuries occur most often from external force and are often associated with pelvic fractures. (About 15% of all pelvic fractures are associated with concomitant bladder or urethral injuries.) latrogenic injury may result from gynecologic and other extensive pelvic procedures as well as from hernia repairs and transurethral operations.
Pathogenesis & Pathology
The bony pelvis protects the urinary bladder very well. When the pelvis is fractured by blunt trauma, fragments from the fracture site may perforate the bladder. These perforations usually result in extraperitoneal rupture. If the urine is infected, extraperitoneal bladder perforations may result in deep pelvic abscess and severe pelvic inflammation.
When the bladder is filled to near capacity, a direct blow to the lower abdomen may result in bladder disruption. This type of disruption ordinarily is intraperitoneal. Since the reflection of the pelvic peritoneum covers the dome of the bladder, a linear laceration will allow urine to flow into the abdominal cavity. If the diagnosis is not established immediately and if the urine is sterile, no symptoms may be noted for several days. If the urine is infected, immediate peritonitis and acute abdomen will develop.
Pelvic fracture accompanies bladder rupture in 90% of cases. The diagnosis of pelvic fracture can be made initially in the emergency room by lateral compression on the bony pelvis, since the fracture site will show crepitus and be painful to the touch. Lower abdominal and suprapubic tenderness is usually present. Pelvic fracture and suprapubic tenderness with acute abdomen suggest intraperitoneal bladder disruption.
A. Symptoms: There is usually a history of lower abdominal trauma. Blunt injury is the usual cause. Patients ordinarily are unable to urinate, but when spontaneous voiding occurs, gross hematuria is usually present. Most patients complain of pelvic or lower abdominal pain.
B. Signs: Heavy bleeding associated with pelvic fracture may result in hemorrhagic shock, usually from venous disruption of pelvic vessels. Evidence of external injury from a gunshot or stab wound in the lower abdomen should make one suspect bladder injury, manifested by marked tenderness of the suprapubic area and lower abdomen. An acute abdomen indicates intraperitoneal bladder rupture. A palpable mass in the lower abdomen usually represents a large pelvic hematoma. On rectal examination, landmarks may be indistinct because of a large pelvic hematoma.
C. Laboratory Findings: Catheterization usually is required in patients with pelvic trauma but not if bloody urethral discharge is noted. Bloody urethral discharge indicates urethral injury, and a urethrogram is necessary before catheterization. When catheterization is done, gross or, less commonly, microscopic hematuria is usually present. Urine taken from the bladder at the initial catheterization should be cultured to determine whether infection is present.
D. X-Ray Findings: A plain abdominal film generally demonstrates pelvic fractures. There may be haziness over the lower abdomen from blood and urine extravasation. An intravenous urogram should be obtained to establish whether kidney and ureteral injuries are present.
Retrogradual cystography (Retroperitoneal rupture)
Bladder disruption is shown on cystography. The bladder should be filled with 300 mL of contrast material and a plain film of the lower abdomen obtained. Contrast medium should be allowed to drain out completely, and a second film of the abdomen should be obtained. The drainage film is extremely important, because it demonstrates areas of extraperitoneal extravasation of blood and urine that may not appear on the filling film. With intraperitoneal extravasation, free contrast medium is visualized in the abdomen, highlighting bowel loops.
Retrogradual cystography (Intraperitoneal rupture)
Retrogradual cystography (Intraperitoneal rupture)
CT cystography is an excellent method for detecting bladder rupture; however, retrograde filling of the bladder with 300 mL of contrast medium is necessary to distend the bladder completely. Incomplete distention with consequent missed diagnosis of bladder rupture often occurs when the urethral catheter is clamped during standard abdominal CT scan with intravenous contrast injection.
E. Instrumental Examination: If urethral injury is suspected (bloody discharge), a urethrogram should be obtained before any attempt is made to catheterize the patient. If there is no evidence of urethral injury, catheterization can be safely accomplished.
Cystoscopy is not indicated, since bleeding and clots obscure visualization and prevent accurate diagnosis.
Abdominal trauma with hematuria may cause injury to the kidney and ureter as well as the bladder. A urogram is indicated for all patients with trauma-related hematuria. Associated injuries to the pelvic vessels and bowel also should be considered.
The urethra may be injured as well as the bladder; this possibility should be considered in any patient with blunt trauma and pelvic fractures. Urethrogra-phy demonstrates disruption of the urethra.
A pelvic abscess may develop from extraperi-toneal bladder rupture; if the urine becomes infected, the pelvic hematoma becomes infected too.
Intraperitoneal bladder rupture with extravasation of urine into the abdominal cavity causes delayed peritonitis.
Partial incontinence may result from bladder injury when the laceration extends into the bladder neck. Meticulous repair may ensure normal urinary control.
A. Emergency Measures: Shock and hemorrhage should be treated.
B. Surgical Measures: A lower midline abdominal incision should be made.
As the bladder is approached in the midline, a pelvic hematoma, which is usually lateral, should be avoided. Entering the pelvic hematoma can result in increased bleeding from release of tamponade and in infection of the hematoma, with subsequent pelvic abscess. The bladder should be opened in the midline and carefully inspected. After repair, a suprapubic cystostomy tube is usually left in place to ensure complete urinary drainage and control of bleeding.
1. Extraperitoneal rupture- Extraperitoneal rupture should be repaired intravesically. As the bladder is opened in the midline, it should be carefully inspected and lacerations closed from within. Polyglycolic acid or chromic absorbable sutures should be used.
Juncture by two-row catgut junctures.
Perivesical space is drainage through obturatorial foramen or ischiorectal space.
Drainage through obturatorial foramen
Extraperitoneal bladder lacerations occasionally extend into the bladder neck and should be repaired meticulously. Fine absorbable sutures should be used to ensure complete reconstruction so that the patient will have urinary control after injury. Such injuries are best managed with indwelling urethral catheterization and suprapubic diversion.
Peritoneotomy should be done and the intraabdominal fluid inspected before the procedure is completed. If abdominal fluid is bloody, complete abdominal exploration should be done to rule out associated injuries.
2. Intraperitoneal rupture Intraperitoneal bladder ruptures should be repaired via a transperitoneal approach after careful transvesical inspection and closure of any other perforations.
The peritoneum must be closed carefully over the area of injury. The bladder is then closed in separate layers by absorbable suture. All extravasated fluid from the peritoneal cavity should be removed before closure. At the time of closure, care should be taken that the suprapubic cystostomy is in the extraperitoneal position.
3. Pelvic fracture Stable fracture of the pubic rami is usually present. In such cases, the patient can be ambulatory within 4-5 days without damage or difficulty. Unstable pelvic fractures requiring external fixation have a more protracted course.
4. Pelvic hematoma There may be heavy uncontrolled bleeding from rupture of pelvic vessels even if the hematoma has not been entered at operation. At exploration and bladder repair, packing the pelvis with laparotomy tapes often controls the problem. If bleeding persists, it may be necessary to leave the tapes in place for 24 h and operate again to remove them. Embolization of pelvic vessels with Gelfoam or skeletal muscle under angiographic control is useful in controlling persistent pelvic bleeding.
C. Medical Measures: The patient whose cystogram shows only a small degree of extravasation can be managed by placing a urethral catheter into the bladder, without operation or suprapubic cystostomy. The urine must be free of infection. Corriere and Sandier (1988) have reported success with such management. Careful observation is necessary because of the potential for pelvic hematoma infection, continued bleeding from the bladder, and clot retention.
With appropriate treatment, the prognosis is excellent. The suprapubic cystostomy tube can be removed within 10 days, and the patient can usually void normally. Patients with lacerations extending into the bladder neck area may be temporarily incontinent, but full control is usually regained. At the time of discharge, urine culture should be performed to determine whether catheterassociated infection requires further treatment.
INJURIES TO THE URETHRA
Urethral injuries are uncommon and occur most often in men, usually associated with pelvic fractures or straddle-type falls. They are rare in women.
Various parts of the urethra may be lacerated, transected, or contused. Management varies according to the level of injury. The urethra can be separated into 2 broad anatomic divisions: the posterior urethra, consisting of the prostatic and membranous portions, and the anterior urethra, consisting of the bulbous and pendulous portions.
INJURIES TO THE POSTERIOR URETHRA
The membranous urethra passes through the urogenital diaphragm and is the portion of the posterior urethra most likely to be injured. The urogenital diaphragm contains most of the voluntary urinary sphincter. It is attached to the pubic rami inferiorly, and when pelvic fractures occur from blunt trauma, the membranous urethra is sheared from the prostatic apex at the prostatomembranous junction. The urethra can be transected by the same mechanism at the interior surface of the membranous urethra.
Pathogenesis & Pathology
Injuries to the posterior urethra commonly occur from blunt trauma and pelvic fractures. The urethra usually is sheared off just proximal to the urogenital diaphragm, and the prostate is displaced superiorly by the developing hematoma in the periprostatic and perivesical spaces.
A. Symptoms: Patients usually complain of lower abdominal pain and inability to urinate. A history of crushing injury to the pelvis is usually obtained.
B. Signs: Blood at the urethral meatus is the single most important sign of urethral injury. The importance of this finding cannot be overemphasized, because an attempt to pass a urethral catheter may result in infection of the periprostatic and perivesical hematoma and conversion of an incomplete laceration to a complete one. The presence of blood at the external urethral meatus indicates that immediate urethrography is necessary to establish the diagnosis.
Suprapubic tenderness and the presence of pelvic fracture are noted on physical examination. A large developing pelvic hematoma may be palpated. Peri-neal or suprapubic contusions are often noted. Rectal examination may reveal a large pelvic hematoma with the prostate displaced superiorly. Rectal examination can be misleading, however, because a tense pelvic hematoma may resemble the prostate on palpation. Superior displacement of the prostate does not occur if the puboprostatic ligaments remain intact. Partial disruption of the membranous urethra (currently 10% of cases) is not accompanied by prostatic displacement.
C. Laboratory Findings: Anemia due to hemorrhage may be noted. Urine usually cannot be obtained initially, since the patient should not void and catheterization should not be attempted.
D. X-Ray Findings: Fractures of the bony pelvis are usually present. A urethrogram (using 20-30 mL of watersoluble contrast material) shows the site of extravasation at the prostatomembranous junction.
(free extravasation of contrast material)
Ordinarily, there is free extravasation of contrast material into the perivesical space. Incomplete prostatomembranous disruption is seen as minor extravasation, with a portion of contrast material passing into the prostatic urethra and bladder.
E. Instrumental Examination: The only instrumentation involved should be for urethrography. Catheterization or urethroscopy should not be done, because these procedures pose an increased risk of hematoma, infection, and further damage to partial urethral disruptions.
Bladder rupture may be associated with posterior urethral injuries. An intravenous urogram should be considered part of the assessment. Delayed films should be obtained to demonstrate the bladder and note extravasation. Cystography cannot be done preoperatively, since a urethral catheter should not be passed. Careful evaluation of the bladder at operation is necessary. The anterior portion of the urethra may be injured as well as the prostatomembranous urethra.
Stricture, impotence, and incontinence as complications of prostatomembranous disruption are among the most severe and debilitating mishaps that result from trauma to the urinary system. Stricture following primary repair and anastomosis occurs in about one-half of cases. If the preferred suprapubic cystostomy approach with delayed repair is used, the incidence of stricture can be reduced to about 5%.
The incidence of impotence after primary repair is 30-80% (mean, about 50%). This figure can be reduced to 10-15% by suprapubic drainage with delayed urethral reconstruction.
Incontinence in primary reanastomosis is noted in one-third of patients. Delayed reconstruction reduces the incidence to less than 5%.
A. Emergency Measures: Shock and hemorrhage should be treated.
B. Surgical Measures: Urethral catheterization should be avoided.
1. Immediate management-Initial management should consist of suprapubic cystostomy to provide urinary drainage.
A midline lower abdominal incision should be made, care being taken to avoid the large pelvic hematoma. The bladder and prostate are usually elevated superiorly by large periprostatic and perivesical hematomas. The bladder often is distended by a large volume of urine accumulated during the period of resuscitation and operative preparation. The urine is often clear and free of blood, but gross hematuria may be present. The bladder should be opened in the midline and carefully inspected for lacerations. If a laceration is present, the bladder should be closed with absorbable suture material and a cystostomy tube inserted for urinary drainage. This approach involves no urethral instrumentation or manipulation. The suprapubic cystostomy is maintained in place for about 3 months. This allows resolution of the pelvic hematoma, and the prostate and bladder will slowly return to their anatomic positions.
Incomplete laceration of the posterior urethra heals spontaneously, and the suprapubic cystostomy can be removed within 2-3 weeks. The cystostomy tube should not be removed before voiding cystourethrography shows that no extravasation persists.
2. Urethral reconstruction-
Reconstruction of the urethra after prostatic disruption can be undertaken within 3 months, assuming there is no pelvic abscess or other evidence of persistent pelvic infection. Before reconstruction, a combined cystogram and urethrogram should be done to determine the exact length of the resulting urethral stricture. This stricture usually is 1-2 cm long and situated immediately posterior to the pubic bone. The preferred approach is a single-stage reconstruction of the urethral rupture defect with direct excision of the strictured area and anastomosis of the bulbous urethra directly to the apex of the prostate. A 16F silicone urethral catheter should be left in place along with a suprapubic cystostomy. Catheters are removed within a month, and the patient is then able to void.
Urethral reconstruction prostatomembranous part of the urethra
3. Immediate urethral realignment-Some surgeons prefer to realign the urethra immediately. Direct suture reconstruction of the prostatomembranous disruption in the acute injury is extremely difficult. Persistent bleeding and surrounding hematoma create technical problems. The incidence of stricture, impotence, and incontinence appears to be higher than with immediate cystostomy and delayed reconstruction. However, several authors have reported success with immediate urethral realignment.
C. General Measures: After delayed reconstruction by a perineal approach, patients are allowed ambulation on the first postoperative day and usually can be discharged within 3 days.
D. Treatment of Complications: Approximately 1 month after the delayed reconstruction, the urethral catheter can be removed and a voiding cystogram obtained through the suprapubic cystostomy tube. If the cystogram shows a patent area of reconstruction free of extravasation, the suprapubic catheter can be removed; if there is extravasation or stricture, suprapubic cystostomy should be maintained. A follow-up urethrogram should be obtained within 2 months to watch for stricture development.
Stricture, if present (< 5%), is usually very short, and urethrotomy under direct vision offers easy and rapid cure.
The patient may be impotent for several months after delayed repair. Impotence is permanent in about 10% of patients. Implantation of a penile prosthesis is indicated if impotence is still present 2 years after reconstruction.
Incontinence seldom follows transpubic or perineal reconstruction. If present, it usually resolves slowly.
If complications can be avoided, the prognosis is excellent. Urinary infections ultimately resolve with appropriate management.
INJURIES TO THE ANTERIOR URETHRA
Etiology The anterior urethra is the portion distal to the urogenital diaphragm. Straddle injury may cause laceration or contusion of the urethra. Self-instrumentation or iatrogenic instrumentation may cause partial disruption.
Pathogenesis & Pathology
A. Contusion: Contusion of the urethra is a sign of crush injury without urethral disruption. Perineal hematoma usually resolves without complications.
B. Laceration: A severe straddle injury may result in laceration of part of the urethral wall, allowing extravasation of urine. If the extravasation is unrecognized, it may extend into the scrotum, along the penile shaft, and up to the abdominal wall. It is limited only by Colics' fascia and often results in sepsis, infection, and serious morbidity.
A. Symptoms: There is usually a history of a fall, and in some cases a history of instrumentation. Bleeding from the urethra is usually present. There is local pain into the perineum and sometimes massive perineal hematoma. If voiding has occurred and extravasation is noted, sudden swelling in the area will be present. If diagnosis has been delayed, sepsis and severe infection may be present.
B. Signs: The perineum is very tender, and a mass may be found. Rectal examination reveals a normal prostate. The patient usually has a desire to void, but voiding should not be allowed until assessment of the urethra is complete. No attempt should be made to pass a urethral catheter, but if the patient's bladder is overdistended, percutaneous suprapubic cystostomy can be done as a temporary procedure.
When presentation of such injuries is delayed, there is massive urinary extravasation and infection in the perineum and the scrotum. The lower abdominal wall may also be involved. The skin is usually swollen and discolored.
C. Laboratory Findings: Blood loss is not usually excessive, particularly if secondary injury has occurred. The white count may be elevated with infection.
D. X-Ray Findings: A urethrogram, with instillation of 15-20 mL of water-soluble contrast material, demonstrates extravasation and the location of injury.
Urethrogram (demonstrates extravasation and the location of injury)
A contused urethra shows no evidence of extravasation.
E. Instrumental Examination: If there is no evidence of extravasation on the urethrogram, a urethral catheter may be passed into the bladder. Extravasation is a contraindication to further instrumentation at this time.
Partial or complete disruption of the prostatomem-branous urethra may occur if pelvic fracture is present. Urethrography usually demonstrates the location and extent of extravasation and its relationship to the urogenital diaphragm.
Heavy bleeding from the corpus spongiosum injury may occur in the perineum as well as through the urethral meatus. Pressure applied to the perineum over the site of the injury usually controls bleeding. If hemorrhage cannot be controlled, immediate operation is required.
The complications of urinary extravasation are chiefly sepsis and infection. Aggressive debridement and drainage are required if there is infection.
Stricture at the site of injury is a common complication, but surgical reconstruction may not be required unless the stricture significantly reduces urinary flow rates.
A. General Measures: Major blood loss usually does not occur from straddle injury. If heavy bleeding does occur, local pressure for control, followed by resuscitation, is required.
B. Specific Measures:
1. Urethral contusion The patient with urethral contusion shows no evidence of extravasation, and the urethra remains intact. After urethrography, the patient is allowed to void; and if the voiding occurs normally, without pain or bleeding, no additional treatment is necessary. If bleeding persists, urethral catheter drainage can be done.
2. Urethral lacerations. Instrumentation of the urethra following urethrography should be avoided. A small midline incision in the suprapubic area readily exposes the dome of the bladder so that a suprapubic cystostomy tube can be inserted, allowing complete urinary diversion while the urethral laceration heals.
Percutaneous cystostomy may also be used in such injuries. If only minor extravasation is noted on the urethrogram, a voiding study can be performed within 7 days after suprapubic catheter drainage to search for extravasation. In more extensive injuries, one should wait 2-3 weeks before doing a voiding study through the suprapubic catheter. Healing at the site of injury may result in stricture formation. Most of these strictures are not severe and do not require surgical reconstruction. The suprapubic cystostomy catheter may be removed if no extravasation is documented. Follow-up with documentation of urinary flow rates will show whether there is urethral obstruction from stricture.
3. Urethral laceration with extensive urinary extravasation- After major laceration, urinary extravasation may involve the perineum, scrotum, and lower abdomen. Drainage of these areas is indicated. Suprapubic cystostomy for urinary diversion is required. Infection and abscess formation are common and require antibiotic therapy.
4. Immediate repair-Immediate repair of urethral lacerations can be performed, but the procedure is difficult and the incidence of associated stricture is high.
C. Treatment of Complications: Strictures at the site of injury may be extensive and require delayed reconstruction.
Urethral stricture is a major complication but in most cases does not require surgical reconstruction. If, when stricture resolves, urinary flow rates are poor and urinary infection and urethral fistula are present, reconstruction is required.
Renal colic is a type of abdominal pain commonly caused by kidney stones.
What are the symptoms of renal colic?
Symptoms of renal colic are related to the formation of crystals in the kidneys. These stones can block urine output, causing pain, swelling and infection.
Patients usually present with severe loin pain which may come suddenly or slowly increase in severity. The pain is caused by stretching of the renal pelvis and capsule as the stone obstructs the drainage of urine and by overactive contractions of the ureter as it attempts to dislodge the obstructing stone passing through it. Pain can be felt anywhere in the region of the kidney and along the course of the ureter, commonly described as ‘loin to groin pain’.
Loin pain usually represents more proximal obstruction with the pain moving more anteriorly and to the groin if and when the stone moves further down the ureter.
As the innervation of the testicle and the kidney is the same, pain may also be referred to the testicle or labia. Other common symptoms include nausea and vomiting, haematuria and lower urinary tract symptoms (usually irritative) either due to a urinary tract infection or as a result of inflammation of the bladder wall because of a stone lodged at the ureteral orifice. Patients may also describe passing a stone or stone debris when they micturate and when possible these should be kept for analysis. A good history will often reveal predisposing and precipitant factors such as intensive exercise, high protein intake, periods of immobility, previous episodes, familial tendency and conditions associated with stone formation such as recurrent urinary tract infection (UTI), inflammatory bowel disease, metabolic disorders (including gout), kidney disease and endocrine disorders.
Unlike a patient with peritonism, who characteristically lies still, a renal colic sufferer will often be more fidgety as they try to find a more comfortable position. Simple observations will often reveal the patient to be tachycardic, usually due to the pain, but beware of a febrile patient who may be showing signs of septic shock. Palpation of the abdomen may reveal tenderness in the areas described above.
Patients with renal colic may undergo several investigations and the timing of each varies depending on the time of presentation.
Dipstick urine testing is readily available to all GPs and is normally the first test to be performed. It will show the presence of blood in 85% of patients with renal colic. Although the absence of blood should alert you to other causes of the pain, it does not exclude renal colic . The presence of nitrites and/or leucocytes obviously raises the suspicion of a UTI and urine should be sent for microscopy and culture. Normal urine is acidic with a pH around 5.5, a urinary pH greater than 7 raises the possibility of infection with urea splitting bacteria and the presence of struvite stones. Alternatively, a pH of 5.4 or less might suggest increased levels of uric acid in the urine and the risk of a uric acid stone (uric acid precipitates at pH 5.4).
Further investigations on the urine, usually via a specialist ‘stone clinic’, will include 24-hour urine collections to measure calcium, phosphate, uric acid and creatinine clearance. In addition, a urine spot test will be performed to detect cystine.
Differential diagnosis of renal colic
Hepatobiliary conditions, for example cholecystitis
Abdominal aortic aneurysm
Inflammatory bowel disease
Ruptured ovarian cysts
Pleurisy, for example lower lobe pneumonia
Quantitative infrared analysis (spectrophotometry) of the stone material will reveal its mineral composition. Patients should be encouraged to collect and keep all stone material that is passed.
Patients will invariably have some form of imaging either in the initial acute period after a referral to the emergency department or in the week following a resolved episode of colic to ensure there is no ongoing obstruction, which depending on the local arrangement, may well be the remit of the GP. Imaging investigations include:
Plain X-ray/intravenous urogram
A plain X-ray of the kidneys, ureter and bladder will often reveal a stone if it contains calcium. For an intravenous urogram, the plain film is followed by the administration of intravenous contrast (assuming there is good renal function)
and repeated X-rays at 30-minute intervals are taken until the contrast is seen to have cleared from the unobstructed side. The contrast will delineate the renal tract and demonstrate ureteric obstruction, which is seen as hydronephrosis and ureteric dilatation above an obstruction.
Non-contrast spiral computed tomography (CT) has the highest degree of diagnostic accuracy and its use is becoming more widespread. Out of hours, however, the availability of a CT scanner with the skilled interpretation needed somewhat limits its use.
Although detecting small stones on ultrasound is difficult, it can be very useful in detecting hydronephrosis, which indicates some degree of obstruction. Ultrasound is often more readily available and is also useful, alongside CT, if there is some diagnostic uncertainty as the radiologist/radiographer will usually be able to screen for an alternative pathology. Magnetic resonance imaging is useful but rarely used as it is time consuming and offers no significant benefit over spiral CT.
Once a diagnosis has been made, which is usually apparent from the history, prompt treatment needs to be given. Analgesia should be the first priority. If, in the general practice setting, the patient cannot be attended to within half an hour, then they should be referred to the local accident and emergency department. This would ordinarily be via an ambulance as a paramedic would be able to give strong analgesia. Non-steroidal anti-inflammatories (NSAIDs), most commonly in the form of intramuscular (IM) or rectal (PR) diclofenac, are the most effective. Subcutaneous or IM opioids (diamorphine, morphine or pethidine) are less effective alternatives when NSAIDs are contraindicated. Antiemetics should also be given, especially if nausea and vomiting is severe or opioid analgesia is used.
The patient should be referred if there is any diagnostic uncertainty as conditions that require immediate intervention often present in a similar fashion to renal colic. Patients with persistent pain, who appear systemically unwell or who have symptoms and signs of infection, should all be referred urgently, as should patients who are anuric, significantly dehydrated or have a solitary or transplanted kidney. Urgent drainage using either a ureteric stent or by means of a nephrostomy is required if the upper urinary tract is both obstructed and infected, as septicaemia (usually with a gram-negative organism) is a very real and life-threatening risk. Similarly, emergency drainage or removal of an obstructing stone is required if renal function deteriorates, the patient becomes anuric, has intractable pain or vomiting or there is obstruction in a solitary or transplanted kidney .
Surgical treatment options
Endoscopic laser lithotripsy
The endoscopic management of renal stones requires a short hospital stay. Under a general anaesthetic, a ureteroscope is passed retrogradely into the ureter until the obstructing stone is identified. The stone can then either be retrieved using a collapsible wire basket or broken up in situ using a laser or ballistic (hydraulic and mechanical) lithotriptor.
The use of baskets and ballistic lithotriptors can be troublesome, and lithotripsy with modern lasers, such as the Holmium: YAG (Ho:YAG) laser, is now the mainstay of treatment. Endoscopic laser lithotripsy has a success rate of around 90% and in combination with extracorporeal shock wave lithotripsy (ESWL) has virtually removed the need for open stone surgery. The Ho:YAG laser works by producing a vaporization bubble at the tip of the fibre-optic cable while in water. Although all lasers have the advantage that they can be delivered via fibre optics, making them ideal for use with flexible ureteroscopes, only modern lasers are able to deliver enough localized energy to break up all types of stone into small enough fragments for routine use. Complication rates for Ho:YAG laser lithotripsy are low at around 4%. Complications may relate to the endoscopy itself (trauma) or residual stone fragments that are themselves large enough to cause colicky symptoms. Localized tissue scarring and fibrosis can occur, leading to ureteral strictures, but this is rare and a rate comparable to non-laser treatments.
Extracorporeal shock wave lithotripsy
ESWL is a non-invasive outpatient procedure that uses focused shock
waves to break stones into smaller fragments, preferably less than
Shock waves, usually produced by
an electromagnet, are propagated through the body with little or no adverse
effect because there is a minimal difference in the density of soft tissues
they pass through. However, at a stone-fluid interface, there is a large
difference in density at which focused shock waves dissipate a large enough
amount of energy to break up the stone. Overall, ESWL achieves stone-free rates
approaching 80%, but this diminishes with large (more than
Percutaneous nephrolithotomy (PCNL) is an inpatient procedure performed under general anaesthesia. A nephroscope is passed via an incision in the loin into the collecting system.
Through this, the stone can be broken up and removed using either a laser or mechanical lithotriptor. It is used when stones are not amenable to an endoscopic approach or ESWL. UTI and catheter problems are fairly common after PCNL but more serious complications including bleeding, septicaemia and pneumothorax are thankfully rare.
If the above measures fail, then open surgery is required but this is now an uncommon occurrence (1–5% of patients).