Transurethral Resection of the prostate what could happen on surgery

Definition: TURP Syndrome, or TUR syndrome, is an uncommon but serious complication of a specific type prostate surgery. During transurethral resection of the prostate surgery, a sterile irrigation solution is used to keep the surgical area clean and to prevent distribution of cancer cells if they are present. This solution is low in sodium. When this solution enters the bloodstream, it can lower the sodium level in the body. Hyponatremia, or low blood sodium, can cause disorientation, nausea, vomiting, fatigue, and in severe cases, brain edema and seizures.Treatment varies based upon the severity of the low sodium, which can be determined by a simple blood test. Treatment may be as simple as restricting fluid intake, or may involve IV medication, or the administration of salt.Also Known As: hyponatremia, low sodium, low blood sodium, Transurethral resection syndrome, transurethral resection of the prostate syndrome, water intoxication

Trans Urethral Resection of Prostate (TURP) is the sec­ond most common surgical procedure (after cataract extrac­tion) done in men over the age of 65 years. Advancement in technology has enabled the urologists to reach all corners of the urinary system using endoscopes, causing minimum trauma to the patient. Endoscopic procedures in the urinary system require the use of irrigating fluids to gently dilate the mucosal spaces, remove blood, cut tissue and debris from the operating field and enable better vision. In spite of the best of efforts to understand and prevent the various compli­cations of endoscopic procedures, incidence of some of the inherent complications have remained the same and still daunt the urologists. Aberrations in the Central Nervous Sys­tem (CNS), Cardio Vascular System (CVS) and other sys­tems which manifest due to the absorption of irrigating fluids during TURP are together known as TURP Syndrome. Though it is called TURP Syndrome, this complication can occur during other endoscopic procedures also namely Uretero-Renoscopy (URS), Percutaneous Nephrolithotomy (PCNL), Trans Cervical Resection of Endometrium (TCRE), etc. Despite improvements in the current surgical and anesthetic management, 2.5 - 20% of patients undergoing TURP show one or more manifestations of TURP syndrome and 0.5% - 5% die perioperatively. Symptoms TURP syndrome may occur at any time perioperatively [1] and has been observed as early as few minutes after surgery has started and as late as several hours after surgery has been completed. When under regional anesthesia, the patient char­acteristically complains of Dizziness Headache Nausea Tight feeling in the chest and throat Shortness of breath Restlessness Confusion Retching Abdominal pain Both systolic and diastolic blood pressures rise and the heart rate decreases. If not treated promptly, the patient may be­come cyanotic and hypotensive and go in for cardiac arrest. Some patients present with neurological symptoms. Ini­tially they become lethargic and then unconscious. Their pupils dilate and react sluggishly to light. This may be fol­lowed by short episodes of tonic-clonic seizures leading to a state of coma. Under General Anesthesia (GA), the diagnosis of TURP Syndrome is difficult and often delayed. The usual signs are unexplained rise and then a fall in BP and refractory brady­cardia. ECG changes such as nodal rhythm, ST changes, U waves and widening of QRS complexes may be observed. Recovery from GA and muscle relaxants may be delayed. Irrigating fluids are used during endourological procedures for better vision. Ideally the irrigation solution should be isotonic, non hemolytic, electrically inert (so that diathermy can be used), non toxic, transparent, easy to sterilize and inexpensive. [2] Unfortunately, a solution having all these qualities is not yet available. Electrolyte solutions such as normal saline or Ringer Lactate do least harm when ab­sorbed into the circulation. However they cause disper­sion of high frequency current from the resectoscope and hence abandoned. A variety of other irrigating fluids have been in use, each having its own merits and demerits. Sterile water: Though sterile water has many qualities of an ideal irrigating fluid, the disadvantage is its extreme hypotonicity, causing hemolysis, dilutional hyponatremia, shock and renal failure. Glycine 1.2%, 1.5%. 2.2%: Glycine, an endogenous amino acid has been suggested as a suitable irrigating fluid considering its many advantages, including the low cost, [3] though not as cheap as sterile water. Glycine is isotonic with plasma only at a concentration of 2.2%, but the side effects of glycine at this concentration are more. The os­molality of 1.5% glycine is 230 mosm/1 compared to se­rum osmolality of 290 mosm/l and hence cardiovascular and renal toxicities can occur at this concentration also. Further lowering of the concentration of glycine can lead to more complications due to hypotonicity and hence can­not be used for irrigation purposes. The distinct advan­tage of 1.5% glycine over sterile water is its tendency to cause less hemolysis and renal failure. Mannitol 3%: Mannitol, though does not have the toxicities of glycine, drives water out of cells and may enhance circulatory overloading. [4] The cost of mannitol is also higher compared to glycine. The elimination of man­nitol through kidney will be decreased in patients with impaired renal function. Glucose 2.5% - 4%: This is not a widely used irrigating fluid since glucose produces tissue charring at the site of resection and associated hyperglycemia produced when glucose is absorbed into the circulation. It also causes stickiness of surgeons' gloves and instruments. Cytal: Cytal, a mixture of sorbitol 2.7% and mannitol 0.54%[5] widely used in USA as an irrigating fluid, has not gained popularity in India due to its high cost and non­availability. In the body, sorbitol is metabolised to fructose, which may present problems in a patient with hypersensi­tivity to fructose. Urea 1%: This produces urea crystallisation on the in­struments during resection and hence not preferred. 1.5% glycine and sterile water are the most widely used irrigating fluids in urological endoscopic surgeries. Pathophysiology 1.Circulatory overload The uptake of small amounts of irrigating fluids has been shown to occur during almost every TURP [6] and TCRE [7],[8] through the venous network of prostatic bed and endometrium respectively. Spontaneous leakage through  Fallopian tube More Detailss increases fluid absorption during TCRE. The fluid absorp­tion has been studied by the expired breath ethanol tests after the addition of ethanol up to a concentration of 1 % to the irrigating fluid. [9] The uptake of I litre of fluid within one hour, which corresponds to an acute decrease in the serum sodium concentration of 5-8 mmols/l, is the volume above which the risk of absorption related symptoms is statistically in­creased. [10],[11] The average rate of fluid absorption during TURP is 20 ml/min. Due to circulatory overload, the blood volume increases, systolic and diastolic pressures increase and the heart may fail. The absorbed fluid dilutes the serum proteins and decreases the oncotic pressure of blood. This, concur­rent with the elevated blood pressure, drives fluid from the vascular to interstitial compartment causing pulmonary and cerebral edema. In addition to direct absorption into the cir­culation, a significant volume (upto 70%) of the irrigation solution has been found to accumulate interstitially, in the periprostatic and retroperitoneal spaces. For every 100 ml of fluid entering the interstitial compartment, 10-15 meq of so­dium also moves with it. Though the duration of surgery has not been conclu­sively proved to be the determinant for the volume of fluid absorbed, morbidity and mortality were found to be defi­nitely higher when surgery was prolonged over 90 min­utes. [12] Intravascular absorption correlates well with the size of the prostate, while interstitial absorption depends primarily on the integrity of prostatic capsule. Circula­tory overload occurs when the weight of the gland is more than 45 grams. Another important factor that determines the rate of absorption of fluid is the hydrostatic pressure at the prostatic bed. This pressure depends on the height of irrigating fluid column and the pressure inside the blad­der during surgery. The ideal height of irrigating fluid is 60 cm so that approximately 300 ml. of fluid is obtained per minute during resection for good vision. 2. Water intoxication Some patients with TURP syndrome present symptoms of water intoxication, [13] a neurological disorder caused by increased water content of the brain. The patient becomes first somnolent and then incoherent and restless. Seizures may also develop leading on to coma in decerebrate posi­tion. There will be clonus and positive Babinski responses. Papilloedema, with dilated, sluggishly reacting pupils can occur. The EEG will show low voltage, bilaterally. The symptoms of water intoxication appear when serum so­dium level falls 15 - 20 meq/l below normal level. 3. Hyponatremia Sodium is essential for proper function of excitatory cells, particularly those of heart and brain. Several mechanisms lead to hyponatremia in TURP patients. [14],[15],[16],[17] Dilution of serum sodium through excessive absorp­tion of irrigation solution. Loss of sodium into the stream of the irrigation fluid from the prostatic resection site. Loss of sodium into pockets of irrigation solution ac­cumulated in the periprostatic and retroperitoneal spaces. Larger amounts of glycine stimulate the release of atrial natriuretic peptide in excess of that expected by the volume load, which further promote natriuresis. The symptoms of hyponatremia are restlessness, con­fusion, incoherence, coma and seizures. When serum so­dium falls below 120 meq/1, hypotension and reduced inyocardial contractility occur. Below 115 meq/1, brady­cardia and widening of QRS complexes, ventricular ectopics and T wave inversion occur. Below 100 meq/1 generalised seizures, coma, respiratory arrest, Ventricular Tachycardia (VT), Ventricular Fibrillation (VF) and car­diac arrest occur. Sodium requirement is calculated by the following formula: Sodium Deficit = Normal serum Na - Estimated serum Na x Volume of body water (Body water is usually 60% of body water) 4. Glycin toxicity Excess of glycine absorbed into circulation is toxic to heart and retina and may lead to hyperammonemia. Experimen­tally glycine has been found to reduce the vitality and sur­vival of isolated cardiomyocytes. [18] In patients, glycine 1.5 % has been associated with subacute effects on the myocar­dium, manifested as depression or inversion of the T wave on the electrocardiogram 24 hr after surgery. [19] Absorption exceeding 500 ml has been shown to double the long-term risk of acute myocardial infarction. [20] This may be one of the reasons for the higher long-term mortality after transurethral versus open prostatectomy, which has been a debate among urologists for some years. TURP seems to depress myocar­dial function, particularly when the operative duration ex­ceeds 1 hr [21] and when glycine is used at room temperature. [22] About 0.5% of patients develop acute myocardial infarction during TURP, [23] though transient myocardial ischemia has been detected during 20% of TURPs. Dilutional hypocalcemia has also been implicated as a source of acute cardiovascular disturbances when glycine is absorbed.[24],[25] However calcium is restored more rapidly, probably due to mobilisation of calcium from bone tissues. Glycine is known to be a major inhibitory neurotrans­mitter in the spinal cord and in the brain stem, probably acting in the same manner as gamma amino butyric acid on the chloride ion channel. Too high a concentration may therefore cause severe depressant effect on the CNS and visual disturbances. Glycolic acid, formate and formaldehyde are other metabolites of glycine and these too can cause visual disturbances. The signs of glycine toxicity [11] are nausea, vomiting, slow respiration, seizures, spells of apnoea and cyanosis, hypotension, oliguria, anuria and then death. When arginine, another nonessential amino acid is added to the glycine infusion, the toxic effect of glycine on the heart is blunted. The mechanism by which arginine protects the heart is unknown. The normal value of serum glycine in man is 13-17 mg/l. Glycine toxicity is very uncommon in TURP patients probably because most of the absorbed glycine is retained in the periprostatic and retroperitoneal spaces, where it has no systemic effect. 5. Ammonia Toxicity Ammonia is a major by-product of glycine metabolism." High ammonia concentration suppresses norepinephrine and dopamine release in the brain. This causes the en­cephalopathy of TURP syndrome. Fortunately ammonia toxicity is rare [27] in man. Characteristically the toxicity oc­curs within one hour after surgey. [28] The patient develops nausea and vomiting and then lapses into coma. Blood ammonia rises above 500 micromols/1 (normal value is 11-35 micromols/1). Hyperammonemia lasts for over ten hours postoperatively, probably because glycine contin­ues to be absorbed from the periprostatic space. It is not clear why hyperammonemia does not develop in all TURP patients. Hyperammonemia implies that the body cannot fully metabolize glycine through the glycine cleavage system, [29] citric acid cycle [30] and conversion to glycolic acid and glyoxylic acid. [31] Another possible ex­planation is arginine deficiency. Ammonia is normally con­verted to urea in the liver via the ornithine cycle. Arginine is one of the intermediary products necessary for this cy­cle. When a patient has arginine deficiency, ornithine cy­cle is not fuelled and thus ammonia accumulates. 6. Hypovolemia, Hypotension The classical hemodynamic signs of the TURP syn­drome, when glycine is used as irrigating fluid, consist of a transient arterial hypertension, that may be absent if the bleeding is profuse, followed by more prolonged hypo­tension. [32],[33] Release of prostatic tissue substances and endotoxins into the circulation and associated metabolic acidosis might contribute to this hypotension. [34],[35],[36] Blood loss during TURP leads to hypovolemia, causing signifi­cant loss in oxygen carrying capacity leading to myocar­dial ischemia and infarction. Blood loss correlates with the size of prostatic gland resected, duration of surgery and skill of the surgeon. [12] The average blood loss during TURP is 10 m1/gram of prostate resected. The treatment of TURP syndrome involves correction of various pathophysiological mechanisms operating in body homeostasis. [16],[24],[25],[47],[48] Ideally the treatment has to be instituted before serious CNS or cardiac complications occur. When TURP syndrome is diagnosed, surgical proce­dure should be terminated as early as possible. Frusemide should be administered in a dose of 1 mg/kg intravenously. However, the use of frusemide to treat TURP syndrome has been questioned [49] because it increases sodium excre­tion. Hence 15% mannitol has been suggested as a better choice, due to its action independent of sodium excretion and its tendency to increase extracellular osmolality. Oxy­gen should be administered by nasal cannula. Pulmonary edema should be managed by tracheal intubation and posi­tive pressure ventilation with 100% oxygen. Arterial blood gases, hemoglobin and serum sodium are to be estimated. Correction of hyponatremia should be done by diuresis and slow administration of 3-5% hyper­tonic saline at the rate of not more than 0.5 meq/1 per hour or not faster than 100 ml/hr. Approximately 200 ml of hypertonic saline is needed for correction of hypo­natremia. Rapid administration of saline leads to pulmo­nary edema and central pontine myelinolysis. Two-thirds of the hypertonic saline restores serum sodium and osmo­lality, while one-third redistributes water from cells to the extracellular space, where it becomes available to diuretic treatment with frusemide. Intravenous calcium may be used to treat acute cardiac disturbances during surgery. Seizures should be managed by diazepam/midazolam/barbiturate/dilantin or a muscle relaxant depending on the severity. Significant blood loss should be managed by adminis­tering packed red cells. In cases of DIC, fibrinogen 3-4 gms should be given intravenously followed by heparin infusion 2000 units bolus (and then 500 units per hour). Fresh Frozen Plasma (FFP) and platelets may also be used depending on the coagulation profile. Surgical drainage of retroperitoneal fluid in cases of perforation can reduce the morbidity and mortality sig­nificantly. [50]

It's really hard to urinate, maybe you have BPH or worst cancer

Benign prostatic hyperplasia (BPH), also known as benign prostatic hypertrophy, is a histologic diagnosis characterized by proliferation of the cellular elements of the prostate. Cellular accumulation and gland enlargement may result from epithelial and stromal proliferation, impaired preprogrammed cell death (apoptosis), or both.

BPH involves the stromal and epithelial elements of the prostate arising in the periurethral and transition zones of the gland (see Pathophysiology). The hyperplasia presumably results in enlargement of the prostate that may restrict the flow of urine from the bladder.

BPH is considered a normal part of the aging process in men and is hormonally dependent on testosterone and dihydrotestosterone (DHT) production. An estimated 50% of men demonstrate histopathologic BPH by age 60 years. This number increases to 90% by age 85 years.

The voiding dysfunction that results from prostate gland enlargement and bladder outlet obstruction (BOO) is termed lower urinary tract symptoms (LUTS). It has also been commonly referred to as prostatism, although this term has decreased in popularity. These entities overlap; not all men with BPH have LUTS, and likewise, not all men with LUTS have BPH. Approximately half of men diagnosed with histopathologic BPH demonstrate moderate-to-severe LUTS.

Clinical manifestations of LUTS include urinary frequency, urgency, nocturia (awakening at night to urinate), decreased or intermittent force of stream, or a sensation of incomplete emptying. Complications occur less commonly but may include acute urinary retention (AUR), impaired bladder emptying, the need for corrective surgery, renal failure, recurrent urinary tract infections, bladder stones, or gross hematuria. (See Clinical Presentation.)

Prostate volume may increase over time in men with BPH. In addition, peak urinary flow, voided volume, and symptoms may worsen over time in men with untreated BPH (see Workup). The risk of AUR and the need for corrective surgery increases with age.

Patients who are not bothered by their symptoms and are not experiencing complications of BPH should be managed with a strategy of watchful waiting. Patients with mild LUTS can be treated initially with medical therapy. Transurethral resection of the prostate (TURP) is considered the criterion standard for relieving bladder outlet obstruction (BOO) secondary to BPH. However, there is considerable interest in the development of minimally invasive therapies to accomplish the goal of TURP while avoiding its adverse effects (see Treatment and Management).

Anatomy

The prostate is a walnut-sized gland that forms part of the male reproductive system. It is located anterior to the rectum and just distal to the urinary bladder. It is in continuum with the urinary tract and connects directly with the penile urethra. It is therefore a conduit between the bladder and the urethra. (See the image below.)

Normal prostate anatomy. The prostate is located at the apex of the bladder and surrounds the proximal urethra.

The gland is composed of several zones or lobes that are enclosed by an outer layer of tissue (capsule). These include the peripheral, central, anterior fibromuscular stroma, and transition zones. BPH originates in the transition zone, which surrounds the urethra.

Pathophysiology

Prostatic enlargement depends on the potent androgen dihydrotestosterone (DHT). In the prostate gland, type II 5-alpha-reductase metabolizes circulating testosterone into DHT, which works locally, not systemically. DHT binds to androgen receptors in the cell nuclei, potentially resulting in BPH.

In vitro studies have shown that large numbers of alpha-1-adrenergic receptors are located in the smooth muscle of the stroma and capsule of the prostate, as well as in the bladder neck. Stimulation of these receptors causes an increase in smooth-muscle tone, which can worsen LUTS. Conversely, blockade of these receptors (see Treatment and Management) can reversibly relax these muscles, with subsequent relief of LUTS.

Microscopically, BPH is characterized as a hyperplastic process. The hyperplasia results in enlargement of the prostate that may restrict the flow of urine from the bladder, resulting in clinical manifestations of BPH. The prostate enlarges with age in a hormonally dependent manner. Notably, castrated males (ie, who are unable to make testosterone) do not develop BPH.

The traditional theory behind BPH is that, as the prostate enlarges, the surrounding capsule prevents it from radially expanding, potentially resulting in urethral compression. However, obstruction-induced bladder dysfunction contributes significantly to LUTS. The bladder wall becomes thickened, trabeculated, and irritable when it is forced to hypertrophy and increase its own contractile force.

This increased sensitivity (detrusor overactivity [DO]), even with small volumes of urine in the bladder, is believed to contribute to urinary frequency and LUTS. The bladder may gradually weaken and lose the ability to empty completely, leading to increased residual urine volume and, possibly, acute or chronic urinary retention.

In the bladder, obstruction leads to smooth-muscle-cell hypertrophy. Biopsy specimens of trabeculated bladders demonstrate evidence of scarce smooth-muscle fibers with an increase in collagen. The collagen fibers limit compliance, leading to higher bladder pressures upon filling. In addition, their presence limits shortening of adjacent smooth muscle cells, leading to impaired emptying and the development of residual urine.

The main function of the prostate gland is to secrete an alkaline fluid that comprises approximately 70% of the seminal volume. The secretions produce lubrication and nutrition for the sperm. The alkaline fluid in the ejaculate results in liquefaction of the seminal plug and helps to neutralize the acidic vaginal environment.

The prostatic urethra is a conduit for semen and prevents retrograde ejaculation (ie, ejaculation resulting in semen being forced backwards into the bladder) by closing off the bladder neck during sexual climax. Ejaculation involves a coordinated contraction of many different components, including the smooth muscles of the seminal vesicles, vasa deferentia, ejaculatory ducts, and the ischiocavernosus and bulbocavernosus muscles.

Epidemiology

BPH is a common problem that affects the quality of life in approximately one third of men older than 50 years. BPH is histologically evident in up to 90% of men by age 85 years. As many as 14 million men in the United States have symptoms of BPH. Worldwide, approximately 30 million men have symptoms related to BPH.

The prevalence of BPH in white and African-American men is similar. However, BPH tends to be more severe and progressive in African-American men, possibly because of the higher testosterone levels, 5-alpha-reductase activity, androgen receptor expression, and growth factor activity in this population. The increased activity leads to an increased rate of prostatic hyperplasia and subsequent enlargement and its sequelae.

Prognosis

In the past, chronic end-stage BOO often led to renal failure and uremia. Although this complication has become much less common, chronic BOO secondary to BPH may lead to urinary retention, renal insufficiency, recurrent urinary tract infections, gross hematuria, and bladder calculi.

Carcinoma of the penis is rare in developed countries. By contrast, it accounts for up to 20 percent of cancers in men some parts of Africa, Asia, and South America. (See "Carcinoma of the penis: Epidemiology, risk factors, and clinical presentation", section on 'Epidemiology'.)

The rarity of this condition, its variable clinical appearance, men's frequent hesitation to seek treatment, and inconsistency in follow-up often lead to long delays in diagnosis and treatment. Furthermore, the data on treatment outcomes are derived primarily from retrospective studies. Number of patients are small and there are no randomized trials and to define the optimal treatment.

Key areas of controversy in the management of penile cancers include:

• The role of penile-sparing treatments versus more aggressive surgery (partial or total penile amputation)
• The need for prophylactic inguinal lymphadenectomy in men without palpable inguinal nodes
• Optimal management of men with locally advanced or metastatic disease

The diagnosis, treatment, and prognosis of penile carcinoma are presented here. The epidemiology, risk factors, and clinical presentation are discussed separately.