What are posterior urethral valves (PUV)?

PUV is an abnormality of the urethra, which is the tube that drains urine from the bladder to the outside of the body for elimination. The abnormality occurs when the urethral valves, which are small leaflets of tissue, have a narrow, slit-like opening that partially impedes urine outflow. Reverse flow occurs and can affect all of the urinary tract organs including the urethra, bladder, ureters, and kidneys. The organs of the urinary tract become engorged with urine and swell, causing tissue and cell damage. The degree of urinary outflow obstruction will determine the severity of the urinary tract problems.





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Treatment varies with its severity and the underlying cause.

1. Patients with hypocalcemia who are severely symptomatic (carpopedal spasm, tetany, seizures, decreased cardiac function, or prolonged QT interval) require rapid correction of calcium levels with intravenous (IV) calcium therapy.

Intravenous calcium — Initially, IV calcium (1 to 2 g of calcium gluconate, in 50 mL of 5 percent dextrose) can be infused over 10 to 20 minutes.

The calcium should not be given more rapidly, because of the risk of serious cardiac dysfunction, including systolic arrest [4]. This dose of calcium gluconate will raise the serum calcium concentration for only two or three hours; as a result, it should be followed by a slow infusion of calcium in patients with persistent hypocalcemia.

then Determine the Cause

2. Asymptomatic patients with an acute decrease in serum corrected calcium to ≤7.5 mg/dL (1.9 mmol/L), who may develop serious complications if untreated. Acute hypocalcemia can occur when there is a rapid and progressive reduction in serum calcium (eg, acute hypoparathyroidism following post-radical neck dissection for head and neck cancer). Treat with IV calcium (1 to 2 g of calcium gluconate, in 50 mL of 5 percent dextrose) can be infused over 10 to 20 minutes.

10 percent calcium gluconate (90 mg of elemental calcium per 10 mL) Calcium gluconate is less likely to cause tissue necrosis if extravasated.

An IV solution containing 1 mg/mL of elemental calcium is prepared by adding 11 g of calcium gluconate (equivalent to 990 mg elemental calcium) to normal saline or 5 percent dextrose water to provide a final volume of 1000 mL. This solution is administered at an initial infusion rate of 50 mL/hour (equivalent to 50 mg/hour). The dose can be adjusted to maintain the serum calcium concentration at the lower end of the normal range (with the serum calcium corrected for any abnormalities in serum albumin as noted above). Patients typically require 0.5 to 1.5 mg/kg of elemental calcium per hour.

The infusion should be prepared with the following considerations:

●The calcium should be diluted in dextrose and water or saline because concentrated calcium solutions are irritating to veins.

●The IV solution should not contain bicarbonate or phosphate, which can form insoluble calcium salts. If these anions are needed, another IV line (in another limb) should be used.

IV calcium should be continued until the patient is receiving an effective regimen of oral calcium and vitamin D. For patients with hypoparathyroidism, calcitriol (in a dose of 0.25 to 0.5 mcg twice daily) and oral calcium (1 to 4 g of elemental calcium carbonate daily in divided doses) should be initiated as soon as possible. Calcitriol is the preferred preparation of vitamin D for patients with severe acute hypocalcemia because of its rapid onset of action (hours). (See "Hypoparathyroidism", section on 'Management'.)

IV calcium is not warranted as initial therapy for asymptomatic hypocalcemia in patients with impaired renal function in whom correction of hyperphosphatemia and of low circulating 1,25-dihyroxyvitamin D are usually the primary goals. (See 'Chronic kidney disease' below.)

Concurrent hypomagnesemia — Hypomagnesemia is a common cause of hypocalcemia, both by inducing resistance to parathyroid hormone (PTH) and by diminishing its secretion. (See "Clinical manifestations of magnesium depletion".)

In patients with hypomagnesemia, hypocalcemia is difficult to correct without first normalizing the serum magnesium concentration. Thus, if the serum magnesium concentration is low, 2 g (16 mEq) of magnesium sulfate should be infused as a 10 percent solution over 10 to 20 minutes, followed by 1 gram (8 mEq) in 100 mL of fluid per hour. Magnesium repletion should be continued as long as the serum magnesium concentration is less than 0.8 mEq/L (1 mg/dL or 0.4 mmol/L). More careful monitoring is required in patients who have impaired renal function who are at greater risk of developing hypermagnesemia.

Persistent hypomagnesemia, as occurs in some patients with ongoing gastrointestinal (eg, malabsorption) or renal losses, requires supplementation with oral magnesium, typically 300 to 400 mg daily divided into three doses. (See "Causes of hypomagnesemia" and "Evaluation and treatment of hypomagnesemia".)


We also suggest IV calcium therapy in asymptomatic patients with an acute decrease in serum corrected calcium to ≤7.5 mg/dL (1.9 mmol/L) (Grade 2C). (See 'Severe acute and/or symptomatic hypocalcemia' above.)


IV calcium is not warranted as initial therapy for asymptomatic hypocalcemia in patients with impaired renal function in whom correction of hyperphosphatemia and of low circulating 1,25-dihyroxyvitamin D are usually the primary goals. (See 'Intravenous calcium' above and 'Chronic kidney disease' above.)

●For those with milder symptoms of neuromuscular irritability (paresthesias) and corrected serum calcium concentrations greater than 7.5 mg/dL (1.9 mmol/L), initial treatment with oral calcium supplementation is sufficient (see 'Mildly symptomatic or chronic hypocalcemia' above). If symptoms do not improve with oral supplementation, IV calcium infusion is required.

IV calcium is also indicated to prevent acute hypocalcemia in patients with milder degrees of hypocalcemia or chronic hypocalcemia (due to hypoparathyroidism) who become unable to take or absorb oral supplements, as may occur after complex surgical procedures requiring prolonged recuperation. (See 'Mildly symptomatic or chronic hypocalcemia' above.)

●To effectively treat hypocalcemia in patients with concurrent magnesium deficiency, hypomagnesemia should be corrected first. (See 'Concurrent hypomagnesemia' above.)


Determine the Cauase



●When hypoparathyroidism (transient or permanent) or vitamin D deficiency are the cause of hypocalcemia, administration of IV calcium is only transiently effective (as long as the infusion continues), and oral calcium may not be well absorbed. In these cases, successful management requires the addition of vitamin D, which often permits a lower dose of calcium supplementation. (See 'Mildly symptomatic or chronic hypocalcemia' above.)

●Most patients with hypoparathyroidism require lifelong calcium and vitamin D supplementation (table 1). For patients with permanent hypoparathyroidism, the goals of therapy are to relieve symptoms, raise and maintain the serum calcium concentration in the low-normal range (eg, 8.0 to 8.5 mg/dL [2.0 to 2.1 mmol/L]), and avoid hypercalciuria (maintain 24-hour urinary calcium below 300 mg). For patients with chronic hypoparathyroidism who cannot maintain stable serum and urinary calcium levels with calcium and vitamin D supplementation, the addition of recombinant parathyroid hormone (1-84) is an option. However, the long-term safety of parathyroid hormone (PTH) has not been established. In addition, recombinant PTH is much more expensive than standard therapy with calcium and calcitriol. (See "Hypoparathyroidism", section on 'Management'.)

●Individuals with hypocalcemia due to vitamin D deficiency require vitamin D repletion. Nutritional deficiency (25-hydroxyvitamin D [25{OH}D] <20 ng/mL [50 nmol/L]) requires initial treatment with 50,000 units of vitamin D2 or D3 orally once per week for six to eight weeks, and then 800 to 1000 international units of vitamin D3 daily thereafter. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment".)


Determine the Cause



Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.


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Question 1 of 1

A 42-year-old African-American man has been diagnosed with hypertension for the past 10 years and treated with medication. One morning, he is found unresponsive by his wife. He is taken to the emergency department and pronounced dead by the physician. An autopsy revealed cardiac hypertrophy and a narrowing of the aorta just distal to the ligamentum arteriosum, with dilation of the intercostal artery's ostia. How could the death have possibly been prevented?



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