Endocrine/​Hematology/​Gastrointestinal/​Renal/​Integumentary Study Guide for the CCRN

Renal/Genitourinary

The kidneys and genitourinary structures play an important role in waste filtering, nutrient absorption, waste elimination, and electrolyte balance. Damage to these structures can cause serious events, including urinary retention, electrolyte imbalance, and sepsis. Patients with these conditions may be treated acutely or have long-term consequences from the damage done.

Acute Genitourinary Trauma

Acute genitourinary trauma can include any of the organs that compose the genitourinary tract. These include the kidneys, ureters, bladder, urethra, and any reproductive organs. Trauma in this area most commonly occurs via blunt force injury or penetrating trauma. Blunt renal trauma makes up the majority of acute genitourinary trauma cases. Other injuries to the genitourinary system can include bladder injuries from blunt abdominal trauma or pelvic fractures; urethral crush or straddle injuries (most common in men); surgical injury during abdominal procedures, or laceration due to abdominal gunshot or stab wounds.

Symptoms and Diagnosis

Hematuria, pain, and bruising are common symptoms of genitourinary trauma. Diagnosis of trauma can be determined based on patient history, clinical symptoms, and any necessary radiographic imaging.

In renal and ureteral injuries, microscopic or gross hematuria is the most common symptom. Progressive or prolonged renal injury can lead to renal failure. CT or MRI imaging may identify a perirenal hematoma in the event of blunt trauma. If renal injury is severe, CT imaging may be delayed to avoid use of IV contrast which can cause further renal impairment. Instead, an IV pyelography may be performed to assess renal function.

Bladder injuries generally present with symptoms of lower abdominal pain, gross hematuria, and difficulty or inability to void. Blood testing may show an increase in serum creatinine as urinary fluids are reabsorbed. A retrograde cystography or voiding cystourethrogram can identify irregularities in the bladder and any areas of perforation.

Urethral injuries are most common in men. They can occur due to crush injuries of the penis or straddle injuries. Symptoms of urethral injury include initial hematuria, decreased ability or inability to void, scrotal swelling, and changes to the penis (erythema, edema). Diagnosis can be obtained via a retrograde urethrogram.

Treatment

Treatment of acute genitourinary trauma can include surgical intervention for ruptured or torn organs (ureters, bladder, or urethra), placement of stents, and prevention of further injury. Patients with bladder injuries should have foley catheters placed to keep the bladder decompressed during healing. If urethral injury is suspected, foley catheter placement should not be attempted without consultation of genitourinary healthcare specialists to help prevent any additional injury. Patients with urethral injury may require the use of a suprapubic catheter to facilitate urinary drainage and bladder compression instead.

Some patients may just require close observation without surgical intervention. Many patients will be placed on prophylactic antibiotics and bed rest during acute recovery. Nurses should monitor patients closely for any changes in urine output, hematuria, and hemodynamics. Common complications of genitourinary trauma include bleeding, hypertension, infection (pyelonephritis), urinary incontinence, and structural changes to the genitourinary tract.

Acute Renal Injury

Acute renal injury is generally classified as either acute kidney injury (AKI), acute renal failure, or acute tubular necrosis (ATN).

AKI

In AKI, a patient has an acute decompensation in renal function. It usually occurs due to decreased perfusion and decreased filtration which in turn increases the reabsorption of metabolic waste. This increases the patient’s serum creatinine and urea.

Levels of Severity

Three levels of severity exist in a diagnosis of AKI: pre-renal, intrarenal or intrinsic, and post-renal. In the pre-renal stage, the kidneys do not receive adequate perfusion. In the intrarenal or intrinsic stage there is a decrease of kidney function. Post-renal AKI results from the inability to effectively drain urine. The mortality rate for AKI can range from 50-80% and is a common diagnosis for critically ill patients. It is more prevalent in patients with previous renal conditions, disorders that rely heavily on the functioning of the kidneys (burns, trauma, infection, transfusion reactions), patients taking nephrotoxic medications, and renal obstruction.

Symptoms

Symptoms of AKI include malaise, fatigue, weakness, darkening urine, decreased urine volume, flank pain, and confusion. Treatment focuses on treating the underlying cause and providing careful fluid and electrolyte replacement. Patients may be prescribed diuretics to increase urine production and low-dose dopamine to increase renal perfusion. Patients should be educated on choosing meals and foods with low sodium, low protein, and low phosphates to comply with the renal diet. In some cases, patients will need short- or long-term hemodialysis to replace the kidneys’ functions.

ATN

Acute tubular necrosis (ATN) is classified by a hypoxic injury to the kidneys causing damage to the glomeruli and ultimately decreased functionality and filtration of the kidneys. This can lead to acute renal failure. ATN may be caused by several systemic complications, including hypotension, hyperbilirubinemia, sepsis, surgery, some medications (chemotherapy, acyclovir, sulfonamides, streptomycin), and complications from birth.

Symptoms

Symptoms of ATN may develop slowly or quickly. Some effects are life-threatening. Common symptoms of ATN include lethargy, nausea, vomiting, hypovolemia, electrolyte imbalance, hypertension, CNS changes, metabolic acidosis, cardiac dysrhythmias, edema, heart failure, sepsis, and disseminated intravascular coagulopathy (DIC). Treatment involves treating underlying causes, supportive measures, maintaining appropriate fluid balance, antibiotics if needed, and dialysis.

Use of Diuretics

Diuretics are medications used to help the body produce and eliminate liquid waste products from the body. Different classes of diuretics work on different parts of the renal system to prevent or enhance absorption of certain electrolytes and fluid.

Loop Diuretics

Loop diuretics are used to prevent reabsorption of sodium and chloride in the ascending loop of Henle. They also work to increase release of calcium, magnesium, and potassium. Patients on loop diuretics must be closely monitored for electrolyte imbalances and dysrhythmias. Nurses should educate patients that common side effects of these medications include frequent urination, postural hypotension, increased blood glucose, and increased uric acid. They are not often used to control hypertension, as their mechanism is short-acting. The most common loop diuretics are bumetanide (Bumex®), ethacrynic acid (Edecrin®), and furosemide (Lasix®). Bumex and Edecrin can be administered intravenously to help reduce preload. Bumex may additionally be given orally as a treatment for heart failure. Lasix can be oral or intravenous and is used to help control congestive heart failure and renal insufficiency. It can also be used after surgery to decrease preload and reduce the incidence of post-perfusion syndrome.

Thiazide Diuretics

Thiazide diuretics work similar to loop diuretics; however, they prevent reabsorption in the early distal tubules. This forces an increase in excretion of sodium and water. Potassium and bicarbonate are also eliminated in this process, and patients taking these diuretics often require potassium supplementation to prevent hypokalemia. These diuretics last longer than the loop diuretics, reaching therapeutic levels 12-72 hours after administration. They can be used to help control hypertension. Some patients will be prescribed this medication daily while others, due to the extended mechanism of action, may only have it three to five days a week. Side effects of thiazide diuretics include dizziness, postural hypotension, headache, blurry vision, itching, and lightheadedness. Patients should be educated that use of these medications can increase photosensitivity and sunscreen should be applied regularly. The most common thiazide diuretics include chlorothiazide (Diuril®), bendroflumethiazide (Naturetin®), chlorthalidone (Hygroton®), and trichlormethiazide (Naqua®).

Potassium-Sparing Diuretics

Potassium-sparing diuretics, just like the loop and thiazide diuretics, prevent the reabsorption of sodium. This, however, is performed in the late distal tubule and collecting duct, rather than prior in the filtration system. These are weaker diuretics but do not have as strong of an effect on the patient’s potassium levels. They are often given with thiazide diuretics to counteract the potassium-depleting effects that thiazide diuretics have. Side effects of potassium-sparing diuretics include blurred vision, dehydration, nausea, insomnia, and nasal congestion. The most common potassium-sparing diuretics include spironolactone (Aldactone®) and eplerenone. Aldactone® is commonly used either orally or intravenously to treat congestive heart failure. Eplerenone may be substituted for Aldactone if side effects are intolerable, as eplerenone has been shown to have similar outcomes with fewer side effects.

Chronic Kidney Disease

Chronic kidney disease (CKD) develops over time as kidney function declines. In this condition, the kidneys become unable to appropriately filter blood through the kidneys, concentrate urine, and maintain electrolyte balances. When greater than 50% of the renal capacity is damaged or destroyed, kidney function declines significantly.

Symptoms

Symptoms of chronic kidney disease include weight loss, ecchymosis, itchy skin, increased BUN, increased creatinine, sodium and fluid retention, edema, hyperkalemia, anemia, and uremic syndrome.

Treatment

Treatment is often supportive, treating the symptoms caused by CKD. In patients with significantly decreased function and increased/imbalanced electrolytes, dialysis will be initiated. Patients may be registered for kidney transplant as well. Patients should be instructed on appropriate choices among the renal diet and understand fluid restrictions to prevent fluid overload. Calcium and vitamin supplementation and phosphate binders may be used to help manage alterations in electrolytes due to the decreased filtration function.

Infections

Pyelonephritis is a kidney infection that generally stems from bacteria in the urine. It can affect one or both of the kidneys. Patients at high risk for urinary tract infections include catheterized patients and patients with immune deficiency, history of urinary tractions, kidney stones, and renal/bladder tumors.

Symptoms and Diagnosis

Symptoms of pyelonephritis include fever, flank pain, chills, back pain, abdominal pain, urinary frequency, urgency, dysuria, nausea, and vomiting. Patients may have blood in their urine or pus. Diagnosis may be made with urinalysis testing, urine culture, and CT scan. Patients with recurrent pyelonephritis should be evaluated for vesicoureteral reflux. This can be assessed with a voiding cystourethrogram.

Treatment

Untreated infection may lead to sepsis or urosepsis classified by fever, hypotension, infection, confusion, nausea/vomiting, and difficulty breathing. Often patients are hospitalized for intravenous antibiotics and supportive therapy. Long-term effects of pyelonephritis may include kidney scarring, hypertension, acute kidney injury, acute tubular necrosis, and kidney failure.

Life-Threatening Electrolyte Imbalances

Electrolyte imbalances may occur under many conditions, including kidney damage or fluid overload. As a nurse, understand the appropriate levels of each of the following electrolytes. Also understand how patients may react based on elevated or depressed levels.

Sodium

Normal sodium levels range from 135 to 145 mEq/L. Levels less than 135 are known as hyponatremia and levels greater than 145 as hypernatremia.

Hyponatremia

Hyponatremia may be caused by decreased sodium intake, diarrhea, vomiting, NG decompression, illness, burns, fever, ketoacidosis, and SIADH. Patients should be monitored for lethargy and changes in level of consciousness. In severe hyponatremia, cerebral edema, seizures, and coma may occur.

Hypernatremia

Hypernatremia may be caused by renal disease, diabetes insipidus, and low fluid volumes. Patients should be monitored for irritability, flushing, and lethargy. Worsening hyperkalemia will lead to muscle weakness, spasms, seizures, and coma. Patients should have their sodium levels monitored closely and fluids replaced to reduce dehydration.

Potassium

Normal potassium levels range from 3.5-5.5 mEq/L. Low potassium levels result in hypokalemia. If levels fall below 2.5 mEq/L, severe complications and even death may occur.

Hypokalemia

Hypokalemia occurs due to diarrhea, vomiting, NG decompression, diuresis, alkalosis, starvation, and nephritis. Symptoms of hypokalemia include lethargy, weakness, vomiting, paresthesias, tetany, dysrhythmias, PVCs, flattened T-waves, muscle cramps, and hypotension. Potassium replacement should not exceed 20 mEq/hour.

Hyperkalemia

Hyperkalemia may be caused by renal disease, adrenal insufficiency, metabolic acidosis, dehydration, burns, trauma, hemolysis, NSAID administration, and potassium-sparing diuretics. Addison’s disease causes reuptake of potassium and hyperkalemia. Symptoms of hyperkalemia include ventricular arrhythmias, weakness, hyperreflexia, diarrhea, and confusion. Patients should limit their potassium intake. Calcium gluconate may help to bind to potassium to improve clearance and reduce cardiac symptoms. Insulin and hypertonic dextrose help to shift potassium into the patient’s cells to reduce serum levels. If critically high, hemodialysis or peritoneal dialysis may be implemented.

Calcium

Normal calcium levels range between 8.2 to 10.2 mg/dL.

Hypocalcemia

Hypocalcemia becomes critical when levels fall lower than 7 mg/dL. Causes of hypocalcemia include hypoparathyroidism, pancreatitis, renal failure, decreased vitamin D levels, alkalosis, magnesium deficiency, and low albumin. Patients with hypocalcemia may experience tetany, tachycardia, changes in mental status, tingling, Trousseau’s sign, positive Chvostek’s sign, and hypocalcemia. Correction of calcium levels may be given orally or via IV depending on the severity. Slow administration of IV calcium is necessary to prevent severe cardiac events.

Hypercalcemia

Hypercalcemia becomes critical when levels are greater than 12 mg/dL. Causes of hypercalcemia include acidosis, kidney disease, hyperparathyroidism, immobilization, and malignancies. Patients with hypercalcemia may experience progressive muscle weakness, hypotonicity, anorexia, nausea, vomiting, constipation, bradycardia, and cardiac arrest. Patients should be addressed for other conditions increasing their calcium levels. Diuretics, fluids, and phosphate may be used to help dilute and expel the excess calcium.

Phosphorus

Normal phosphorus levels range from 2.4 to 4.5 mEq/L.

Hypophosphatemia

Hypophosphatemia can occur with severe malnutrition, excessive antacid exposure (with magnesium), increased calcium, increased albumin levels, hyperventilation, burns, and DKA. Symptoms of hypophosphatemia include irritability, tremors, hemolytic anemia, seizures, respiratory failure, and coma. Treatment of hypophosphatemia includes correcting other abnormal electrolytes and phosphorus replacement.

Hyperphosphatemia

Hyperphosphatemia is often related to kidney failure, hypoparathyroidism, phosphorus intake, neoplastic disease, DKA, muscle necrosis, and chemotherapy. The primary symptom of hyperphosphatemia is tachycardia. Patients may also experience cramping, hyperreflexia, tetany, nausea, and diarrhea. Patients should be evaluated for reasons causing hyperphosphatemia and have those conditions corrected. Treatment of decreased calcium levels, antacids, and dialysis are also possible therapies to correct this condition.

Magnesium

Normal magnesium levels range between 1.6 to 2.6 mEq/L. Levels less than 1.2 mg/dL or greater than 4.9 mg/dL are considered to be critical.

Hypomagnesemia

Hypomagnesemia may occur due to chronic diarrhea, CKD, pancreatitis, diuretics, laxative use, hyperthyroidism, hypoparathyroidism, burns, and diaphoresis. Symptoms of hypomagnesemia include muscular excitability, confusion, headaches, dizziness, seizures, tachycardia, ventricular arrhythmias, respiratory depression, and coma. Treatment focuses on correcting the patient’s magnesium levels via IV magnesium. Administration of magnesium IV should not exceed 2 grams per hour and patients should be monitored closely for hypotension.

Hypermagnesemia

Hypermagnesemia may occur in patients with renal failure, decreased renal function, DKA, hypothyroidism, and Addison’s disease. Symptoms of hypermagnesemia include irritability, muscle weakness, dysphagia, tachycardia, hypotension, and seizures. Patients should be assessed for underlying causes of the hypermagnesemia. IV fluid administration and calcium replacement may help to drive down magnesium levels. Patients who have persistent elevated levels may need dialysis.

Metabolic Acidosis and Alkalosis

Acidosis

Metabolic acidosis occurs when the body is unable to excrete excess acids or maintain base levels. Conditions such as DKA, lactic acidosis, diarrhea, starvation, renal failure, shock, and renal tubular acidosis are all potential causes for this condition. Patients with metabolic acidosis can have compensation by driving out \(CO_2\) levels through tachypnea. Respiratory acidosis, on the other hand, relies on the metabolic system to provide bicarbonate, \(HCO_3\), to increase the excretion of hydrogen to help neutralize a patient’s pH. Patients with uncompensated metabolic acidosis and arterial blood gas will show decreased pH, decreased \(HCO_3\), and normal \(PCO_2\). If the patient experiences compensation, their \(PCO_2\) will decrease and their pH will begin to normalize.

Alkalosis

Metabolic alkalosis occurs when the body has decreased acid balance or increased base presence. It may occur due to vomiting, gastric suction, diuretics, decreased potassium levels, increased mineralocorticoids, and \(NaHCO_3\) intake. Patients can have compensation of this condition if the body is triggered to retain \(CO_2\). Respiratory alkalosis can be compensated when \(HCO_3\) is excreted by the kidneys. In an uncompensated patient, lab results will show an increased pH, increased \(HCO_3\), and normal \(PCO_2\). If the patient becomes compensated, their \(PCO_2\) will increase and the pH will begin to normalize.