I.

II.

Clinical assessment of renal function. Kidneys receive 20-25% of cardiac output. Plasma is filtered at a rate of 180 L/day. Renal
function can be evaluated with laboratory tests that reflext glomerulat giltration rate and renal tubular )unction
a. Gfr alterations in gfr are associated with predictable changes in erythropeietic activity. Clinical manifestations of uremia
generally appear when the gfr is less than 15 mL/min/1.73m2 (normal values is at least 90 ml/min/1.73m2
b. Creatineine clearance. The creatinine clearance correlates with the gfr and is the most reliable maeasure of gfr. Creatinine
clearance does not depend on corrections for age or the presence of a steady state. Preoperatively patients with creatinine
clerances of 10-25 mL/min are considered at risk of developing prolonged or adverse responses to drugs that depend on
renal excretion for their clearance from plasma.
c. Serum creatinine. Levels of serium creatinine can be used to estimate the gfr. Normal serium creatinine concentrations
range from 0.6 to 1.0mg/dL in women and 0.8 to 1.3 mg/dL in men. Serium creatinin values are slow to reflect acute changes
in renal function.
d. BUN BUN greater than 50 mg/dL reflex a decreased GFR. BUN vary with the gfr, dietary protein intake, coexisting diseae,
intravascular fluid and increase protein catabolism (fever).
e. Renal tubular function and integrity
i. Urine concentrating ability. Renal tubular dysfunction is present if the kidneys do not produce appropriately
concentratied urine in the presence of a physiologic stimulus for the release of ADH. In the absence of diuretic
therapy or glycosuria, urine pscific gravity greater than 1.018 suggests that the ability of renal tubules to
concentrate urine is adequate.
ii. Proteinuria: transient proteinuria may be associated with fever, chf, seizure acivity, pancreatitis, and exercise and
resolves with the resolution of the underlying stimuls or illness. Orthostatic proteinuria is benign, occurring in up to
5% of adolescents while in the upright position and not in the recumbent position. Proteinuria connotes significant
renal disease.
iii. Fractional urinary sodium excretion: an fena that is greater than 2 % or a urinary sodium concecntration that is
greater than 40 mEq/L reflects decreased ability of the renal tubules to conserve sodium or drug-induced diuresis.
Urine osmolarity is likely to be less than 350 mOsm/L. drug-induced diuresis is associated with increased urinary
excretion of sodium.
iv. Urinalysis: can detect the presence of protein, glucose, acetoacetate, blood and leukocytes. The urin pH and solute
concentrations (specific gravity) are determined, and sediment microscopy is used to determine the presence of
cells, casts, microorganisms and crytsla.s
v. Novel biomarkers of renal function
Acute kidney injury: aki is achracterized by deterioration of renal function over a period of hours to days, resulting in failure of the
kidnyes to excrete nitrogenous waste products and to maintain fluid and electrolyte homeostasis. AKI may be oliguric (urinary output
below 400 mL/day) or nonoliguric(urinary output greater than 400 mL/day). The mortalility rate of severe aki requiring dialysis
remains high. Aki is associated with a number of other systemic disease, acute clinical conditions, drug treatments, and interventional
therapies.
a. Etiology
i. Prerenal azotemia (decreased renal blood flow): nearly of hospital acquired aki cases consis of prerenal azotemia,
which predisposes patients to ischemia-induced acute tubular necrosis (ATN). Prerenal azotemia is rapidly
reversibnle if the underlying cause (hypovolemia, chf) is corrected. Elderly patients are susceptible to prerenal
azotemia because of their predisposition to hypovolemia (poor fluid intake) nad high incidence of renovascular
disease. Urinary indices may help distinguish prerenal from intrinsic aki.
ii. Renalazotemia (intrinsic): intrinsic renal diseases that result in aki are categorized according to the site of injury
(renal tubules, interstitium, glomerulus, renal vasculature). Injury to the renal tubules is most often ischemic or
nephrotoxic (aminoglycoside antibiotics, radiographic contrast agents). Ischemia and toxins often combine to cause
aki in severel ill patients with conditions usch as sepsis or acquired immunodeficiency sundrome (aids). Aki resulting
from acute interstitial nephritis is usually caused by allergic reations to drugs.
iii. Postrenal azotemia (obstructive): AKI occurs when urinary outflow tracts are obstructed (prostatic hypertrophy,
cancer of the prostate or cervix). The potential for recovery is inversely related to the duration of the obstruction.
Renal ultrasonography is the best diagnostic test.
b. Risk factors: co-existing renal disease, advanced age, chf, symptomatic cardiovascular disease, and major operative
procedures (cardiopulmonary bypass, abdominal naaeurysm resection) are risk factors for development of aki. Sepsis and
multiple organ system dysfunction caused by trauma introduce the risk of aki. Iatrogenic causes include inadequate fluid
replacement, delayed treatment of sepsis, and administration of nephrotoxic drugs or dyes.
c. Diagnosis: aki is usually diagnosed based on an acute rise in serium creatinine; signs and symptoms are often absent early
and are nonspecific (malaise, dyspnea, edema, HTN). Urinalysis may be helpful in diagnosis whether aki is likely to be
prerenal, intrarenal or post renal.
d. Complications associated with acute kidney injury
e. Treatment: treatment of aki is aimed at limiting further renal injury and correcting the water, electrolyte, and acid-base
derangements. Underlying causes should be sought and terminated or reversed, if possible.
i. Fluids. Prompt and adequate correction of hypovolemia and hypotension is much more important than the type of
fluid used. Hetastarch may exacerbate injury, and ns may exacerbate hyperfhloremic metabolic acidis. Lr or ther
bicarbonate containing balance salt solution may be best choice.
ii. Vasopressors. Agents may increase renal vasoconstriction and exacerbate aki and should be used with caution. The
use of dopamine to treat or prevent aki is not supported by the literature. Vasopressin may be effective.
iii. Diuretics: the practice of trtying to convert oliguric to nonoliguri aki with diuretic is not advised. Mannitol yields
better outcomes in posttransplantation atn and in combination with forced alkaline diuresis to prevent aki in severe
crush injuries.
iv. N-acetylcesteine. This agent may reduce aki in high-risk patients exposed to radiocontrast dye.
v. Activated protein c and steroid replacement. Steroids and activated protein c reduce mortality in patients with
severe sepsis.
vi. Dialysis. Is a mainstay of severe aki.
f.
Prognosis. For patients with hospital-acquired aki the prognosis is poor, with current mortaility rates of more than 20%, and
50% or more once dialysis is required. Only 15% of patients hwo develop aki will fully recover their renal function.
g. Drug dosage in patients with renal impairment: the rate of elimination of drugs excreted by the kidneys isproportional to the
gfr. If the patient is oliguric, use 5 mL/min for creatinine clearance.
i. Loading dose guidelines. If extracellular fluid volume looks normal, use a normal loading dose. If ecf is contracted,
reduce the loading dose, if ecg is expanded, use a higher loading dose.
ii. Repeat dosing. A combination of increasing the dosage interval and decreasing the dose is often used (analgesics).

iii. Drugs removed by hemodialysis. Usually given towards the end because they are removed by dialysis.
Anesthetic management. Because of high morbidity and mortality, only life-saving surgery should be undertaken in patients
with acute aki. Principles are maintentenance of an adequate mean sbp and o and the avoidance of further renal insults
Chronic kidney disease. Is progressive ifrreversible deterioration of renal function that results from a wide variety of diseases. Dm is
the leading cause of esrd followed by htn.
a. Diagnosis. Signs are foten undetectable, and symptoms are nonspecific (fatigue, malaise anorexia.) in most patients the
diagnosis is established through routine testing, such as serium cretinin level and urinary sediment analysis.
b. Progression. Stages of ckd. Inrarenal hemodynamic changes (glomerular htn, glomerular hyperfiltration and permeability
changes, glomerulosclerosis) are likely responsible for progression of renal disease.
i. Systemic HTN. A major risk factor is systemic htn. Administration of ace inhibitors and or arbs appears to be
renoprotective (decreased proteinuria and slowed progression of glomerular sclerosis) compared with other
antihypertensive regimens.
ii. Dietary factors. New guidelines call for moderate protein restriction in all patients with renal insufficiency.
iii. Strict control of Blood glucose concentrations. This can delay the onset of proteinuria and slow the progression of
nephropathy, neuropathy, and retinopathy.
c. S/S. symptoms of ckd include general malaise and anorexia. Volume overload(peripheral edema, dyspnea, chf) and
electrolyte or acid-base disturbances are late signs of ckd. Other symptoms include cognitive impairment, peripheral
neurpathy, infertility and increased susceptibility to infection.
d. Complications
i. Uremic syndrome. Uremic syndrome is a constellation of signs and symptoms( anorexia, n/v, pruritus, anemia,
fatigue, coagulopathy) that reflect the kidneys progressive inability to performe its excretory secretory, and
regulatory functions. Bun concentration is a useful clinical indicator of the severity of the uremic syndrome and the
patients response to therapy (dietary protein restriction). Serium cretinine concecntration correlates poorly with
uremic symptoms.
ii. Renal osteodystrophy. A complication of ckd is renal osteodystrophy. As the gfr decreases, phostphate
concentrations increase and serium calcium concentrations decrease, stimulating parathyroid hormone secretion
and causing bone resoprtion and calcium release. Treatment of renal osteodystrophy is restriction of dietary
phosphate, administration of oral calcium supplements and vitamin D therapy.
iii. Anemia. Because of decreased erythropoietin production by the kidneys, anemia occurs. Tx is recombinant hyman
erythropoietin (epoetin), eliminating the ned for blood transfusions and avoiding the sx of anemia in most patietnts.
Blood transfusion are avoided if possible, as the resultant sensitization to human leukocyte antigents (HLAs) makes
kidney transpaltation less successful.
iv. Uremic bleeding. Patietns with chronic renal failure have an increased tendency to bleed despite normal findings of
laboratory coatulation studies. Treatment of uremic bleedimg may include the administration of cryoprecipitate to
provide factor 8 (vwf) complex or DDAVP.
e. Treatment. Treatment of ckd includes aggressive treatment of the underlying cause (DM or htn), pharmacologic therapy to
delay the progress, and renal replacement therapy as esrd ensues.
i. Htn. Aces or arbs are used to treat htn. 1st drug of choice is ace inhibitors, which is then titrated upward into the
moderate to high dose range as tolerated. Arbs are the preferred choice in theose with type 2 dm with ckd and
proteinuria. Bb and ccbs may also be useful.
ii. Dm. goal of treatment is to achieve less than 7% glycosylated hemoglobin (Hb). Euglycemia is associated with
reversal of the typical lesions see in diabetic nephropathy and a reduction in albuminuria. Diatery protein intake of
0.6 g/kg/day reduces the rate of progression of renal disease in patients with diabetes but should not be undertaken
at the expense of nutrition in anocrexic patients. Dietary phosphorus should be restricted to 800 to 1000mg/day
when serium phosphorus or pth levels are elevated. Vitamin d supplementation may e helpful. Sodium intake
should be restircited to less than 2.4 g/day.
iii. Anemia responds to treatment with eythropeoritin in all stages of ckd. Hb, is the rpeferred method for assessing
anemia. Anemia is defined for males hb <13 F<12mg/dL regardless of age.
iv. Renal replacement therapy when gfr approaches 30 mL/min/1.73m2, renal replacement therapy is considered.
1. Hemodialysis. Is usually instritubed by the time gfr is 15 mL/min/1.72m2. objectives include adequate
dialysis, adequate nutrition, maintenance of vascular access, correction of hormonal deficiencies,
minimiazation of hostpilatizations and prolongation of life while enhancing its quality. Vascular access for
hemodialysis is established surgically (native av fistula, grafts, or temporary hemodialysis iv catheters).
a. Complications associated with hemodialysis
i. Hypotension. During dialysis, hypotention and hypersensitivity reactions to
polyacrylonitrile in dialysis membranes (most common in patients taking aceis may
occur
ii. Hypersensitivity reactions. Reactions may occur to the ethelene oxide used to seterilize
dialysis equipment or to apolyacylonitrile in dialysis membrames reactions to the latter
due to aceis.
iii. Dialysis disequilibrium syndrome. Syndrome consis of nausea, headaches, and fatigue
but can progress to seizures and coma. It is thourhg t o result from rapid changes in ph
and solute concenctration in the cns. Treatment includes reducing the rate of dialysis and
blood flow.
iv. Muscle cramps. Caused due to changes in K concentration.
v. Fluid,vitamin, and electrolyte balance. Patietnts on hemodialysis have decreased total
body potassium and tolerance of hyperkalemia. Water-soluable vitamins are removed by
hemodialysis and should be replaced. Between treatments, a weight gain of 3-4% of
body mass in 2 days is appropriate. Insuli requirements may decrease owing to
decreased catabolism of insulin.
vi. Cardiovascular disease. Cardiovascular disease caused by accelerated atherosclerosis
and impaired oxygen delivery during uremia accounts for nearly 50% of all deaths in
patients on hemodialysis, fluid retention is the most likely cause of systemic HTN in most
patients who require hemodialysis. Essential htn may require treatment with
antihypertensive drugs in addition to hemodialysis. Pericarditis may result from
inadequate hemodialysis.
vii. Bleeding. Caused by altered plt function is partially corrected by hemodialysis.
h.

III.

viii.

IV.

Infection. Theres is increased susceptibitli to infection caused by impatired phagocytosis

and chemotaxis. All patients on hemodialysis are vaccinated agasints pneumococcus and
if appropriate hep B. tb is usuall extrapulmonary; symtoms may be atypical, with anergy
on skin testing. Unexplainted weight loss with or without fever should propmto further
testing to rul out tb actual hep b and c infection may be asymptomatic. Man
yhemodialysis patients have antibodites to hep c. dose adjustments of drugs used to
treate aids are note required for hemodialysis and isolation of patients with adis or use of
dedicated hemodialysis machine is not necessary.
ix. Peritoneal dialysis. This form of dialysis is simple to perform and may be useful in patient
with severe vascular disease or chf ( more gradual fluid shifts, no need for vascular
access). Peritonitis is the most common serious complication.
x. Drug clearance in patients undergoing dialysis. Drug clearance may dictate adjustment
of dosage intervals and supolemental administration if drugs are cleared by dialysis
( lMWH, Water soluble agents, non-protein bound drugs).
xi. Perioperative hemodialysis. Platients should undergo adequate hemodialysis before
elective surgery to minimize the likelihood of uremic bleeding, pulmonary edema, and
impaired arterial oxygenation.
f.
Anesthetic management of patients with CKD
i. Preoperative evaluation. Fluid status, electrolyte balance, glucose management, and degree of anemia are
evaluated preoperatively. Digoxin tocivity should be a concentr in patients being treated with dig. Antihyperteincive
drug thereapy is continued (ecept ace inhibitors and arbs, which may be withheld to reduce risk of intratoperative
hypotension. Patient on hemodialysis should undergo dialysis during the 24 hours preceidgin elective surgery.
Preoperative ddavp may be considered. Prerioperaite h2 receptor blcokers should be dose-adjusted for renail
failure.
ii. Intraoperative considerations
1. Induction. Hypotension on induction is common, particularly in patients taking aceis. Decreased protein
binding of drugs may result in the availability of more unbound drugs at receptor sites. Potassium release
after administration of succ is not exaggerated in pts with ckd, but caution is indicated if preoperative
serium potassium concentration is in the high-normal range.
2. Maintenance of anesthesia. There is no evidence that patients with co-existing renal disease are at
increased risk of renal dysfunction with sevoflurane. Selection of nondepolarizing muscle relaxants should
consider the clearance mechanisms of these drugs. Clearance of ve and roc is slowed, wheras coearance
of mivacurium, atracurium and ciatracurium from plasma is independent of renal function. LR solurtion or
other potassium containing fluids should not be administered to anuric patients. In anuricc (dialysis)
patients, noninvasive operations require areplacemnt of only insensible water losses with 5% glucose in
water (5-10 mL/kg) iV. Measurein cvp may be useful for guiding fluid replacement. Areterial cannulation
should be avoided if possible, to avoid injury to vessels that may be required for future dialysis access.
Patient positioning should include attention to protecting vascular access fistulas. Regional anesthesia is
useful for placing the vascular shunts necessary for chronic hemodialysis.
3. Opioids. The use of iopiods may minimiase the need for va agents. Morphine and meperidine undergo
methabolism to poteintially neutorix compoiunts the rely on renal clearance. Morphine metabolit
M6glcuronide can accumulate in patieents with ckd, rresuilting in respirtoary depression.
Hydromorphonemay accumulate in ckd but is safely used with dose adjustment. Alfent, fent, remi, and
sufent lack acrtive metabolies, but fent eilimination be be delayed in ckd.
iii. Postoperative management. Attention must be give n to inadequate reversal of muscle relaxant in unfunctional
kidney patients who show signs of skeletal muscle weakness during the posop period. Other considerations are
sensitive t oopiods, arrhythmias r/t hyperkalemia and oxygen supplementation in anemic patients. Meperiding is
avoided for postoperative analgesia because its metabolites may accumulate in patients wit hrenal failre, causing
seizures.
Renal transplant
a. Management of anesthesia
i. General anesthesia. Renal function after kidney transplantation is not influednced by the volatile anesthetic
administered. Goals are mainteneance of CO and tissue oxygen delivery to promote renal perfusion. A high-normal
sbp is desirable to maintain adequate urine flow. Atra, cis, and miva are resasonable muscle relaxants beacause of
lack of dependence on renal clearance, although the transplated kidney will clear MR similarly to a normal kidney.
Cvp monitoring is useful to guide fluid infusions. Diuretics facilitate urine formation by the newly transplanted
kidney. With relase of the vascular clamps, potassium from the preservative solution and acid metabolites hass bee
reported to lead to carida arrest. Hypotension results from the additional 300 mL capacity of the new kidney vacular
bed. Tx is fluid administration.
ii. Regional anesthesia. Blockade of the peripheral sympathetic nervious system can complicate control of sbp.
iii. Posop complications
1. Acute rejection affecting the kidney vasculature. Rejection can be so rapid that inadequate circulation is
evident almost immediately after the blood supply to the kkidney is established. The only treatment is
removal of the transplanted kidney; dic occurs. Postoperative graft hematomas can cause vascular or
ureteral obstruction.
2. Delayed graft rejection. Signs include fever, local tenderness, and deterioration of urine output. Treatemet
is with high dosese of corticosteroids and antilymphocyte globuline.
3. Acute tubular necrosis. In the transplanted kidney, ATN secondary to prolonged ischemia usually responds
to hemodialysis.
4. Cyclosporine toxicity. Cyclosporine toxicity may also cause aki. US and needle biopsy are performed to
differentiate between the possible causes of kidney malfunction.
5. Opportunistic infections. Infections caused by long-term immunosuppression are common after renal
transplantation.
6. Cancer. Large cell lymphoma is a well recognized complication of renal transplantation and occurs almost
exclusively in patients with evidence of Epstein-barr virus infection.
b. Anesthetic considerations for renal transplant recipiencts. Renal transplant recipients are often elderly and have co-existing
cardiovascul;ar disease and dm. the side effects of immunosuprpressant drugs (systemic HTN, lowered seizure thersholds,
anemia, thrombocytopenia) must be considered. Gfr and rbcf are likely to be lowered than in healthy individuals, and the

V.

Primary
a.

b.

c.
d.
e.
f.
g.

h.

i.

j.

k.

l.
m.

n.

acivity of drugs excreted by the kindey s may be prolonged. Drugs that are ptoetnially nephrotoxic or dependent on renal
clearance are avoided. Diuretics are administered only with carful evaluation of the patients intravascular fluid volume
status.
disease of the kidneys
Glomerulonephritis. Is usually caused by deposition of antigen-antibody complxes in the glomeruli. The source of antigens
may be exogenous (poststerptococcal infection) or endogenous (collagen disease). Clinical manifestations of glomerular
disease include hematuria, proteinuria, htn, edema, and increased plama creatinin conc. And the presence of rbc casts in the
urine.
Nephrotic syndrome is defined by daily urinary protein excretion exceeding 3.5 g associated with sodium retension,
hypoerlipopoteinemia, and thromboembolic and infectious complicastion. Diabetic nephropathy is the most common cause
of nephrotic proteinuria.
i. s/s . HTN, proteinuria, hematuria, na retention, edema , hypoveoleia, thromboembolism, hyperlipidemia, infectious
complications.
ii. complications of nephrotic syndrome
1. thrombo embolic
a. renal vein thrombosis
b. pulmonary embolism
c. dvt
2. infectious
a. pneumococcal peritonitis
3. decreased plasma protein binding
a. decreased lvlvs of vitamins and hormones
4. edema
a. generalized; should be treated slowly with loop diuretics and thiazides.
Good pastures syndrome. A combination of pulmonary hemorrhage and glomerulonephritis, good pastures syndrome occurs
most often in young males. Prognosis is poor, wit h no known effective therapy to prevent progression to RF, usually within 1
year of the diagnosis.
Interstitial nephritis. Allergic reaction to drugs, including sulfonamides, allopurinol, phenytoid, and diuretics, can cause
interstitial nephritis. Other, less common causes invlude auto immume diseases ( lupus erythematosus) and infiltrative
disease (sarcoidosis). Patients exhibit decreased urine-concentrating ability, proteinuria, and systemic hhtn.
Hereditary nephritis (alports syndrome). Hereditaroy nephritis is often accompanied by hearing loss and ocular
abnormalities. Drug therapy has not prove successful, although aceis may slow progression of renal disease.
Polycystic renal disease. Is an autosomal dominant disease, polycystic renal disease typically progresses slowly until renal
failure occurs during middle age. Mild systemic htn and proteinuria are common. Hemodialysis or renal transplantation is
eventually necessary in most patients.
Fanconis syndrome. Results from inherited or acquired disturbances of proximal renal tubular function, causing
hyperamoniacidura, gluycosuria, and hyperophaphaturia. Symptoms include poly uria, polydipsia, metabolic acidosis cause d
by loss of bicarbonate ions, and skeletal muscle weakness related to hypokalemia. Dwarfism and osteomalacia, reflexting
loss of phosphate, are prominent in these patients.
Barters and gitel mans syndromes. These are inherited renal salt- wasting disorders caused by defects in sodium chloride
and postssium hcannesl in the ascending limb of the disctal convoluted tubule. Juxtaglomerular hyperplasia,
hyperaldosteronism and hypokalemic acidosis are pathognomonic. Tetment is with aceis, spironolactone, and sodium and
potassium supplementation.
Renal tubular acidosis. Causes metabolic acidosis resulting from ainappropriate acidification of the urine type 1 rta is caused
by impaired bicarbonate reabsorption in the proxima renal tubule. Type 2 rta is caused by impaired secretion of hydrogen ion
in the distal tubule. Both are characterized by hypokalemic, hyperochloremic metabolic acidosis and inappropriately basic
urine. The condition can be hereditary or acquired. Type 4 rta is associated with hyperkalemia rather than hypokalemia and
is often seen in pateihs with ckd.
Nephrolithiasis. Renal stones passing down the ureter can produce intense flank pain, often radiating to the groin, associated
with c/v and mimicking an acute abdominal surgical emergency. Hematuria is common, and ureteral obstruction may cause
signs and symptoms of renal failure.
i. Types of stone
1. Calcium oxalate stones. Causes of hypercalcemia (hyperparathyroidism, sargoidosis, cancer,
hyperoxaluria, hyperouricosuria, idiopathic hypercalciuria) must be considered in these patients.
2. Mg ammonium phosphate stones these stones may result forom urinary tract infection with urea-splitting
organisms that produce ammonia. Ex alkaline urine (usually caused by chronic bacterial infection).
3. Uric acid stones these stones occur in persons with persistently acidi urine (pH greater than 6.0), which
decreases the solubility of uric acid. Approximately 50% of patients with uric acid stones have gout.
4. Cysteine stone due to cystinuria.
ii. Treatment. Treatment depends on identifying the composition of the stone and correcting the predisposing factors,
such as hyperparathyroidism, UTI, or gout, extracorporeal shock wave lithotripsy is noninvasive treatment.
Renal hypertension. Renal disease is the most common cause of secondary systemic htn. The sudden onset of a marked
increase in sbp or the present of htn before the age of 30 years should arouse suspicion of renovascular disease. A bruit may
be audible on auscultation of the abdomen over the kidneys. Systemic htn caused by renovascular disease does not respond
well to treatment wit antibhypertensive drugs. Treatment of renovascular hypertenstion is with renal artery endarterectomy
or nephrectomy.
Uric acid nephropathy. Occurs when uric acid crystals are precipitated in the renal collecting tubules or ureters, producing
acute oliguric renal gailure. The condition is particularly likely to cocur in patients with myeloproliferative disorders being
treated with chemotherpeurtic drugs.
Hepatorenal syndrome. Hepatorenal syndrome is acute oliguria manifesting in patients with decompensated cirrhosis of the
liver. Associated signs include deep jauncdice, ascited, hypoalbuminemia, and hypoprothrombinemia. Treatment is directed
at intravascular fluid volume replacement. In some patients a circulating toxin may be responsible for extreme renal
vasoconstricon and aki. Nevertheless, hemodialysis has no been reliable for eliminating suspected hepatic toxins.
Benign prostatic hyperplasia. Is a nonmalignant enlargement of the prostatne. Transurethral resection of the prostate (TURP
and open prostatectomy have been the traditional treatments for men with symptomatic bph. Laser ablation thertrapy is a
recent tehique allowing for brief operating times. Medical therapy consistrs of finasteride (inhibits 5 alpha reductase to
reduce prostate size and alpha adrenergic antagnists(terazosin,doxazosin, tamsulosin) to decrease prostatic smooth muscle
tone, improving urinary flow.

i.

Turp syndrome. Is characterized by intravascular fluid volume shifts and plasma solute effects caused by absorption
of irrigation solution. Hypo-osmolality is pthe principal factor contributing to the neurologic and hypovolemic
changes associated with TURP syndrome.
1.

2.
3.
4.

5.

6.

Intravascular fluid volume expansion. Rapid intravascular fluid volume expansion caused by systemic
absorption of irricgating fluids (absorption rates may reach 200 mL/min) can cause systemic htn and reflex
bradycardia. Patients with poor left ventricular function may develop pulmonary edema. The most widely
used indicator of intravascular fluid volume gain is hyponatremia.
Intravascular fluid volume loss. Hyponatremia in associateion with systemic htn may result in water flux
along osmotic and hydrostatic pressure gradients out of the intravascular space aand into the lungs, with
resultant pulmonary edema and hypovolemic shock.
Hyponatremia. Hyponatremia caused by intravascular absorption of sodium free irrigating fluids may casue
confusion, agitation, visual disturbances, pulmonary edema, cardiovascular collapse and seizures.
Hypoosmolality. The crucial physiologic derangement leading to central nerouvs system dysfunction during
turp is hypoosmolality. Cerebral edema caused byacut e hypoosmolality can result in increased intracranial
pressure with resultant bradycardia and htn. Diuretics may accentuate hyponatremia nad hypo-osmolality.
No intervention is needed if the serium osmolality is near normal. when treatment is undertaken serium
osmolality should be monitored and corrected aggressively with hypertonic saline only until symptoms
resovle susbtantiallyl; then correction should be consitnued slowly (serium sodium concentrations increase
1.5 meq/l/hr)
Hyperammonemia. Hyperammonemia is the result of systemic absorption of glycine and its oxidative
damination to glyoxylic acid and ammonia.
Hyperglycinemia. Glycine is the most likely cause of visual disturbances, invluding transient blindness,
during turp syndrome, reflexting the role of glycine as an inhibitory NT in the retinal. Vision resturns to

normal within 24 hrs as serum glycine concentrations approach normal. reassurance is the best treatment.
Glycine may also exert toxic effects on the kidneys.