Chapter

88
Acute Kidney Injury

INTRODUCTION AND EPIDEMIOLOGY

Acute kidney injury is the deterioration of renal function over hours
or days resulting in the accumulation of toxic wastes and the loss of
internal homeostasis.































Community-acquired renal failure is diagnosed in only 1% of
hospital admissions at the time of presentation and is usually
secondary to volume depletion

Hospital-acquired renal failure is only apparent after admission.
Hospital factors include:

advanced patient age

potential nephrotoxic

exposures in a hospital setting

sepsis

multiorgan system illness in hospitalized patient

PATHOPHYSIOLOGY

Renal insult is classified as
o prerenal - decreased perfusion of a normal kidney
o intrinsic - pathologic change within the kidney itself
o postobstructive - obstruction to urine outflow

Functions of the kidneys:
o glomerular filtration
o tubular reabsorption
o secretion

Normal glomerular filtration rate (GFR) in early adulthood is

approximately 120 mL/min/1.73 m2 and typically decreases by 8
mL/min/1.73 m2 every decade thereafter

Prerenal failure - tubular and glomerular functions are still
maintained. Restoration of circulating blood volume is usually
sufficient to restore function.

Postobstructive renal failure initially results in an increase in tubular
pressure, which decreases the driving force for filtration

Intrinsic renal failure occurs with diseases of the glomerulus, small
vessels, interstitium, or tubule and is associated with the release of
renal vasoconstrictors.
MC cause of intrinsic renal failure ischemic injury or ischemic
tubular necrosis (also historically called acute tubular necrosis)

Tubular injury is a direct consequence of
o vasoconstriction,
o inflammation,
o endothelial changes,
o disruption of cell-cell and cell-matrix connections
o apoptotic changes

CLINICAL FEATURES
A. HISTORY AND COMORBIDITIES
Prerenal acute renal failure
thirst
orthostatic light-headedness
decreased urine output
Excessive vomiting, diarrhea, urination, hemorrhage, fever, or
sweating reduce circulating volume acute renal failure.
Causes of endothelial leak and third spacing, such as sepsis,
pancreatitis, burns, and hepatic failure prerenal failure
Progression of heart failure from any cause or overdiuresis of the
patient with compensated congestive heart failure renal failure
After cardiac arrest, in severe sepsis, or with other causes of systemic
hypotension Ischemic acute kidney injury
.
Renal failure from crystal-induced nephropathy, nephrolithiasis,
and papillary necrosis -- flank pain and hematuria
Rhabdomyolysis or hemolysis after recent BT-- pigment-induced
renal failure
Acute glomerulonephritis -- Darkening urine and edema with or
without fever, malaise, and rash
-- may have been preceded by pharyngitis or cutaneous infection
Acute interstitial nephritis -- Fever, arthralgia, and rash
Acute renal arterial occlusion -- severe flank pain
Goodpastures syndrome or Wegeners granulomatosis - Cough,
dyspnea, and hemoptysis
Postrenal failure - - men with prostatic disease or advanced
age and patients with indwelling bladder catheters.
Obstruction -- Anuria
-- Alternating oliguria and polyuria (pathognomonic of obstruction)

DIAGNOSIS
o
o
o
o

CBC,
electrolyte - Mg and P
hepatic function tests
blood cultures

o
o
o

urinalysis
urine osmolality
urine culture

ECG - fastest screening test for hyperkalemia

Chest radiography - evaluate for increased volume, effusions,
and pneumonia from or precipitate renal failure
Bedside US to assess urinary bladder volume
o large postvoid bladder residual volume (>125 mL)
bladder outlet obstruction
Anuria - 100 mL urine per day -- prerenal, postrenal, or
intrinsic kidney disease

LABORATORY EVALUATION
A. Creatinine and Glomerular Filtration Rate
Creatinine - mainstay for measuring renal function
- breakdown product of skeletal muscle protein creatine
- level is thus linked to muscle mass.
GFR = 0 serum Cr increases 1 to 3 milligrams/dL/day
Lesser increases in Cr -- residual renal function
faster increases -- rhabdomyolysis.
- Elevation of serum Cr may take 48 hours to accumulate
Cr clearance - estimate GFR
- lower muscle mass (e.g., older patients and women)
lower actual GFRs for any given Cr level
tubular secretion of Cr
o

Glomerulonephritis

tubular secretion of Cr
o
o
o

trimethoprim
cimetidine
salicylates

Normal kidney function is a GFR >90 mL/min/1.73 m2,

Stages of kidney disease are characterized by GFR:

Stage 1 GFR 90 mL/min/1.73 m2

Stage 2 GFR 60 to 89 mL/min/1.73 m2

Stage 3 GFR 30 to 59 mL/min/1.73 m2

Stage 4 GFR 15 to 29 mL/min/1.73 m2

Stage 5 GFR <15 mL/min/1.73 m2

B. PHYSICAL EXAMINATION
Identify dehydration -- evaluate
o
o
o

mucous membranes
jugular vein distention
lung auscultation

o
o

peripheral edema
tissue turgor

o
o

oxygen saturation
US

Indicators of hypovolemia
o
o
o

Base deficit
lactate level
Central venous pressure

Assess for rashes, evidence of vasculitis, jaundice, abdominal or

pelvic masses, or a distended palpable urinary bladder
On cardiac exam, check for atrial fibrillation, abdominal aortic
aneurysm, and signs of heart failure, and assess extremity pulses

B. BUN:Cr Ratio

can suggest hypovolemia

Both -- passively filtered at the glomerulus

Cr -- remains within the tubule

urea -- passively reabsorbed with sodium

avid sodium retention -- urea clearance is as low as 30% of GFR

adequate volume and sodium -- can to 70% to 100% of GFR

Prerenal failure -- B:Cr ratio typically >10

BUN

BUN

malnutrition
hepatic synthetic dysfunction

protein loading
GI hemorrhage
trauma

C. Fractional Excretion of Sodium

FeNa = UNa/PNa UCr/PCr

- indicator to identify hypovolemia *has important limitations

Noncontrast CT has sensitivity for hydronephrosis equivalent to

US and added advantage of demonstrating the site and often the
cause of obstruction.
Radionuclide scans and magnetic resonance urographs - before
and after administration of diuretics
-- functional obstruction in presence of dilated GU tract

TREATMENT

Resuscitation is the first priority

Treat hypovolemia, and identify and treat sepsis, myocardial
ischemia, and occult GI or retroperitoneal hemorrhage
Correct intravascular volume deficits with crystalloid
Bedside US can give some guidance for fluid resuscitation
Inspiratory collapsibility of the intrahepatic segment of the
inferior vena cava -- noninvasive measure of volume status and
fluid responsiveness
Most community-acquired AKI encountered in ED is prerenal
Renal dose adjustments made for medication
Renal function assessed before radiographic contrast studies.
IV contrast studies in patients GFR of 30 to 59 mL/min/1.73 m2
weigh benefits of study against risk of renal function decline
GFR <30 mL/min/1.73 m2, -- avoid IV contrast studies
Benefits typically outweigh risk Emergency contrast studies
o major trauma
o aortic dissection
o STsegment elevation myocardial infarction.
Avoid gadolinium for GFR <30 mL/min/1.73 m2.

PRERENAL FAILURE

D. Urinalysis
Acute glomerulonephritis RBCs enter filtrate at glomerulus
appear as casts and dysmorphic cells due to increased tonicity of
the renal medulla
Acute tubular necrosis -- tubular epithelium breaks down and
allows protein to leak into the filtrate tubular epithelial cells
Prerenal failure -- Hyaline casts are common
Ischemic or toxic tubular injury - pigmented granular casts
Hemoglobinuria or myoglobinuria - Brown granular casts
Myoglobinuria - hemoglobin on urine dipstick with no red cells
glomerulonephritis or autoimmune disease - Red cell casts and
proteinuria
E. Imaging
Renal US - test of choice for urologic imaging in AKI
- approximately 90% sensitivity and specificity for
detecting hydronephrosis due to mechanical obstruction
Chronic renal failure - kidney dimension of <9 cm
Renal parenchyma should be isoechoic or hypoechoic compared
with that liver and spleen
Hyperechogenicity indicates diffuse parenchymal disease
Color flow Doppler US -- assessment of renal perfusion and can
allow diagnosis of large-vessel causes of renal failure.
Resistive index -- ratio of the difference between systolic and
diastolic flow to systolic flow
- [(Vmax Vmin)/Vmax] normal ratio is <0.7
Intermittent or partial obstruction -- hydronephrosis may not be
present
May even be absent in complete obstruction in the setting of
retroperitoneal fibrosis

causes of prerenal azotemia: volume loss, hypotension, and

diseases of the large and small renal arteries
common precursor to ischemic and nephrotoxic conditions
intrinsic renal failure

POSTOBSTRUCTIVE RENAL FAILURE

5% to 17% of all community-acquired disease

elderly population as high as 22%
Risk factors: extremes of age, male sex, malignancy,
nephrolithiasis, retroperitoneal disease, GU surgery, and
indwelling urinary catheters
Timely relief of obstruction - essential for return of normal renal
function
Permanent loss of renal function - 10 to 14 days in the setting of
complete obstruction
risk of permanent renal failure significantly if complicated
by UTI

CRYSTAL-INDUCED NEPHROPATHY

precipitation of crystals within the renal tubules mechanical

and inflammatory injuries of the tubular epithelium
Chronic renal insufficiency and hypovolemia predispose patients
Urinary pH affects the formation of crystals
MCC: Elevated uric acid levels in the tumor lysis syndrome and
some medications acyclovir, sulfonamides, indinavir, and
triamterene

ANGIOTENSIN-CONVERTING ENZYME
INHIBITORS

can simultaneously GFR and renal blood flow

in Cr are observed after initiation of ACE inhibitor therapy
Overt AKI in ACE inhibitor initiation should prompt
consideration of bilateral renal artery stenosis
Volume depletion and vasoconstricting medications are
common precipitators of ACE inhibitorinduced renal failure
Angiotensin receptor blockers (ARBs) have similar effects
Hyperkalemia common complication of ACE inhibitor
renal insufficiency and renal failure are not contraindications
to the use of ACE inhibitors in appropriate patients

NONSTEROIDAL ANTI-INFLAMMATORY
DRUGS

INTRINSIC RENAL FAILURE

NOT common in patients with community acquired disease

MCC in hospitalized patients
Injury to glomerulus, tubule, interstitium, and vasculature
Community-acquired -- drugs and infection
Hospital -- toxic and ischemic insults
Radiocontrast-induced nephropathy imaging with IV contrast
o Incidence - 2% to 12%,
o Course: increasing Cr level, 25% above baseline, over 3 to
5 days complete resolution
o Risk factors

chronic renal insufficiency

diabetes

heart failure

liver disease

hypertension

Cyclooxygenase inhibitors can also cause renal failure

synthesis of vasodilatory prostaglandins of both GFR
and renal blood flow
Risk factors for adverse reactions:
o older age
o chronic renal insufficiency
o CHF, diabetes
o volume depletion
o use of diuretics or ACE inhibitors
Edema & renal insufficiency - observed early & dose dependent

ANTIBIOTICS

particularly aminoglycosides, fluoroquinolones

trough concentration - more relevant in predicting renal injury
once-daily dosing can reduce incidence of nephrotoxicity
trough levels used with vancomycin rates of AKI

PIGMENTS

Hemoglobin and myoglobin deposited in renal tubules

tubular obstruction and direct toxicity renal injury
Large-volume crystalloid infusion is the cornerstone of
treatment for rhabdomyolysis and hemoglobinuria
Myeloma lightchain nephropathy may also cause tubular
obstruction.

TREATMENT OF INTRINSIC RENAL FAILURE

Low (renal)-dose dopamine does not improve renal recovery

or decrease mortality
Fenoldopam is a potent dopamine D1-selective receptor agonist
blood flow to the renal cortex and outer medulla while
lowering systemic blood pressure
o reduces mortality and provides renal protection
o titratable and reliably controls severe hypertension
o agent of choice - HPN emergency w/ renal dysfunction
Venodilators (nitrates) and dialysis tx for volume overload
Diuretics - helpful for volume overload
o high-dose furosemide ototoxic & no benefit in AKI
Calcium channel blockers and mannitol - no role in tx of AKI

Chapter 89 Rhabdomyolysis
INTRODUCTION AND EPIDEMIOLOGY

MCC ADULTS: alcohol and drugs of abuse

followed by:
o medication
o immobility
o
muscle diseases
o infection
o
trauma
o strenuous physical activity
o
NMS
o heat-related illness
o seizures

children - less common and more benign

MCC CHILDREN of nonrecurrent trauma, viral myositis,
and connective tissue disease
adults and children recurrent: inherited metabolic disorders if
associated with exercise intolerance
Coma - risk for rhabdomyolysis from unrelieved pressure on
gravity-dependent body parts
Alcohol consumption - secondary to coma-induced muscle
compression and a direct toxic effect
Nutritional compromise, hypokalemia, hypomagnesemia, and
hypophosphatemia common in alcoholics
Statin-related myopathies - myalgias w/ or w/o elevation of
CK level, muscle weakness, and rhabdomyolysis
Statin-related rhabdomyolysis -rare, varies w/statin, dose related
Drug combinations - +cyclosporine, macrolide antibiotics,
warfarin, digoxin, and dual statin therapy
Strenuous physical activity - athletes, marathon runners, military
recruits, and outdoor laborers
Physical activity that produces high-force eccentric contractions
- strength training or heavy lifting greater breakdown in
muscle higher levels of creatine kinase VS. concentric
contractions - endurance-based exercises
risk
o poor physical conditioning
o high ambient T
o
inadequate fluid intake
o high humidity levels
o wearing of restrictive clothing

RADIOCONTRAST-INDUCED NEPHROPATHY

Risk is related to existing renal insufficiency and presence of

renal insults -DM, hypovolemia, sepsis, use of nephrotoxic meds
significant concern when GFR is <60 mL/min/1.73 m2
Do not give gadolinium based contrast for MRI if the GFR is
30 mL/min/1.73 m2 -- risk of nephrogenic systemic fibrosis.
The use of sodium bicarbonate appears promising

destruction of skeletal muscle, caused by any mechanism that

results in injury to myocytes and their membranes
Direct muscle injury and genetic and biochemical factors
rhabdomyolysis
Acute necrosis of skeletal muscle fibers and the leakage of
cellular contents into the circulation myoglobinuria

PATHOPHYSIOLOGY

syndrome characterized by injury to skeletal muscle with

subsequent effects from the release of intracellular contents

o
o
o
o

myoglobin
creatine kinase
aldolase
lactate dehydrogenase

o
o
o

aspartate
aminotransferase
potassium

disruption of the Na+K+ATPase pump and calcium transport

intracellular calcium and subsequent muscle cell necrosis
calcium activates phospholipase A2 and various vasoactive
molecules and proteases production of free oxygen radicals

acute in onset
o myalgias
o stiffness
o weakness

o
o
o

malaise
low-grade fever
dark (usually brown) urine

Muscle symptoms - only half of cases

severe rhabdomyolysis
o N&V
o abdominal pain
o tachycardia
Urea-induced encephalopathy - Mental status changes
Swelling and tenderness of the involved muscle groups and
hemorrhagic discoloration of overlying skin
MC: postural muscles of the thighs, calves, and lower back
may be present w/o any SSx, may have Normal PE
diagnosis after soliciting a historical clue or elevated serum
CK level or presence of dark urine on routine lab test

DIAGNOSIS

CLINICAL FEATURES

DIFFERENTIAL DIAGNOSIS

serum creatine kinase - most sensitive and reliable indicator

of muscle injury
degree of elevation = amount of muscle injury and the severity
of illness, NOT development of renal failure or other morbidity
requirement for the diagnosis of rhabdomyolysis - a 5x or
greater above the upper threshold of normal in serum CK
level, in the absence of cardiac or brain injury
begins to rise - 2 to 12 hours after the onset of muscle injury
peaks - 24 to 72 hours
declines - relatively constant rate of 39% of previous days value
Ongoing muscle necrosis - elevated values that fail to
isoenzyme CK-MM - skeletal and cardiac muscle; responsible in
large part for elevation in serum CK
CK-MB - primarily in cardiac; should not exceed 5% of total CK
Myoglobin - oxygen-binding protein found in skeletal and
cardiac muscle and is involved in oxidative metabolism
Myoglobinuria - skeletal muscle injury is >100 grams
Myoglobin elevation occurs before CK elevation rapidly
cleared from plasmarenal excretion & metabolism to bilirubin
Myoglobin enters urine when plasma concentration is >1.5
mg/dL causes reddish brown discoloration when urine
myoglobin level is >100 mg/dL
myoglobin contains heme, qualitative tests such as the dipstick
test do not differentiate among hemoglobin, myoglobin, & RBC
suspect myoglobinuria when urine dipstick test is + for blood
but no RBC present on microscopic examination
Radioimmunoassay - slightly more sensitive than the dipstick
technique in identifying myoglobinuria
myoglobin levels - return to normal within 1 to 6 hours after
onset of muscle necrosis absence of elevated serum
myoglobin level or myoglobinuria does not exclude diagnosis
Serum electrolyte, calcium, phosphorus, and uric acid levels
Urinalysis should be obtained for all patients
Serum creatinine and BUN - identify acute renal failure
CBC & coagulopathic screen DIC potential complication
levels of aldolase, LDH , urea, creatine, & aminotransferases

acute myopathies, periodic paralysis, polymyositis or

dermatomyositis, GBS
Rhabdomyolysis associated w/ strenuous exercise or fasting or
repeat episodes inherited metabolic myopathy

TREATMENT
A. PREHOSPITAL CARE

crush injury or accident victims with prolonged extrication and

transport times early and vigorous IV fluid resuscitation
Once limb is extricated NS @ 1 L/h
After extrication NS @ 500 mL alternate w/ D5%NS @ 1L/h
Avoid potassium or lactate containing solutions
no evidence that administration of NaHCO3 is beneficial

B. ED CARE

Once in ED continue aggressive IV rehydration 24 to 72 H

One method: rapid correction of fluid deficit with IV
crystalloids followed by infusion of 2.5 mL/kg/h goal:
maintaining minimum UO of 2 mL/kg/h
Another method: goal of 200 to 300 mL UO each hour
No prospective controlled studies have demonstrated benefit
from alkalinization of urine w/ NaHCO3 or forced diuresis
with mannitol or loop diuretics
Bicarbonate - widely recommended but w/o an evidence base
If bicarbonate is given maintain an isotonic solution and
avoid metabolic alkalosis or hypokalemia
Mannitol - may be harmful may cause osmotic diuresis in
hypovolemic patients
IFC - critical pts and acute renal failure to monitor UO
cardiac monitoring - electrolyte and metabolic complications
can cause dysrhythmias
pts w/ heart disease, comorbid conditions, or preexisting renal
disease or for elderly patients hemodynamic monitoring to
avoid fluid overload
Serial measurements:
o urine pH
o phosphorus
o electrolytes
o
BUN
o creatine kinase
o
creatinine
o
calcium
Hypocalcemia - early in rhabdomyolysis usually no tx
Calcium - given only to treat hyperkalemia-induced
cardiotoxicity or profound signs and symptoms of hypocalcemia
hypercalcemia is symptomatic continue saline diuresis
hyperphosphatemia >7 milligrams/dL - oral phosphate binders
Tx hypophosphatemia when <1 milligram/dL
Hyperkalemia - most severe in the first 12 to 36 hours
o insulin and glucose therapy may not be as effective in
rhabdomyolysis-induced hyperkalemia
o use of ion-exchange resins is effective
o Dialysis may be needed
Avoid prostaglandin inhibitors (NSAID) - vasoconstrictive
effects on the kidney

DISEASE COMPLICATIONS

Factors that contribute to rhabdomyolysis-induced acute renal

failure: hypovolemia, acidosis or aciduria, tubular obstruction,
and the nephrotoxic effects of myoglobin
exertional rhabdomyolysis - acute renal failure is rare without
the presence of factors like dehydration, heat stress, trauma, or
underlying disease such as sickle cell anemia
Renal tubular obstruction 2 to precipitation of uric acid and
myoglobin
Ferrihemate - breakdown product of myoglobin; responsible for
the direct toxic effect on the kidneys appears to occur only in
the presence of hypovolemia and aciduria (pH <5.6).
Renal failure may be oliguric (MC) or nonoliguric
w/ initially elevated creatinine and BUN and a large base deficit
have risk for rhabdomyolysis-induced acute renal failure
neither the presence of myoglobinuria nor the degree of CK
elevation is predictive of acute renal failure
Anticipate serum K level due to release of potassium from
injured skeletal muscle
Renal function - most important determinant of degree of
elevation
Hyperkalemia - significant complication of rhabdomyolysis if
acute renal failure occurs
uric acid levels - in crush injures due to release of muscle
adenosine nucleotides and the subsequent conversion to uric
acid by the liver
Uric acid - correlate with serum CK levels
Serum phosphorus - initially may be elevated due to the
leakage of phosphorus from injured muscle
Hypocalcemia - occurs early; asymptomatic deposition of
calcium salts in necrotic muscle due to hyperphosphatemia
and levels of 1,25-dihydroxycholecalciferol
Soft tissue calcifications on radiographs of involved limb
Hypocalcemia can occur w/o levels of phosphorus as
calcium is mobilized from damaged muscle hypercalcemia
DIC - severe rhabdomyolysis hemorrhagic complications
mechanical complications of rhabdomyolysis compartment
syndrome and peripheral nerve injury
muscle swelling may exert pressure on peripheral nerves
neuronal ischemia paresthesias or paralysis
Nerve injury is often proximal, and multiple nerves may be
involved in the same extremity
Compartment syndrome - 2 to marked swelling and edema of
the involved muscle groups

half of HD and PD patients will be alive 3 years after starting

therapy cardiac causes account for about half of all deaths

PATHOPHYSIOLOGY

Uremia - contamination of the blood with urine

Azotemia - buildup of nitrogen in the blood
Excretory failure - leads to elevated levels of >70 chemicals in
uremic plasma, which gives rise to the hypothesis that these
toxins, individually or in combination, cause uremic organ
dysfunction and produce the symptoms of uremia
dialysis DOES not reverse uremia because many toxins are
highly protein bound and nondialyzable
Biosynthetic failure - aspects of uremia caused by loss of the
renal hormones 1,25(OH)2-vitamin D3 and erythropoietin.
kidneys - responsible for the secretion of erythropoietin and 1hydroxylase produce the active form of vitamin D3
85% of erythropoietin is produced in the kidneys ESRD
levels of erythropoietin anemia
Vitamin D3 deficiency GI calcium absorption secondary
hyperparathyroidism renal bone disease
Regulatory failure oversecretion of hormones uremia
disruption of normal feedback mechanisms
uremic state excess free oxygen radicals react with
carbohydrates, lipids, and amino acids advanced glycation
end products atherosclerosis and amyloidosis

CLINICAL FEATURES OF UREMIA

Uremia - clinical syndrome; no single symptom, sign, or

laboratory test result reflects all aspects of uremia
correlation exists between the symptoms of uremia and low
GFR (8 to 10 mL/min/1.73 m2)
BUN and serum creatinine levels - inaccurate markers

DISPOSITION AND FOLLOW-UP

healthy patients w/ exertional rhabdomyolysis and w/o

comorbidities tx w/ oral or IV rehydration observed in the
ED released
Otherwise, patients should be admitted for IV hydration,
diuresis, management of complications, and treatment of the
underlying cause
initial 24 to 48 hours monitored bed to identify dysrhythmias
nephrology service evaluate the need for dialysis patients
with hyperkalemia unresponsive to therapy

Chapter 90 End-Stage Renal Disease

INTRODUCTION AND EPIDEMIOLOGY

irreversible loss of renal function, resulting in the accumulation

of toxins and the loss of internal homeostasis
Uremia - clinical syndrome resulting from ESRD, is universally
fatal without some form of renal replacement therapy
renal replacement therapy - two basic modalities: renal
transplant and dialytic therapy HD or PD
Hemodialysis - initial therapy in new cases of adult ESRD
most children receive transplants

MC reasons for E dialysis:

o hyperkalemia,
o severe acid-base disturbances
o pulmonary edema resistant to usual therapy

NEUROLOGIC COMPLICATIONS

Stroke - 6% of HD pts; half hemorrhagic and half ischemic

Subdural hematomas 10x more frequently in HD pts
Uremic encephalopathy - constellation of nonspecific central
neurologic symptoms associated with renal failure
Uremic encephalopathy - best diagnosed after eliminating
structural, vascular, infectious, toxic, and metabolic causes of
neurologic dysfunction
Dialysis dementia - nonspecific
o manifestation and treatment is progressive
o 2- to 4-year survival - 24%
o becomes evident after at least 2 years of HD
o fails to respond to in dialysis frequency or renal
transplantation
Peripheral neuropathy - most frequent neurologic
manifestation; lower > upper limb involvement
o most frequent clinical features large-fiber involvement:
paresthesias, reduction in deep tendon reflexes, impaired
vibration sense, muscle wasting, and weakness
o Autonomic dysfunction impotence, postural dizziness,
gastric fullness, bowel dysfunction, and reduced sweating
o HD - does not improve autonomic dysfunction
o daily short HD and long nocturnal HD may reduce elevated
sympathetic activity

Mortality from CV disease is 10-30x higher in HD patients

CAD, LV hypertrophy, and CHF are common
Etiology of CV disease in ESRD patients is multifactorial
preexisting conditions, uremia, and dialysis-related conditions
Dx of ischemic CV disease in ESRD patients clouded by
misconception that serum protein markers of myocardial
damage (troponins I and T) are unreliable in HD patients
troponin I and T are common even in asymptomatic HD
patients LV hypertrophy and microvascular disease
Asymptomatic elevations long-term risks of CAD
MI - >20% dynamic rise of baseline levels of troponin T and I
Management of hypertension - control of blood volume
If unsuccessful adrenergic blocking agents, ACE inhibitors,
or vasodilating agents - hydralazine or minoxidil
Heart failure most commonly results from hypertension,
followed by coronary artery disease and valvular defects
Natriuretic peptide levels are elevated in HD patients from
concomitant LV hypertrophy and systolic dysfunction
Uremic cardiomyopathy - diagnosis of exclusion
LV dysfunction - related to ischemic heart disease, hypertension,
and hypoalbuminemia
Dialysis rarely improves left ventricular function
Pulmonary edema - ascribed to fluid overload, but acute MI can
also trigger depressed LV function
Cornerstones of therapy:
o supplemental oxygen
o bilevel positive airway pressure
o nitrates
o ACE inhibitors
Loop diuretics - furosemide (60 to 100 milligrams IV), may aid
even in minimal UO from short-lived vasodilatory actions
HD - ultimate treatment for fluid overload in ESRD patients
Preload reduction by inducing diarrhea with sorbitol or by
phlebotomy may help in low resource situations
o Removing as little as 150 mL of blood is safe and effective
o Improved oxygenation offsets the in oxygen-carrying
capacity due to in hemoglobin
o Blood withdrawn should be collected in transfusion bags,
so plasma can be extracted by the blood bank and the RBC
transfused back to the patient later during dialysis

hypotension, heart size on chest radiograph suggest

effusion and potential tamponade
o Bedside US - best method to detect pericardial effusion and
tamponade
o Hemodynamically significant pericardial effusions require
pericardiocentesis under fluoroscopic or US guidance
o Bedside pericardiocentesis - only in hemodynamically
unstable patients because of its high complication rate
Pericarditis is usually due to uremia
o linked to fluid overload, abnormal platelet function, and
increased fibrinolysis and inflammation
o Pericardial contents are sterile unless infected and are
o causes pericardial friction rubs
o unique features of uninfected uremic pericarditis inflammatory cells do not penetrate into the myocardium,
so typical ECG changes of acute pericarditis are absent
o When ECG has features typical of acute pericarditis,
infection should be suspected
Dialysis-related pericarditis MC during periods of
catabolism (trauma and sepsis) or inadequate dialysis due to
missed sessions or vascular access problems
o Pathophysiology: buildup of middle molecules and
hyperparathyroidism.
o more common during HD than during PD
o Pericardial effusion - most important complication and
tends to be recurrent
Intensive dialysis - management of uremic and dialysis-related
pericarditis in patients in hemodynamically stable condition
HD is preferred - higher clearance rates effective usually after
10 to 14 days
Indomethacin, colchicine, and steroids - not useful
Anterior pericardiectomy - if pericardial effusion persists for
longer than 10 to 14 days with intensive dialysis
Total pericardiectomy - reserved for constrictive pericarditis
o

CARDIOVASCULAR COMPLICATIONS

PD does not remove volume fast enough to have a significant

impact on pulmonary edema
Cardiac tamponade is a concern in any critically ill ESRD
patient, often presenting without classic findings.
o signs of cardiac tamponade instead include:

changes in mental status

interdialytic weight gain

hypotension
edema

SOB
intradialytic hypotension

HEMATOLOGIC COMPLICATIONS

Anemia is multifactorial, caused by:

o
erythropoietin
o
blood loss from dialysis
o
frequent phlebotomy
o
RBC survival times
factitious anemia - wide fluctuations in plasma blood volume
Without treatment, hematocrit should stabilize at 15% to 20%,
with normocytic and normochromic RBC
Anemia - regular infusions of human recombinant erythropoietin
Erythropoietin replacement therapy - increasing exercise
capacity and tolerance
bleeding diathesis of ESRD patients:
o
risks of GI tract bleeding
o subdural hematomas
o subcapsular liver hematomas
o
intraocular bleeding
Uremic bleeding :
o platelet function
o anemia,
o
abnormal plateleto abnormal guanidinosuccinic
vessel wall interactions
acid dependent production
o
altered vWF
of nitric oxide

Skin bleeding test - best predictor of clinically important defects

in hemostasis
Improvement in bleeding times with infusions of desmopressin
(benefit in 1 h), cryoprecipitate (benefit in 4 h), or conjugated
estrogens (benefit in 6 h)
Dialysis does not improve the immune function and may
exacerbate immunodeficiency

GI COMPLICATIONS

Anorexia, nausea, and vomiting are common Sx of uremia

incidence of gastritis and UGIB in ESRD patients
Chronic constipation - common secondary to decreased fluid
intake and the use of phosphate-bonding gels
ESRD patients incidence of diverticular disease and colonic
perforation, especially patients with polycystic kidney disease
Dialysis-related ascites 2 to:
o fluid overload
o portal hypertension from polycystic liver disease
o osmotic disequilibrium
peritoneovenous shunts - treatment of refractory ascites

RENAL BONE DISEASE

GFR falls phosphate excretion serum phosphate

calcium phosphate product [Ca2+ (mg/dL) X PO4 (mg/dL)] is
higher than 70 80 metastatic calcification
Pseudogout - Joint pain develops from calcification of synovial
membranelined joints
Metastatic calcification in small vessels skin and finger
necrosis, life-threatening calcifications in the cardiac and
pulmonary systems
Short-term mortality rate is higher w/ a calcium-phosphate
product of >72
Treatment: low-calcium dialysate and phosphate-binding gels
ESRD progresses calciphylaxis and vitamin D3 deficiency
depressed ionized calcium levels and stimulation of the
parathyroid gland Hyperparathyroidism
o production of parathyroid hormone high bone
turnover weakened bones susceptible to fracture, bone
pain and muscle weakness
o High alkaline phosphatase and parathyroid hormone levels
make the diagnosis
o Treatment: control of serum phosphate levels with binding
gels, vitamin D3 replacement, subtotal parathyroidectomy
Osteomalacia - a defect in bone calcification
o S/Sx: weakened bones, bone pain, and muscle weakness
o characterized by low to normal alkaline phosphatase levels
and low parathyroid hormone levels
o confirming the dx: serum aluminum and bone aluminum
o Treatment: desferrioxamine helps aluminum bone disease

B. COMPLICATIONS OF VASCULAR ACCESS

2-MICROGLOBULIN AMYLOIDOSIS

Dialysis-related amyloidosis - in dialysis patients >50 years of

age and on dialysis for >10 years
Advanced glycation end products amyloidosis
Amyloid deposits are found in the GI tract, bones, and joints
Complications: GI perforation, bone cysts with pathologic
fractures, and arthropathies - carpal tunnel syndrome and rotator
cuff tears

HEMODIALYSIS
A. TECHNICAL ASPECTS OF HEMODIALYSIS

HD substitutes a filter for the glomerulus to produce an

ultrafiltrate of plasma
IV heparin 1000 to 2000 u - used to prevent thrombosis at the
vascular access site

HD sessions typically take 3 to 4 hours

Adjustment of the pressure gradient across the hemodialyzer
filter controls the amount of fluid removal (ultrafiltration)
Solute removal (clearance) during HD depends on:
o filter pore size
o amount of ultrafiltration (solute drag)
o concentration gradient across the filter (diffusion)
During HD - blood is removed from the vascular access site by
large-bore needles (typically 15 gauge), circulated through the
dialysis machine at rates of 300 to 500 mL/min, and returned
dialysate usually flows at a rate of 500 to 800 mL/min through
the dialysis filter in the direction opposite to blood flow

cases native artery or vein is not suitable for AV fistula creation,

interposing vascular graft made of autologous vein,
polytetrafluoroethylene, or bovine carotid artery must be used
o associated with a higher complication rate and shorter
functional life expectancies than natural AV fistulas
tunneled-cuffed catheters 3rd form of vascular access
o MC site for tunneled-cuffed catheter placement: R IJ vein
o tunneled-cuffed catheters should not be removed by pulling
Complications of vascular access account for more inpatient
hospital days than any other complication of HD
MC complications of HD vascular access - failure to provide
adequate flow (300 mL/min) and infection
If referred to the ED for inadequate access flow that impairs
dialysis, missing a single session should not result in uremic
encephalopathy, allowing emergency dialysis for those with
hyperkalemia and fluid overload in the ED
MC causes of inadequate dialysis flow: Thrombosis and
stenosis of the vascular access
o Grafts have a higher rate of stenosis than do fistulas
o presents with loss of bruit and thrill over the access.
o can be treated within 24 hours by angiographic clot
removal or angioplasty
o Thrombosis tx with direct injection of alteplase
Vascular access infections occur in 2% to 5% of AV fistulas
and approximately 10% of grafts
o present with fever, hypotension, or WBC count
o classic signs of infection: pain, erythema, swelling, and
discharge from infected vascular access are often missing
o After 6 months with a dialysis catheter, approximately half
of patients develop bacteremia, with serious complication
occurring in 5%-10% of patients with bacteremia
o A four-fold higher colony count in the catheter blood
culture than in the peripheral blood culture suggests the
catheter as the source of bacteremia
MC Staphylococcus aureus, followed by gram-negative bacteria
Patients usually require hospital admission, and vancomycin is
the DOC (15 milligrams/kg or 1 gram IV) because of its
effectiveness against methicillin-resistant organisms and long
half-life (5 to 7 days) in dialysis patients
Aminoglycoside - gentamicin 100 mg IV initially and after each
dialysis treatment - is added if gram-neg organisms are
suspected; monitor closely because of toxicity
Alternatives or adjuncts:
o removal and delayed replacement of the catheter
o catheter exchange over a guidewire
o use of antimicrobial/citrate lock solutions
Hemorrhage from vascular access - rare but life-threatening
o Hemorrhage can result from: aneurysms, anastomosis
rupture, or over anticoagulation
o Control bleeding: with manual pressure applied to the
puncture sites for 5 to 10 minutes, and observe the patient
for 1 to 2 hours if ceased
o Consult a vascular surgeon when simple methods fail

Vascular access aneurysms - from repeated punctures

true aneurysms are very rare
o Most aneurysms are asymptomatic; occasionally pain or
associated peripheral impingement neuropathy
o Aneurysms rarely rupture
Vascular access pseudoaneurysms - from subcutaneous
extravasation of blood from puncture sites
o Signs: bleeding and infection
o Dx: Arterial Doppler US
o if detected vascular surgeon should be consulted
Vascular insufficiency of the extremity distal to the vascular
access occurs in approximately 1% of all patients
o steal syndrome - result of preferential shunting of arterial
blood to the venous side of the access
o S/Sx:exercise pain, nonhealing ulcers, cool, pulseless digits
o Dx: Doppler US or angiography
o Tx: surgical
High-output heart failure can occur when >20% of the cardiac
output is diverted through the access
o Branham sign - a drop in heart rate after temporary access
occlusion; useful for detecting this complication
o Dx: Doppler US - can accurately measure access flow rate
o Tx: Surgical banding to flow and treat heart failure

C. COMPLICATIONS DURING HD

Hypotension - most frequent complication of hemodialysis,

occurring during 50% of treatments

Fluid removal during HD averages 1 to 3 L over a 4-hour

session, but removal of up to 2 L/h is possible
Maintenance of a normal BP during ultrafiltration depends on
cardiovascular compensatory mechanisms and refilling of the
vascular space by fluid shifts from the interstitial and
intracellular compartments
MC cause of hypotension - Excessive ultrafiltration due to
underestimation of the patients ideal blood volume (dry weight)
Optimal dry weight clinically defined when hypotension

prevents further fluid removal

DDx of intradialytic hypotension: Myocardial dysfunction from
ischemia, hypoxia, arrhythmias, and early pericardial tamponade
sepsis or antihypertensive meds also contribute to hypotension
Vascular refilling enhanced by:
o improving nutrition
o performing ultrafiltration before dialysis
o sodium concentration of the dialysate solution
Hypotension early in HD session - preexisting hypovolemia
o Predialysis losses - patient starts HD at weight below his or
her dry weight consider GI bleeding, sepsis, vomiting,
diarrhea, or intake of salt and water
o Intradialytic blood loss can occur from blood tubing or
hemodialyzer filter leaks
Hypotension near the end of HD - result of excessive
ultrafiltration, but pericardial or cardiac disease is possible
Intradialytic hypotension
o S/SX: nausea, vomiting, and anxiety, orthostatic
hypotension, tachycardia, dizziness, and syncope
o Tx: halt HD and place patient in Trendelenburg position
o
hypotension persists patient is given salt by mouth
(broth) or normal saline, 100 to 200 mL IV
PT is transferred to the ED for further evaluation assess for
adequacy of volume status, impairment of cardiac function,
pericardial disease, infection, and GI bleeding
Dialysis disequilibrium - clinical syndrome occurring at end of
dialysis and is characterized by nausea, vomiting, and
hypertension can progress to seizure, coma, and death
o occurs when large solute clearances occur during HD
patients 1st dialysis session or during hypercatabolic states
o cause is believed to be cerebral edema from an osmolar
imbalance between the brain and the blood
o During high solute removal blood has a transiently
lower osmolality than the brain favors water movement
into the brain and causes cerebral edema
o prevented by limiting solute clearance when initiating HD
o Tx: STOP HD and administering mannitol IV to serum
osmolality.
Air embolism
o clinical presentation depends on the patients body position
o Sitting - air passes retrograde through the internal jugular
vein cerebral circulation ICP and neurologic sx
o Recumbent position - air goes into the right ventricle and
pulmonary circulation pulmonary hypertension and
systemic hypotension
o passage of air through a right-to-left shunt creates an
arterial air embolism lodge in the coronary or cerebral
circulation MI or stroke.
o Sx: acute dyspnea, chest tightness, LOC and cardiac arrest
o S: cyanosis and churning sound in the heart from air
bubbles in the blood
o Tx: clamp the venous blood line and place patient supine
o Give 100% oxygen to aid reabsorption of the air
o Other therapies:

percutaneous aspiration of air from the right ventricle

IV administration of steroids

full heparinization,

hyperbaric oxygen treatment

Electrolyte abnormalities - errors in mixing the dialysate
concentrate w/waterresults in rapid osmolar shifts &hemolysis
o In some communities, water contains high concentrations
of Ca and Mg produces final dialysate high in minerals
o Use of this dialysate result in hard water syndrome
hypercalcemia and hypermagnesemia
o develop nausea, vomiting, headaches, burning skin, muscle
weakness, lethargy, and hypertension
o Tx: properly filtering the dialysis water to lower calcium
and magnesium concentrations

Hypoglycemia occurs in diabetic and nondiabetic

o drugs, malnutrition and sepsis are important causes

D. ED EVALUATION OF HD PATIENTS

Pts on HD may develop complications related to ESRD or HD

Medical history is very important

B. COMPLICATIONS OF CONTINUOUS
AMBULATORY PERITONEAL DIALYSIS

Repeated episodes of intradialytic hypotension may provide

important early clues to pericardial tamponade or MI
Repeated access infections - worsening immunologic status
Note all missed sessions and reasons
uremic symptoms - markers of inadequate hemodialysis
if the native kidneys are retained - sources of hypertension,
infection, and nephrolithiasis

Examine the access site: look for presence of flow by identifying

a bruit and thrill
The classic signs of infection erythema, swelling, tenderness,
and purulent dischargeare often limited until the infection is
far advanced
Look for congestive heart failure, effusion, or high-output
fistula-related heart failure; peripheral edema, hepatojugular
reflux, and jugular venous distention can be present in both fluid
overload and pericardial tamponade
loud cardiac murmur - represent flow secondary to anemia or
the arteriovenous access
Neurologic dysfunction - generally diffuse and nonfocal
Any focal neurologic findings require neuroimaging
GI bleeding - DRE and occult blood testing
Doppler US examination if any question about vascular
insufficiency, aneurysm, or pseudoaneurysm exists

exchanges of solution throughout the day

Continuous cyclic PD - through multiple exchanges at night
while the patient sleeps

Peritonitis MC complication of PD
o Mortality rates: range between 2.5% and 12.5%
o S/Sx: fever, abdominal pain, and rebound tenderness
o Cloudy effluent suggests peritonitis; confirmed by Gram
stain, cell count, and culture.
o The cell count in PD-related peritonitis is usually >100
leukocytes/mm3 with >50% neutrophils
o Gram staining - positive in only 10% - 40% of cases
o Organisms isolated in PD-related peritonitis

Staphylococcus epidermidis (approximately 40%)

S. aureus (10%)

Streptococcus species (15% to 20%)

Gram-negative bacteria (15% to 20%)

Anaerobic bacteria (5%)

Fungi (5%)
o Empiric therapy: few rapid exchanges of fluid lavaged to
the # of inflammatory cells in peritoneum + heparin (500 to
1000 units/L dialysate) to fibrin clot formation
o First-generation cephalosporin can be mixed with the
dialysate, 500 mg/L with the first exchange and 200 mg/L
with subsequent exchanges
o In penicillin-allergic patients vancomycin 500 mg/L and
maintenance doses of 50 mg/L per exchange
o Gram-negative coverage: add gentamicin 100 mg/L and
maintenance doses of 4 to 8 mg/L per exchange
o Recommend tx for 7 days after the first negative culture
results, usually resulting in a total of 10 days of therapy
o Admission based on the patients clinical appearance.
o Parenteral antibiotics are not used
Infections around a PD catheter
o pain, erythema, swelling, and discharge around catheter site
o MC causative bacteria are S. aureus and Pseudomonas
aeruginosa.
o Empiric therapy: oral first-generation cephalosporin or
ciprofloxacin for outpatient therapy
o Refer patients to their continuous ambulatory PD centers
for follow-up the next day
Abdominal wall hernias occur in 10% to 15% of PD patients
o Immediate surgical repair of pericatheter hernias
because of the high risk of incarceration

C. ED EVALUATION OF PD PATIENTS

PERITONEAL DIALYSIS
A. TECHNICAL ASPECTS OF PD

peritoneal membrane is the blooddialysate interface

PD relies on separate processes of clearance (solute removal) &
ultrafiltration (fluid removal) to replace functions of nephron
solute removal occurs via diffusion down chemical gradients
established by altering dialysate electrolyte concentration
Dialysate - supplied in 1.5% and 4.25% glucose formulations,
which can be alternated to or ultrafiltration
Typical PD regimens: 4 exchanges daily, with 2 L of dialysate
infused and left in place for several hours before draining
During the day, approximately 8 L is infused and about 10 L is
drained, for a removal of approximately 2 L/d of fluid
PD can be accomplished in an acute setting
o Continuous ambulatory PD - over the long term via

PE focuses on the abdomen: signs of infection of the

peritoneum, tunnel, and exit site should be identified

Chapter 91 Urinary Tract Infections and Hematuria

URINARY TRACT INFECTIONS

2010 UTI 6TH MC diagnosis in women age 15 - 64 years and

4TH MC diagnosis in women age 65 years and older
Self-reported annual incidence of UTI in women - 12%, by age
32 years, half of all women report having at least one UTI
younger women are more likely to be affected than men by a
ratio of 35:1; gender gap to 2:1 by age 66, most likely due to
bph and need for instrumentation in elderly men
All age groups from neonates to the elderly are affected,
carrying risks in special populations

E. COMPLICATED UTI

PATHOPHYSIOLOGY AND DEFINITIONS

Symptomatic patients, low-colony-count infections with 102 to

103 CFU/mL are clinically valid

UTIs can be grouped based on the anatomic site involved as

well as patient characteristics
classifications are important when determining tx modalities

infection involving a functional or anatomically abnormal

urinary tract or infection in the presence of comorbidities that
place the patient at risk for more serious adverse outcomes
diagnostic criterion: isolation of 105 CFU/mL of urine culture
patients are more likely to be infected w/ resistant organisms
Uncomplicated pyelonephritis - clinical syndrome of fever and
flank pain or tenderness with or without vomiting in a patient
with an anatomically normal urinary tract without comorbidities
recommended management of patients with uncomplicated
pyelonephritis is similar to recommendations for patients with
complicated UTI and differs from the management of patients
with uncomplicated cystitis

A. ASYMPTOMATIC BACTERIURIA

presence of >100,000 (>105) CFU/mL of a single pathogen on

two successive urine cultures in a patient without symptoms
Prevalence 10% in pregnantwoman, 40% in male and 50% in
female residents of nursing homes, and up to 100% in patients
with indwelling catheters for more than 1 month
Tx: recommended only in pregnant woman and in patients
immediately prior to invasive urinary procedures

B. URETHRITIS AND CYSTITIS

Infections of lower urinary tract include urethritis and cystitis

Acute cystitis - infection isolated to the bladder
W/O coexisting pyelonephritis in healthy, nonpregnant young
females with no obstruction is a benign illness
Competent ureteral valves prevent ascent of the bacteria into the
kidneys in most cases
Diagnostic criterion in acutely symptomatic patients: positive
urine culture of 102 to >103 CFU/mL
Urethritis - commonly associated with STDs, presents with
similar symptoms but typically is associated with a vaginal
discharge or irritation

C. PYELONEPHRITIS

Pyelonephritis is an infection of the upper urinary tract.

involves the renal parenchymal and pelvicalyceal system
differentiated from cystitis primarily by clinical findings:
o a syndrome of flank pain or CVA tenderness
o with or without fever
o positive urine culture of 105 CFU/mL
o other systemic symptoms such as nausea or vomiting
can progress into three patterns of renal infection not commonly
considered part of the UTI spectrum:
o acute bacterial nephritis
o renal abscess
o emphysematous pyelonephritis

D. UNCOMPLICATED UTI

UTI in a patient w/o structural or functional abnormalities

within the urinary tract or kidney parenchyma, w/o relevant
comorbidities that place patient at risk for more serious adverse
outcome, and not associated with GU tract instrumentation
Classification is thus limited to young, healthy, nonpregnant
women with normal anatomic and functioning urinary tracts
Women are more susceptible than men to UTI due to a shorter
urethra for uropathogenic bacteria to ascend
Traditional diagnostic criterion dating from 1960: positive urine
culture of 105 CFU/mL

F. RECURRENT URINARY TRACT INFECTION

two uncomplicated UTIs in 6 months or three or more

uncomplicated UTIs in the preceding 12 months
classified into two different categories that affect treatment
decisions: relapse and reinfection
Relapse - recurrence of a UTI within 2 weeks of treatment
completion caused by the same organism from a focus within
the urinary system, and represents treatment failure
Reinfection - recurrent UTI caused by a different bacterial
isolate or by the previously isolated bacteria after a negative
intervening culture or a period of 2 weeks between infections
Reinfection is more common than relapse
Behavioral factors can lead to risk for uncomplicated UTIs
concentration of bacteria in the female bladder may 10-fold
after sexual intercourse
use of a diaphragm and spermicide is also associated with
recurrent UTI spermicide enhances vaginal colonization with
Escherichia coli

MICROBIOLOGY

arise from ascending infection from the urethra to the bladder,

although hematogenous and lymphatic spread can occur

Uropathogenic organisms often have adhesins, fibrillae, or pili

that allow bacteria to adhere to and invade the uroepithelium
E. coli remains the most common pathogen by a large margin

C. PYELONEPHRITIS

Cystitis - Flank pain, CVA tenderness, or specific renal

tenderness to deep palpation, because of referred pain
if in association with fever, chills, nausea, vomiting, or
prostration acute pyelonephritis
presentation may be subtle, and difficult to distinguish lower
from upper UTI, especially in patients who do not experience
pain normally (spinal cord injury), immunocompromised
patients, and the aged
missed pyelonephritis could lead to untreated sepsis

D. UROSEPSIS

community acquired extended-spectrum -lactamaseproducing

E. coli - small but growing source of antibiotic resistance,
affecting approximately 4% to 6% of outpatients with UTI
Emergence of this resistant isolate of E. coli has important
implications for treatment and can mortality
Several anatomic, genetic, and age-related factors risks for
bacterial invasion of the urinary tract
Select women have specific uroepithelial cell E. colibinding
glycolipids that promote fecal coliform colonization of vagina
postmenopausal women - estrogen has been associated with a
conversion of vaginal flora from lactobacillus to E. coli and
other Enterobacteriaceae
Incomplete bladder emptying disrupts the bladders ability to
eradicate bacteria from its mucosal surface, its susceptibility
to infection, especially in patients with neurogenic bladder,
women with uterine prolapse, and men w/ prostate hypertrophy

E. COMPLICATED UTI

CLINICAL FEATURES
vary by anatomic site involved and the patients risks for
complicated UTI
Asymptomatic bacteriuria is a laboratory based diagnosis

A. URETHRITIS

In males, dysuria + urethral discharge indicates urethritis

UTI is uncommon in healthy young adult males, but if the
clinical diagnosis does not suggest urethritis or prostatitis in a
male with dysuria, bacteriuria is likely due to UTI
In women, Chlamydia infection should be suspected in the
following settings:
o a new sexual partner
o
partner with urethritis
o examination findings of cervicitis
o low-grade pyuria with no bacteria seen on urinalysis
Concurrent gonorrhea is common with Chlamydia infections

S/Sx: frequency, urgency, hesitancy, suprapubic pain, visible

(gross) hematuria, and/or suprapubic tenderness
Nature and severity of symptoms are determined by:
o etiologic organism(s)
o portions of the urinary tract involved
o patients ability to mount immune & inflammatory response
History of vaginal discharge or irritation is more often
associated with vaginitis, cervicitis, or pelvic inflammatory
disease than with UTI
Fever is uncommon with simple cystitis

clinical features and classic presenting S/Sx may vary widely or

be entirely absent
Suspect UTI in more complicated cases involving patients with
atypical and diverse S/Sx: weakness, malaise, altered mental
status, fever, and flank or abdominal pain
Guidelines suggest the following criteria be used to define
symptomatic catheter-associated UTI:
o new onset or
o acute hematuria
worsening of fever
o pelvic discomfort
o rigors
o in those whose catheters
o altered mental status
have been removed
o malaise
o dysuria
o lethargy with no other
o urgent or frequent
identified cause
urination
o flank pain
o suprapubic pain or
o CVA tenderness
tenderness
patients with spinal cord injury - spasticity, autonomic
dysreflexia, and sense of unease compatible with catheterassociated UTI

DIAGNOSIS

B. CYSTITIS

may or may not exhibit symptoms for cystitis or pyelonephritis

European Section for Infections in Urology
Simple urosepsis presents with
o temperature change (>38C or <36C)
o rising heart rate (>90 beats/min)
o elevated respiratory rate (>20 breaths/min)
o leukocytosis
Severe urosepsis
o Hypotension
o and/or organ dysfunction
o and/or hypoperfusion - evidenced by lactic acidosis,
oliguria, or acute altered mental status.
Uroseptic shock - adds the criteria of hypotension or ongoing
evidence of hypoperfusion despite adequate fluid resuscitation

Definitive diagnosis: historical findings + lab confirmation

clinical diagnosis of acute uncomplicated cystitis can be made
with a moderate probability based on:
o history of dysuria
o frequency
o urgency
o in the absence of vaginal discharge or irritation
o in women who have no risk factors for complicated UTIs
false-positive rate for the dx of UTI based on history alone: 33%
in outpatients and as high as 43% in ED patients
Although empiric treatment of uncomplicated cystitis based on
history alone continues to be advocated by some experts, three
systematic reviews do not recommend history-based diagnosis
due to inaccuracy, and other authors advocate lab confirmation
to reduce the growing problem of antibiotic resistance

URINALYSIS

Clean-catch, midstream voiding specimen - as accurate as urine

obtained by catheterization
Bacteria in urine double each hour at room temperature
refrigerated if not sent directly to the laboratory
Catheterization - indicated if patient cannot void spontaneously,
is too ill or immobilized, or is extremely obese
Avoid unnecessary catheterization 1% to 2% of patients
develop a UTI after a single catheter insertion

E. COMBINED RESULTS OF DIPSTICK

TESTING, URINE CELL COUNTS, AND
HISTORICAL INFORMATION

A. NITRITE REACTION BY DIPSTICK TEST

Urine nitrite reaction - very high specificity (>90%), and a

o useful in confirming UTI caused by bacteria that convert
nitrates to nitrite coliform bacteria, including E. coli.
o Enterococcus, Pseudomonas, and Acinetobacter species do
not convert nitrates to nitrites not detected by nitrite test
low sensitivity (~50%) - not always useful as a screening
examination negative result does not exclude the dx of UTI

Overall sensitivity of 48% to 86% and a specificity of 17% to

93% for identifying infection
In the ED, using culture findings of 105 CFU/mL as the criterion,
a positive leukocyte esterase reaction result has a sensitivity of
77% and a specificity of 54%
(+) urinary dipstick nitrite or leukocyte esterase test result
supports the dx of UTI, but a () test result does not exclude it

C. URINE WBC COUNT OR PYURIA BY

MICROSCOPY

Assessment of pyuria using standard centrifuged urine is

imperfect due to variable specimen preparation techniques
WBC count of >5 cells/HPF in a centrifuged specimen from a
symptomatic patient is abnormal
Symptomatic patient who has <5 WBCs/HPF in a centrifuged
specimen, other causes of false-negative pyuria should be
considered such: dilute precentrifuged urine, systemic
leukopenia, or patient self treatment with leftover antibiotics
Pyuria may be intermittent or absent if the patient has an
obstructed and infected kidney
In men, >1 or 2 WBCs/HPF in a centrifuged specimen can
be significant when bacteria are present
Urethritis and prostatitis are far more likely causes of pyuria in
young males who are sexually active and complain of dysuria,
regardless of the presence or absence of urethral discharge

D. BACTERIURIA BY MICROSCOPY

sensitive tool for detection of UTI in symptomatic patient

Presence of any bacteria on a Gram-stained specimen of
uncentrifuged urine (>1 bacterium/HPF or 1000x) is
significant & highly correlates w/ culture results of >105
CFU/mL
For Gram-stained centrifuged specimens, >1 bacterium/HPF
(1000x) is 95% sensitive and >60% specific to predict a culture
with 104 CFU/mL
o Both fail to detect low-colony-count UTI or infection

classic historical findings of cystitis - weak predictors of

positive culture or failed to predict cystitis
Vaginal discharge weakly likelihood of cystitis
diagnostic accuracy was significantly improved using dipstick
testing, particularly a positive test for nitrites
no single historical variable of cystitis could rule in or rule out
infection, but a dipstick test positive for nitrates, moderate
pyuria, and/or bacteriuria were accurate predictors of a UTI
no single test or combination of testing results can effectively
rule out UTI in women presenting to ED w/ sx of cystitis
subset of women for whom test results are equivocal who should
either be treated empirically or receive phone-in treatment based
on culture, if follow-up cannot be assured in 2 to 3 days

F. URINE AND BLOOD CULTURE

B. LEUKOCYTE ESTERASE REACTION BY

DIPSTICK TEST

caused by Chlamydia
Female patients with symptoms suggestive of UTI and vaginal
discharge or dyspareunia should have a pelvic examination to
investigate for PID

Patient with typical symptoms of cystitis or an uncomplicated

UTI and positive findings on urinalysis
o pyuria on microscopic examination
o bacteria in a Gram-stained specimen
o
positive leukocyte esterase test result
o and/or positive urine nitrite test result
o urine culture is not required
Vast majority of patients respond to empiric therapy.
Urine culture should be performed for the following patients:
o those with complicated UTI
o pregnant women
o adult males
o patients with relapse or reinfection
o septic patients
patient is symptomatic single (+) culture result is significant
organisms in blood culture match those in urine culture in 97%
of cases; blood culture results usually do not alter management
primary indication for blood cultures in patients with suspected
UTI is clinical sepsis

IMAGING

Renal imaging studies - not indicated in healthy patients with

acute pyelonephritis who can be managed as outpatients
Male, elderly, diabetic, or severely ill patients with acute
pyelonephritis - considered for imaging, particularly if there is a
renal stone or a poor initial response to antibiotic therapy
Plain film radiography and US - poor sensitivity for detection of
intrarenal gas formation in emphysematous pyelonephritis
Kidney or ureteral stones or emphysematous pyelonephritis are
suspected - CT is the best imaging modality

oral cephalosporins due to enterobacteria

o Aminopenicillins - not recommended as first-line
therapy in uncomplicated UTI

B. ACUTE PYELONEPHRITIS AND

COMPLICATED URINARY TRACT INFECTION

After clinical improvement has been achieved with parenteral

antibiotics, treatment should be changed to oral
Patients may require fluid resuscitation with crystalloids to
replace fluid losses due to vomiting or sweating
Guidelines recommend a total of 7 to 14 days of therapy,
regardless of whether or not parenteral therapy is used
Men with UTI without immunocompromise may have improved
outcomes with therapy for 7 days, rather than 14 days
sepsis syndrome - a total of 21 days of treatment

C. RECURRENT INFECTION

TREATMENT
A. ACUTE CYSTITIS AND UNCOMPLICATED
URINARY TRACT INFECTION

Selection of antibiotics depends on:

o organism suspected of causing infection
o
patients ability to adhere to treatment regimen
o
local resistance patterns
o
potential drug toxicity
o
cost

DISPOSITION AND FOLLOW-UP

Three-day regimens are recommended for uncomplicated

infections in nonpregnant women
Total of 3 to 6 days of therapy is sufficient for treating
uncomplicated UTIs in elderly women
Trimethoprim-sulfamethoxazole continues to be recommended
because it is inexpensive and has limited side effects
Fosfomycin - less efficacy than short courses of other regimens
Avoid trimethoprim-sulfamethoxazole as the first-line empiric
agent of choice unless treating based on culture with sensitivity
Nitrofurantoin - treatment of UTI in pregnancy, although it is
not effective against Staphylococcus saprophyticus
5-day course of extended-release nitrofurantoin is as effective as
3 days of trimethoprim-sulfamethoxazole
A single 3-gram dose of fosfomycin is a first-line choice for
uncomplicated UTI resistance rate is only 2%
Both nitrofurantoin and fosfomycin are recommended oral
agents in the event of extended-spectrum -lactamaseproducing
E. coli infection, resistance only 6% and 3%, respectively
Third-gen cephalosporins - effective against enterobacteria
First-gen cephalosporins - effective against staphylococci
Amoxicillin-clavulanate - less effective than fluoroquinolones or

Women w/ history of >2 UTIs in 6 months or >3 UTIs in 12

months cultured, treated empirically, and referred to a
primary care physician in 1 to 2 weeks for repeat culture and
possible prophylaxis
Tx: same tx for uncomplicated cystitis including 3-day
regimens, unless the recurrence is relapse
Tx relapse: alternative agent, same for complicated UTI

decision to admit based on:

o age
o host factors
o response to initial ED interventions
Admit: unable to retain fluids and medication or those w/
systemic signs of UTI and a stone

84% are discharged

Adjunctive therapies at discharge: increased fluids and frequent
voiding diminish tissue contact with bacteria
Oral bladder analgesic - phenazopyridine (200 milligrams PO
three times daily) reduces dysuria
Cranberry juice - mildly effective in reducing the incidence of
recurrent infection
Unfavorable prognosis:
o advanced age and general debility
o renal calculi or obstruction
o history of recent hospitalization or instrumentation
o
diabetes mellitus
o evidence of chronic nephropathy
o sickle cell anemia
o underlying carcinoma
o immunocompromised state
Dangerous complications of acute pyelonephritis:
o acute papillary necrosis with possible ureter obstruction
o septic shock
o perinephric abscesses
o emphysematous pyelonephritis

SPECIAL POPULATIONS
PATIENTS WITH HIV/AIDS

resistance to TMP-SMX is due largely to its use in

Pneumocystis jiroveci prophylaxis
Initial antibiotic: Fluoroquinolones - unless urine C&S available
caused by typical pathogens or common STD organisms
Close outpatient follow-up (recheck in 1 week) and possible
infectious disease consultation

HEMATURIA
A. INTRODUCTION AND EPIDEMIOLOGY

Gross hematuria - visible to the eye

Microscopic hematuria - laboratory diagnosis.
Myoglobin - discolor urine and simulate gross hematuria
MCC: UTI associated with urgency, dysuria, and nocturia
Sx also common in pt diagnosed with cancer of the urinary tract
Painless hematuria - neoplastic, hyperplastic, & vascular causes
Approx.1 mL of whole blood/L of urine visible hematuria
Gross hematuria result in false proteinuria
Gross hematuria is more common in premenopausal women due
to UTIs and contamination with menstrual blood
American Urological Association Microscopic hematuria: 3
RBCs/HPF (400X) on a properly collected and centrifuged
urinary specimen in the absence of an obvious benign cause
Hematuria from malignant causes is frequently intermittent

B. PATHOPHYSIOLOGY

Any process that results in infection, inflammation, or injury to

the kidneys, ureters, bladder, prostate, male genitalia, or urethra
may result in hematuria

Men >50 years old - tumors of the prostate or elsewhere in the

ejaculatory system and benign prostatic hypertrophy
patients <40 years - common causes:
o infections and inflammatory conditions
prostatitis
urethritis
sexually transmitted diseases
epididymo-orchitis
calculi with inflammation
tuberculosis
Testicular tumors may occur in men <50 years old
Free hemoglobin, myoglobin, or porphyrins in the urine result in
a positive urine test strip reaction for blood

by bacteria resulting in shedding and bleeding; resolves with

appropriate antibiotic treatment
patients taking anticoagulants appropriate coagulation studies
+ imaging at follow-up for older patients to exclude malignancy
UTI: normal RBCs on microscopic examination + bacteriuria
and leukocytes in a young healthy patient
Presence of normal RBCs without evidence of infection
further urologic evaluation
stable patients without an urgent cause suggested by history and
physical examination OPD

F. IMAGING

C. CLINICAL FEATURES

Initial hematuria - appearance of blood at the beginning of

micturition, with subsequent clearing suggests urethral
disease including cancer
Gross hematuria - lower tract cause
Microscopic hematuria, younger patients -nephrolithiasis or UTI
hematuria in patients >50 years old warrants follow-up because
renal, bladder, and prostate cancer frequency
Risk factors for uroepithelial cancer are:
o age >50 years
o male sex
o smoking
o family history of bladder cancer
o occupational exposures chemical, rubber, or leather ind
o excessive analgesic use
Expanding abdominal aortic aneurysms may erode to urogenital
tract or cause inflammation or obstruction from direct pressure
Malignant hypertension, embolic renal infarction, and renal vein
thrombosis are other serious diagnoses that can cause hematuria
Pregnancy - associated w/ UTI, nephrolithiasis, or pre-eclampsia
Recent instrumentation may produce hematuria
Hematuria in HIV-infected patients is 18% to 50%
o UTI
o thrombocytopenia
o chlamydial
o subclinical uroepithelial
o gonococcal urethritis
Kaposis sarcoma
o
glomerulonephritis
o urethral trauma
o neurogenic bladder
Hypertension and edema nephrotic syndrome
Full genital-urinary examination - essential for males & females

Noncontrast helical CT or renal US - Initial upper and lower

urinary tract imaging for hematuria
Helical CT - delineates most renal tumors, obstructions, or
stones and their precise location
Renal US - screening for obstruction, hydronephrosis, or AAA
o Study of choice in pregnant pt w/ suspected nephrolithiasis
Renal US also does not provide any assessment of renal function
Helical CT with contrast provides this important information
Gross hematuria in patients with blunt or penetrating trauma to
the abdomen, flank, or back aggressive approach to identify
the source of bleeding and to guide management

G. TREATMENT, DISPOSITION, AND

FOLLOW-UP

Treatment of hematuria is directed at the cause

Hemodynamically stable condition OPD management
Urgency for follow-up depends on the presence of gross
hematuria or risk factors for significant disease

Patients with gross hematuria or listed significant risk factors

should ideally be reevaluated at follow-up within 2 weeks
American Urological Association guideline: referral to urology
to assess for urinary tract malignancy in all patients with
microscopic hematuria without an obvious benign cause
Follow-up within 1 month - for patients with microscopic
hematuria without significant risk factors
Gross hematuria intravesical clot formation and bladder
outlet obstruction
ADMIT + specialist consult
o intractable pain
o intolerance of oral fluids and medications
o significant comorbid illness
o bladder outlet obstruction
o evidence of hemodynamic instability
o possible life-threatening causes of hematuria

D. DIAGNOSIS

Potential causes of hematuria are suggested by considering:

o patients age
o potential risk factors
o sex
o history of recent GU
o demographic characteristics
instrumentation
o habits
o comorbidities

E. LABORATORY TESTING

clean-catch midstream urine collection

Catheter-collected specimens - for women with a vaginal
discharge or menstrual or vaginal bleeding
urethral catheterization induces hematuria in 15% of patients
Glomerular source - Brown or smoke-colored urine, along with
dysmorphic RBCs, cellular casts, and proteinuria
Source below the kidneys - Red, clotted blood in the urine
urine dipstick test detect as little as 150 mg/L of free hmg,
corresponding to 5 - 20 intact RBCs/mL on microscopic analysis
False-negative:
o
high concentration of ascorbic acid (>5 mg/dL)
o
high SG
False-positive:
o presence of free hemoglobin, myoglobin, or porphyrins
Hemorrhagic cystitis with invasive infection of the bladder wall

Chapter 92
Acute Urinary Retention

INTRODUCTION AND EPIDEMIOLOGY

common painful urologic emergency characterized by a sudden

inability to pass urine + lower abdominal distention or pain.
elderly men with benign prostatic hyperplasia
20% recurrence within 6 months after an episode of AUR
mortality rate at 1 year increases from 4.1% in patients age 45 to
54 years to 32.8% in those age 85 years and older

PATHOPHYSIOLOGY

The voiding process, or micturition, involves the complex

integration and coordination of high cortical neurologic
(sympathetic, parasympathetic, and somatic) and muscular
(detrusor and sphincter smooth muscle) functions
sensory impulse of bladder distention transmits cortical
centers coordinate voluntary urination
Continent urine storage in the bladder requires
o relaxation of the detrusor muscle through -adrenergic
stimulation and parasympathetic inhibition
o contraction of the bladder neck and internal sphincter
through -adrenergic stimulation
smooth urination
o contraction of bladder detrusor muscle by cholinergic
muscarinic receptors
o relaxation of both the internal sphincter of bladder neck
and the urethral sphincter by -adrenergic inhibition
any causes that interfere with the neurologic control of the
voiding process voiding dysfunction
Urinary retention - inability to void voluntarily despite a
distended bladder & results from dysfunction of the detrusor
muscle and its coordination with the control of the bladder outlet
Bladder outlet obstruction progressively urine stream
strength & size despite forceful &prolonged detrusor contraction

CLINICAL FEATURES

o
o
o
o
o
o
o

Detailed history of present illness and PE, especially neurologic

examination, supported by imaging and urodynamic studies,
reveal the cause in the majority of patients
MC presentation: elderly male with inability to void for several
hours and lower abdominal distention or pain, 2 to BPH
PMH to look for:
history of prostatism
o Hx of urinary urgency,
prostate or UB cancer
frequency, or hesitancy
bladder calculi
o force and caliber of
IFC or injury to urethra
stream
prostate surgery
o nocturia
pelvic radiation therapy
o incontinence
terminal dribbling
Gross hematuria infection, bladder calculi, or neoplasm
Urethral stricture history of Foley catheter insertion,
cystoscopy, trauma, or previous radiation therapy or infection
History of new medications common cold preparations,
anticholinergics, sympathomimetic agents, and psychogenic and
other potential agents
Detailed neurologic history - look for a causative lesion from
high cortical function down to peripheral nerves that determine
end-organ function
Possible spinal cord injury hx of trauma
Infection or sepsis - Fever,tachycardic,tachypnea, &hypotension
Hypertension or tachycardia - may be transient and may resolve
after bladder decompression

Abdominal examination - palpitate or percuss from the epigastric

area to the lower abdomen to identify a painful mass (distended
bladder) in the lean patient
External genitalia - identify phimosis, paraphimosis, meatal
stenosis or stricture, or evidence of urethral or penile trauma
DRE (either before or after relief of obstruction) - evaluate the
anal-rectal area and prostate, assessing anal tone, perineal
sensation, prostate enlargement, stool impaction, and any
possibility of malignancy
Nodular or rock-hard prostate may suggest prostate cancer
Women with urinary retention - pelvic examination to detect
possible inflammatory lesions or pelvic or adnexal masses
After successful drainage of the distended bladder - repeat PE of
the lower abdomen to help exclude an unresolved extraurinary
bladder problem needing further management

DIAGNOSIS

Bedside US can easily identify urinary retention

Obtain a urine culture to identify urinary tract infection.
Hematuria secondary to the physical trauma of catheter insertion
that clears over time is common
CBC - patients with suspected severe infection, massive
hematuria with possible hypovolemia, or hematologic diseases
Renal function studies and serum electrolytes - prolonged
obstruction impaired renal function and electrolyte imbalance
Formal abdominal US or CT may be indicated to identify pelvic
or abdominal masses, bladder stones, or hydronephrosis, not
routinely needed if symptoms resolve after catheter placement
Neuroimaging or spinal imaging is needed if examination
identifies neurologic deficits
Cystourethrography may be required eventually to evaluate the
pathology in the lower urinary tract; not an ED procedure

TREATMENT

URETHRAL CATHETERIZATION TECHNIQUE

SUPRAPUBIC CATHETERIZATION
TECHNIQUE

Bladder decompression - urethral or suprapubic catheterization

Difficult catheterization in males - from urethral stricture,
prostatic enlargement, or postsurgical bladder neck contractures
recently underwent urologic surgery consult the urologist
before attempts at catheter placement.

retrograde injection of 10 to 15 mL of water-soluble anesthetic

lubricant (e.g., 2% lidocaine jelly) 5 to 10 minutes before
inserting the catheter can alleviate patient discomfort
Retract the foreskin when inserting the catheter
Catheter is in place when urine is freely draining
Do not inflate the retention balloon until urine begins to flow
through the catheter into the clear extension tube
Urethra can be injured from inflation of the retention balloon
within the urethra
If the catheter balloon is inflated in the prostatic urethra and not
the bladder, urine may or may not drain freely, and balloon
inflation causes extreme pain
Forceful attempts at catheter removal with the balloon still
inflated can cause edema and tears to the urethra
If attempts at passage of a straight 14- to 18-French Foley
catheter fail, use a firm angulated coud. catheter, positioned so
the tip points anteriorly
During insertion, a false lumen can be created, or the catheter
may kink in the urethra, especially in patients with underlying
urethral strictures or prostate enlargement
Consult urology for management
If catheterization produces gross blood, deflate the balloon,
remove the catheter, and do not attempt reinsertion because a
false passage may have been produced through the penile
soft tissue instead of the urethra
Management may require urology consultation for the use of a
guidewire, flexible filiforms, and dilation followers for
progressive dilation of the urethra to place a catheter

performed in patients after failure of several attempts of urethral

catheterization and as long as there is no obvious pelvic trauma
or abnormal anatomy in the lower abdomen
may be the only option to decompress an extremely painful,
distended bladder when urethral catheterization is not possible
US- guided suprapubic catheterization - low complication rate
Prepare the suprapubic area with betadine and local anesthesia
Visualize the distended bladder with US
advance a 22-gauge spinal needle with 10-mL syringe
posteriorly and caudally at a 30-degree angle from the true
vertical and 60 degrees from the horizontal plane of the
abdomen, 3 to 4 cm above the pubic symphysis in the midline
Advance the needle while withdrawing on the syringe
US visualization of the needle in the bladder and urine return
indicates correct placement
Use the depth and position of this attempt to direct the
placement of the obturator
Make a small skin incision in the midline at the point of prior
needle removal
cystostomy catheter and obturator assembly are then placed in
similar manner as the spinal needle, again aspirating for urine
After inflating the retention balloon, withdraw the obturator and
leave the catheter in the bladder
Secure the catheter with a suture.
If a guidewire is used for catheter insertion, remove the pullapart sheath after successful bladder placement

POSTCATHETERIZATION CARE

Patients with long-standing obstruction are at risk for

postobstructive diuresis and postobstructive renal failure
Monitor for 4 hours minimum for significant hourly urinary
output (>200 mL/h over input) after initial return
If this degree of output continues ADMIT the patient with

volume replacement adjusted hourly according to urine output

Pts w/ significant elevations of BUN or creatinine ADMIT
Reassess pt after Foley insertion for resolution of symptoms
Routine use of antibiotics for the prevention of bacteriuria or for
the treatment of asymptomatic bacteriuria is not suggested
Antibiotics are reserved for symptomatic urinary tract infection
Pharmacologic therapy with an -adrenergic receptor blocker,
which exerts its effects on the bladder neck and prostate, may
relax bladder smooth muscle, reducing outlet resistance to
urinary flow
-Adrenergic blockers such as alfuzosin, 10 mg daily, or
tamsulosin, 0.4 mg daily, increase the success of spontaneous
voiding after the catheter is removed
Warn patients, especially elderly - possible postural hypotension
-Adrenergic blockers may also shorten the interval of time
before a successful voiding trial and prevent recurrent episodes

DISPOSITION AND FOLLOW-UP

majority of patients with urinary retention are discharged

Patients should be educated in Foley catheter care and bag
drainage and given a list of alarm symptoms
o fever, return of symptoms, repeated vomiting, abdominal
pain, catheter blockage, or penile pain
o Penile pain - migration of the balloon into proximal urethra
Feelings of urgency or bladder spasm can be treated with
oxybutynin, 2.5 mg PO two or three times a day.
Oxybutynin has anticholinergic properties and can cause the
same adverse effects as any anticholinergic agent
There is NO satisfactory tx for urinary leakage around the IFC
Placement of a larger catheter is not typically effective
Recommend urology follow-up within 3 to 7 days.
longer period of Foley drainage is encouraged in patients with
retention vol >1.3 L to improve chances of successful voiding
serum prostate-specific antigen assay and long-term use of a 5reductase inhibitor could be evaluated at urology follow-up
Discontinue offending medications.
Patients with clot retention, hematuria and coagulopathy, sepsis,
possible neurologic cause of urinary retention, or other
significant comorbidities ADMIT

SPECIAL CONSIDERATIONS
A.FEMALES WITH URINARY RETENTION

Urinary retention in women is uncommon

Obstructive causes of urinary retention in women are usually
related to gynecologic problems, but neurogenic causes can
develop in both men and women
Mx: catheterization and attending to any treatable cause
Ideal selection of catheterization method, depends on the clinical
assessment of precipitating factors and underlying conditions.
-Adrenergic blockers do not appear to be helpful in women
with urinary retention
If there is no apparent cause, refer to a gynecologic urologist for
urodynamic studies

B. GROSS HEMATURIA AND CLOT RETENTION

Gross hematuria clot retention, resulting in pain and

hypertension and tachycardia from acute bladder distention
Mx: placement of a 20- to 24-French triple-lumen catheter (one
port each - urine drainage, balloon inflation, bladder irrigation)
and irrigation with saline until clear to evacuate clots
Pts may require admission, because clot retention may reoccur
and may require cystoscopic clot removal
Gross hematuria from coagulopathy - clotting parameters
corrected as appropriate and be admitted

C. POSTOPERATIVE URINARY RETENTION

Treatment is discussed in chapter 87

W/ retention after GU or pelvic procedures consult surgeon
patients with normal renal function and no obstruction, bladder
catheterization to relieve symptoms and then removal of the
catheter and a trial of voiding are usually all that is necessary