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Diseases of Urinary System Dr. Maged El-Ashker Associate Professor of Internal Medicine
Urinary system is composed of: 1
• Kidney
2
• Ureters
3
• UB
4
• Urethra
Functions of the kidney
1.
2.
3.
4.
Removes nitrogenous wastes Urea Uric acid Creatinine Ammonia Maintains homeostasis Fluid balance Electrolyte balance Acid-base balance Excretory Organ Via blood filtration & formation of urine Regulation of Blood Pressure Juxtaglomerular apparatus RAA system Renin Angiotensin Aldosterone
Urine formation 1. Filtration – Occurs in renal corpuscle 2. Reabsorption – Occurs in proximal convoluted tubule – Also occurs in distal convoluted tubule – It takes things back into blood 3. Secretion – Occurs in distal convoluted tubule – Blood gives things up to the urine 4. Concentration – Occurs in collecting tubules
Kidney
Nephron functional unit:
Principles of renal insufficiency Renal function depends upon the number and functionality of the individual nephrons. The potential causes of renal Insufficiency are: 1.
The rate of renal blood flow
2.
The glomerular filtration rate
3.
The efficiency of tubular reabsorption (the latter two are intrinsic)
Causes of renal insufficiency and uremia
Prerenal
Renal insufficiency Postrenal
Renal
Pre-renal causes of Insufficiency (Hemodynamic causes)
Congestive heart failure Acute circulatory failure Dehydration
N.B: Proximal tubular function is affected by
renal ischemia to a much greater extent than the Glomerulus or distal tubules; this is because of the high metabolic demands of the proximal tubules
Renal causes of Insufficiency Glomerulonephritis, pyelonephritis, Interstitial nephritis, Embolic nephritis, Toxic nephrosis, Amyloidosis
Post renal of Insufficiency 1.
Obstructive uroloithiasis
2.
Rupture of any part of urethers, UB or
urthera
Pathogenesis of renal insufficiency and renal failure
1.
Damage to the glomerular epithelium destroys its selective permeability and
permits the passage of plasma proteins into the glomerular filtrate
If the damage is complete and extensive:
Glomerular filtration may cease completely particularly if there is acute swelling of the kidney, but it is believed that anuria in the terminal stages of acute renal disease is caused by back diffusion of all glomerular
filtrate
through
the
damaged
tubular
epithelium rather than failure of filtration.
When renal damage is less severe:
The
remaining
maintain
total
nephrons
compensate
to
glomerular
filtration
by,
increasing their filtration rates. When this occurs, the volume of glomerular filtrate may exceed the capacity of the tubular
epithelium to reabsorb fluid and solutes
Decreased glomerular filtration results in: Retention of metabolic waste products such as urea and creatinine (uremia) 2. Retention of sulfate that contributes to metabolic acidosis in renal insufficiency 3. Retention of phosphate that leads to hyperphosphatemia and hypocalcemia (Renal Rickets) 4. Hyperkalemia which cause myocardial asthenia and fatal heart failure 1.
Loss of tubular resorptive function leads to: 1.
2.
3.
Continued loss of sodium and chloride causing hyponatremia and hypochloremia The continuous loss of large quantities of fluid due to solute diuresis can cause clinical dehydration Protein loss into the urine leading to hypoproteinemia, muscular weakness
Collectively 1.
Prolonged
hypoproteinemia,
metabolic
acidosis, hyponatremia and hyperkalemia result in rapid loss of body condition and
muscle weakness. 2.
Hypocalcemia may be sufficient to contribute to circulatory failure and to nervous signs .
Clinical signs of renal failure: In general, the clinical syndrome is variable and is rarely diagnostic for renal failure. However, weakness, lethargy, inappetence and, with extensive glomerular lesions, dependent edema due to hypoproteinemia
Bleeding diathesis can also be present in severely uremic animals.
Renal failure is characterized biochemically by: An increase in blood levels of urea and
creatinine (azotemia) and by retention of other solutes as described above.
Clinical features of urinary tract disease Principal manifestationS of UTD: 1. 2.
3. 4.
5. 6. 7. 8.
Abnormal constituents of urine Variations in daily urine flow Abdominal pain, painful urination (stranguria) Difficult urination (dysuria) Abnormal size of kidneys Abnormalities of the bladder and urethra Urachal leakage. Uremia
Abnormal constituents of the urine 1. 2.
3. 4. 5. 6.
Proteinuria Casts and cells Hematuria Hemoglobinuria Myoglobinuria Pyuria
7. Bacteriuria 8. Crystalluria 9. Glucosuria 10. Ketonuria 11. Indicanuria
Proteinuria can be..
Prerenal Renal
Post renal
Prerenal proteinuria Prerenal proteinuria is due to an abnormal plasma content of proteins that traverse
glomerular capillary walls as in hemoglobin, myoglobin, immunoglobulin
….. Renal proteinuria
Functional
Pathological
Intense exercise
Glomerular
Fever
Interstitial Tubular
Postrenal proteinuria
Urinary
• Due to the entry of proteins derived from hemorrhagic or exudative processes affecting the renal pelvis, ureter, UB, and urethra
Extraurinary
• Due to entry of proteins derived from the genital tract or external genitalia during voiding or in the process of collecting urine for analysis.
2. Casts and cells They occur only when the kidney is involved
in the disease process. If present in the urine, it indicates an
inflammatory or degenerative changes in the kidney
3. Hematuria Prerenal Renal
Postrenal
• Vascular damage • Septicemia • Purpura hemorrhagica. • Glomerulonephritis, • Renal infarction, embolism of the renal artery, • Tubular damage as caused by toxic insult, • pyelonephritis.
• Urolithiasis • Cystitis. • Enzootic hematuria
4. Hemoglobinuria 1.
False hemoglobinuria!
2.
True hemoglobinuria
Examples: (Intravascular hemolysis) 1. 2.
3. 4. 5.
6.
Babesiosis Water intoxication Bacillary Hburia Hypoposphatemia Copper poisoning Leptospirosis
5. Myoglobinuria Its presence in the urine is an evidence of severe muscle damage. The only notable occurrence in animals is azoturia of horses. Myoglobinuria does not occur commonly in enzootic muscular dystrophy, possibly because there is insufficient myoglobin in the muscles of young animals.
6. Pyuria Leukocytes or pus in urine indicates
inflammatory exudation at some point in the urinary tract, usually the renal pelvis or
bladder.
7. Bacteriuria Diagnosis of urinary tract infection is based on finding a clinically relevant bacteriuria in urine collected by free catch (midstream collection into a sterile container), catheterization or cystocentesis. > 40 000 (cfu)/mL from free-catch specimens, and more
than
specimens
1000
cfu/mL
from
catheterized
8. Crystalluria The presence of crystals in the urine of herbivorous animals have no special significance
unless they occur in very large numbers and are associated with clinical signs of irritation of UT. The presence of calcium carbonate crystals in the peritoneal fluid of a neonatal foal has been used to confirm a diagnosis of ruptured bladder
9. Glucosuria 1. 2.
3. 4. 5.
6.
Glucosuria in combination with ketonuria occurs only in diabetes mellitus Enterotoxemia due to Clostridium perfringens type D Parenteral treatment with dextrose solutions, Adrenocorticotropic hormones or glucocorticoid analogs. Horses with tumor of the pars intermedia of the pituitary gland Acute tubular nephrosis as a result of failure of tubular reabsorption.
10. Ketonuria 1.
Starvation
2.
Prergnancy toxemia
3.
Ketosis
11. Indicanuria Indicates autointoxication either due to constipation or intestinal obstruction
Variations in daily urine flow: • • • 1. Polyuria •
Increase in the volume of urine produced eg: Diabetes (insipidus and mellitus) IV fluid therapy, Osmotic diuresis, Diuritics, corticosteroids Chronic renal failure
2. Oliguria
• Dehydration • Congestive heart failure, circulatory failure • Acute Heart failure
3. Anuria
• Obstructive urolithiasis • Acute tubular nephrosis.
4. Pollakiuria
5. Dribbling
• Abnormally frequent passage of urine with or without an increase in the volume of urine excreted • Examples: Cystitis, UB calculi, uretheritis, partial obstruction of urthera
• is a steady, intermittent passage of small volumes of urine, sometimes precipitated by a change in posture or increase in intra-abdominal pressure • As in partial obstructive urolithiasis
3. Abdominal pain (dysuria and stranguria) A. Dysuria or painful/difficult urination occurs in [cystitis, UB calculus, and urethritis] Manifested clinically by….. 1. Frequent passage of small amounts of urine. 2. Grunting may occur with painful urination 3. The animal may remain in the typical posture after urination is completed.
Continue.. B. Stranguria is slow and painful urination
associated with disease of the lower urinary tract including cystitis, vesical calculus,
urethral obstruction, and urethritis. The animal strains to pass each drop of urine.
4. Abnormalities of kidneys and ureters
Enlargement or decreased size of kidneys may be
palpable on rectal examination or detected by ultrasonography. Examples pyelonephritis, hydronephrosis Increase size of ureters as in uretritis, hydroureters
5. Abnormalities of UB and urethra 1. 2. 3. 4. 5.
6.
Gross enlargement of the bladder Rupture of the bladder A shrunken bladder following rupture Cystic calculi Enlargement and pain of the pelvic urethra and its external aspects in male cattle with obstructive urolithiasis Obstruction of the urethral process of male sheep with obstructive urolithiasis
6. Uremia Is the systemic state that occurs in the terminal stages of renal insufficiency.
The uremic animal is depressed and anorexic with muscular weakness and tremor.
In chronic uremia, the body condition is poor as a result of continued loss of protein in the urine, dehydration and anorexia.
Continue..
Tachycardia because of terminal dehydration and myocardial asthenia but the temperature remains normal
Ammoniacal or uriniferous smell on the breath is often described but is usually undetectable.
Tongue dip necrosis, GIT ulcerations
Recumbency, coma, death
Special examination of the urinary system
Specific Gravity
PH
Urine
Glucose, protein, Urea, Sodium,FE Na Creatinine
Enzymuria
Enzymuria
Serum biomarkers to detect AKI
DIAGNOSTIC EXAMINATION TECHNIQUES 1.
Sonography
2.
Endoscopy
3.
Radiography
4.
Biopsy
5.
Urinalysis
6.
Serum biomarkers
Principles of Treatment of UTD
Removing the primary cause and restoring
normal
fluid
dehydration,
balance acid-base
by
correcting
disorders,
electrolyte abnormalities
Antimicrobial therapy (If needed)
Antiinflammatory agents
and
Note………………………….. Ruminants with acute and chronic renal failure typically have………………. 1. Hyponatremia, 2. hypochloremia, 3. Hypocalcemia, hypokalemia because of inappetence 4. Hyperphosphatemia [only in ARF]
Note…………………….
Horses with acute or chronic renal failure
have similar electrolyte changes to those in ruminants, with the marked difference being
the
presence
of
hypophosphatemia.
hypercalcemia
and
Note……………………
If the patient has anuria or oliguria after the fluid volume deficit is corrected, a diuretic should be administered to help restore urine flow. Furosemide (1-2 mg/kg BW every 2 h) or mannitol (0.25-2.0 g/kg BW in a 20% solution) may be used, but furosemide is preferred because of its much lower cost and ease of administration.
Notes……………………..
Animals non-responsive to fluid loading and diuretics could be administered low-dose (,renal dose') dopamine as a continuous
intravenous infusion (2-5ug/kg BW/min) with dopamine being diluted in 0.9% NaCl, 5%
dextrose or lactated Ringer's solution.
Note…………………..
Appropriate first-line antimicrobials include penicillin, ampicillin, amoxicillin, ceftiofur,
and
cefquinome
in
ruminants
and
trimethoprim-sulfa and ceftiofur in horses.
Antimicrobial therapy for lower UTI should
continue for at least 7 days and for 2-4 weeks for upper UTI.
Note………………………
B complex vitamins should be frequently administered because their rate of loss in the
urine is anticipated to be higher than normal in animals with renal failure.
Diseases of the Kidney 1. 2. 3. 4. 5. 6. 7.
Pyelonephritis Renal ischemia Glomerulonephritis Toxic nephrosis Interstitial nephritis Embolic nephritis Hydronephrosis
Pyelonephritis It is a bacterial inflammation of the renal pelvis and the kidney caused mainly by ascending infection from the
lower urinary tract. Clinically it is characterized by
Pyuria Hematuria Cystitis Ureteritis Suppurative nephritis.
Etiology Secondary to bacterial infections of the lower urinary tract 2. Spread from embolic nephritis of hematological origin such as septicemia in cattle (Pseudomonus. aeruginosa) 3. Specific pyelonephritides associated with C. renale in cattle and pigs 4. In association with nephroliths 1.
Pathogenesis Pyelonephritis develops when:
Bacteria
Urine stasis
Reflux of urine from UB
What are the causes of urine stasis? Blocking of the ureters by: Inflammatory swelling Debris By a pressure from the uterus in pregnant females By obstructive urolithiasis
What happens !!!! Initially, the renal pelvis and medulla are affected (because they are relatively more hypoxic and localized tissue hypertonicity
depresses
the
phagocytic
function
of
leukocytes), then the infection in may extend
to the cortex.
Notes If renal involvement is bilateral
Fever
Toxemia
Pyelonephritis in cattle and C. renale infection
Very common but the clinical disease has
been decreased markedly.
Now, the majority of pyelonephritis in cattle
is caused by E. coli.
The reason for the decrease in C. renaIe isolation from clinical cases is probably due to: 1.
A change in diet towards concentrates with an associated decrease in urine pH (acidic)
2.
The widespread use of beta-lactam antibiotics
3.
The marked decrease in urethral catheterization in order to obtain a urine sample in cows suspected to be ketotic.
Important notes C. renale attaches most efficiently in alkaline pH E coli attaches most efficiently in acidic pH
Clinical findings 1. 2.
3. 4. 5. 6. 7.
The first observed sign is hematuria In other cases, the first sign is colic !!! Fluctuating fever (39.5 c) Capricious appetite Fall in milk yield over weeks Loss of body condition The most obvious signs are the presence of pus, mucous, tissue debris and blood in urine (last portion of urine voided)
Continue……… 8. Dysuria, stanguria, dribbling of urine 9. Rectal examination of UB may be –ve in the early stages, but
later there is detectable thickening of its wall 10. RE, left kidney show enlargement and absence of lobulation
and becomes tender 11. In chronic cases: no clinical signs except a history of chronic
weight loss
Clinical pathology: Uremia (BUN, Cr are Elevated) Urinalysis RBCs Protein Pus Depris Mucous
Treatment 1.
General principles of UT infections
2.
Change of urine pH
3.
Antibacterial agents for at least 3 weeks
4.
Unilateral nephrectomy (but this should
only be done in non azotemic animals)
Differential Diagnosis The presence of pus and blood in the urine may suggest
Cystitis
Embolic nephritis
Pyelonephritis
It may be difficult to distinguish between these diseases but renal enlargement or pain on rectal palpation of the
kidney indicates renal involvement.
Continue…… Ultrasonographic
changes
associated
with
pyelonephritis include: A dilated renal collecting system, renal or ureteral calculi,
increased
corticomedullary
echogenicity,
echogenicity
and
loss
of
subjective
enlargement of the kidney with acute disease or a small irregular kidney with chronic disease
2. Renal Ischemia Reduced blood flow through the kidneys
usually results from general circulatory failure. There is transitory oliguria followed by
anuria and uremia if the Circulatory failure is not corrected
Causes and pathogenesis Hemodynamic causes !!!
Decreased Venous return Decreased Cardiac output Decreased circulating blood volume
Continue…. When COP is decreased compensatory vasoconstriction of the renal blood vessels Decreased GFR Oliguria, retention of waste product (Urea, Creatinine) leads to prerenal azotemia
Continue…
Up to a certain stage, the degenerative
changes are reversible by restoration of renal blood flow, but if ischemia is severe
enough and of sufficient duration, the renal damage is permanent
N.B The parenchymatous lesions vary from
tubular necrosis to diffuse cortical necrosis in which both tubules and glomeruli are affected.
In cases of hemoglobinuria and myoglobinuria It appears that vasoconstriction of renal vessels is mostly prevalent rather than a direct toxic effect of Hb, Mb on renal tubules.
Uremia in both cases may be exacerbated by plugging
of
the
coagulated protein.
tubules
with
casts
of
Clinical signs Renal
ischemia does not appear as a
distinct disease. Its signs are masked by the clinical signs of the primary disease. In
most cases, oliguria and azotemia will
go unnoticed if the circulatory defect is corrected in the early stages.
Continue… The
general clinical picture is one of acute
renal failure as described under uremia.
CLINICAL PATHOLOGY Urinalysis
as well as serum urea nitrogen and creatinine concentrations are most commonly used as indices. On urinalysis, proteinuria is an early indication of renal damage The passage of large volumes of urine of low specific gravity after a period of oliguria is usually a good indication of a return of normal glomerular and tubular function
Treatment
Treating the primary cause
Correcting fluid, electrolyte and acid-base disturbances
If renal damage has occurred, supportive treatment as suggested for the treatment of acute renal failure
should be instituted.
Glomerulonephritis
Glomerulonephritis can occurs either
Primary
Secondary
• The disease involves only the Kidney (Glomeruli) although the inflammatory process extends to affect the surrounding interstitial tissue and blood vessels.
• As a component of diseases affecting several body systems, such as Equine infectious anemia and chronic swine fever
N.B
The
primary
and
secondary
glomerulonephritis are rare causes of clinical disease in farm animals.
Continue…… The disease is sometimes associated with other chronic, systemic illness such as in:
Cows with Johne's disease Bovine virus diarrhea Leptospirosis Pigs with hog cholera African swine fever Horses with equine infectious anemia and S. equi infection
Pathogenesis
Glomerular injury can be initiated by an immune response whereby antibodies are directed against intrinsic glomerular antigens or by foreign antigens planted in the glomerulus.
Alternatively, and more commonly, circulating antigen-antibody complexes may be deposited in the glomerulus.
Continue..
As the complexes accumulate, they stimulate an inflammatory
response
that
damages
the
glomerular filtration system.
Inflammatory damage to the glomerulus alters the selective permeability of the filtration system allowing plasma protein, particularly albumin, to pass into the glomerular filtrate
Clinical findings Chronic
diarrhea Proteinuria hypoalbuminemia Weight loss Oliguria……anuria uremia
Treatment
Unrewarding
TOXIC NEPHROSIS
Nephrosis is the process in which cloudy swelling till caseation and sloughing of the affected part then proliferartive changes are occurred resulting in formation of scar tissues instead of original kidney tissues.
Causes
Most cases of nephrosis are caused by the
direct action of toxins but hemodynamic changes may contribute to the pathogenesis. A.
Hemodynamic causes (Dehydration, CHF, Mburea, Hburea)
B. Toxins 1. Metals
• Mercury, arsenic, cadmium, selenium and organic copper compouds
2. Antibacterial
• Aminoglycosides (Genta,Neomycin) • Tetracyclin (Daily LA tetracyclin) • Sulfonamides
3.Vitamins
• VitaminK3 (IM or IV) • Vitamin D2 orD3
Continue… 4. NSAIDS
• Phenylbutazone • Flunixin meglumin
5. Benzimidazole
• Thiabendazole anthelmintics
6. Monensin
• In ruminants
Continue.. 7. Oxalate
• In plants • In fungi • In ethylene glycol or ascorbic acid,
8. Aldrin
• Insecticide
9. Mycotoxins
• Ochratoxins and Citrinins
9. Bacterial toxins
Pathogenesis 1.
Hemodynamic causes
Decrease renal flow, with
susequent decrease GFR (The same as in Renal ischemia) 2.
Toxins as well as Mb or Hb causes either destruction or plugging of renal tubules, causing interstitial edema resulting decrease GFR (Acute nephrosis)
3.
If there is sufficient tubular damage, there may be back leakage of glomerular filtrate into the interstitium.
Clinical findings Clinical signs may not be referable to the urinary system. In acute nephrosis there is………………….. Oliguria and proteinuria with clinical signs of uremia in the terminal stages (depression, dehydration, anorexia, hypothermia, a slow or an elevated heart rate, and weak pulse and diarrhea)
Clinicopathological findings
Urinalysis abnormalities are usually present before serum urea and creatinine concentration are
increased.
Proteinuria, glucosuria, enzymuria (GGT) and Hypoproteinemia
In acute renal disease of horses, hypercalcemia and hypophosphatemia can be present
Treatment
Treatment should be directed at general supportive care for acute renal disease as before
Remove the source of toxins
Hemodialysis was used successfully to treat a foal with presumed oxytetracycline nephrotoxicosis.
Interstitial nephritis
Interstitial nephritis is rarely recognized as a cause of clinical disease in farm animals although it is a frequent postmortem finding in some species.
It is a common disease in dog and less in other animals
It may be acute diffuse or chronic focal non suppurative.
White spotted kidney
Continue…
Acute type is caused by leptospirosis in dogs
Focal interstitial nephritis of cattle is not associated with leptospirosis or active
bacterial infection
Clinical findings (in dogs)/Treatment
Polyuria Polydepsia Vomition Fever Treatment Restoration of fluid and electrolyte balance AB administration
Embolic nephritis
Embolic lesions in the kidney do not cause clinical signs unless they are very extensive, in which
case septicemia may be followed by uremia.
Even though embolic nephritis may not be clinically evident, transient proteinuria and pyuria may be observed if urine samples are examined at frequent intervals.
Etiology 1. Usually occurs after any septicemia or bacteremia when bacteria lodge in renal tissue. Examples: Valvular endocarditis Suppurative lesions in uterus, udder, navel, peritoneal cavity in cattle
2. or be associated with systemic infections such as: Septicemia in neonatal animals, including
Actinobacillus equuli infection in foals and E. coli septicemia in calvesErysipelas in pigs,
Corynebacterium, pseudotuberculosis in sheep and goats. Septicemic or bacteremic Streptococcus equi
infection in horses.
Pathogenesis
Bacterial emboli either localize in renal tissue
cause the development of focal suppurative lesion
Continue…………
Or block of a blood vessel
Infarction
Continue… The gradual enlargement of focal embolic lesions leads to the development of toxemia and gradual loss
of renal function. If the urine is checked repeatedly, the sudden appearance of proteinuria, casts, and microscopic hematuria, without other signs of renal disease, suggests the occurrence of a renal infarct.
Clinical signs
Usually there is insufficient renal damage to
cause signs of renal disease, If so, Signs of toxemia and the primary disease are usually
present.
The kidney is enlarged on rectal examination
Clinical pathology Hematuria, proteinuria and pyuria are present in the urine. Positive urine culture at the onset of proteinuria
Differential Diagnosis
Differentiation from pyelonephritis is difficult unless the latter is accompanied by signs of lower urinary tract infection such as cystitis or urethritis.
The kidney is enlarged in both conditions and the findings on urinalysis are the same when embolic nephritis invades the renal pelvis.
Hydronephrosis
Hydronephrosis is a dilatation of the renal pelvis with progressive atrophy of the renal parenchyma.
It occurs as a congenital or an acquired condition following obstruction of the urinary tract.
Any urinary tract obstruction can lead to
hydronephrosis
Diseases of Urinary bladder
1. Cystitis It means Inflammation of the bladder. Usually associated with bacterial infection. Characterized
clinically (pollakiuria
by
frequent, and
painful
dysuria),
urination hematuria,
inflammatory cells and bacteria in the urine.
Etiolgy 1. 2. 3. 4. 5. 6. 7.
Ascending infection from lower UT Secondary to cystic calculus Difficult parturition Contaminated uretheral catheter Late pregnancy As a sequel to paralysis of the bladder. Secondary to pyelonephritis
Pathogenesis Bacteria frequently gain entrance to the bladder but are usually removed by the flushing action of voided urine before they invade the mucosa.
Mucosal injury and stagnation of urine facilitate invasion of the bacteria
Bacteria usually enter the bladder by ascending the urethra but descending infection from embolic nephritis may also occur.
CLINICAL FINDINGS (acute cases) 1. Frequent urination occurs and is accompanied by pain (treading with the hind feet, kicking at the belly and swishing with the tail ) and sometimes grunting. 2. The animal remains in the urination posture for some minutes after the flow has ceased 3. The urethritis that usually accompanies cystitis causes painful sensations and the desire to urinate. (Bladder is
always nearly empty)
Continue… 4. The volume of urine passed on each occasion is usually small. 5. Moderate febrile reaction 6. Acute retention of urine may develop if the urethra becomes
blocked with pus or blood, but this is unusual. 7. On RE, no palpable abnormality may be detected but pain may be evidenced
Continue….(Chronic cases) • There is a similar syndrome but the signs are less marked. • Frequent urination and small volume are the characteristic signs. • The bladder wall may feel thickened on rectal examination.
Clinical pathology
Blood and pus in the urine is typical of acute cases and the urine may have a strong ammonia odor.
In less severe cases the urine may be only turbid and in chronic cases there may be no
abnormality on gross inspection.
Continue…. Microscopic examination of urine sediment will reveal: RBCs Leukocytes Desquamated epithelial cells. Quantitative bacterial culture is necessary to confirm the diagnosis and to guide treatment selection.
Treatment
Antimicrobial agents are indicated to control the infection for a minimum of 7 and preferably 14 days.
Repeated bacterial culture of urine at least once during and again within 7-10 days after completion of
treatment used to assess the success of therapy.
Recurrence of the infection is usually due to failure to
eliminate foci of infection
Paralysis of the urinary bladder It is uncommon in large animals. Paralysis usually occurs as a result of neurological diseases affecting the lumbosacral spinal cord such as equine herpes myelopathy and cauda equina syndrome,
and
particularly
ascending
meningitis in lambs after tail docking.
spinal
Continue…. Compression
of the lumbar spinal cord by neoplasia or infected tissue can cause paralysis of the bladder. Excessive tension on the tail, such as with tail ropes or use of the tail for restraint in cattle, can injure the cauda equina and cause bladder paralysis. In horses, spinal cord degeneration following consumption of sorghum can lead to bladder paralysis
continue
epidural injection of an excessive quantity of alcohol.
Equine protozoal myeloencephalitis
idiopathic bladder paralysis Due to atony of UB following UT obstruction
Clinical signs 1. Incontinence with constant or intermittent dribbling of urine (during walking)
2. Urine flow is often increased during exercise. 3. The bladder is enlarged on examination per rectum and urine can be easily expressed by manual compression.
Treatment 1.
2. 3. 4.
5. 6.
Treatment is supportive and aimed at relieving bladder distension by regular catheterization and lavage. During catheterization, care must be taken to avoid introducing infection. Administration of parasympathomimetic agents such as bethanechol (Evacuate the bladder) Nerve tonic Prohylactic antibacterial agents NB.The prognosis in poor
Obstruction of Urinary tract Uroliths
Inflammatory
debris
Blood
Tumors
(bovine enzootic hematurea), squamous cell carcinoma
Urolithiasis in ruminants Urolithiasis is a common disorder among
ruminants raised in management systems where the ration is composed primarily of
grain or where animals graze certain types of pasture
Urolithiasis becomes an important clinical
disease of castrated male ruminants when calculi cause urinary tract obstruction,
usually obstruction of the urethra
Urethral obstruction is characterized clinically by: Complete retention of urine, Frequent unsuccessful attempts to urinate Distension of the bladder.
Urethral perforation and rupture of the bladder can be sequelae
There are three main groups of factors that contribute to urolithiasis:
1. Factors favors the development of a nidus
2. Factors facilitate precipitation of solutes on to the nidus 3. Factors favor concretion by cementing precipitated salts to the developing calculus.
I. Factors favors Nidus formation Vitamin A deficiency
Stilbestrol as grwoth promotors
Nidus UT infection
Estrogen adminstration
II. Factors favor precipitation of solutes
N.B: Although the urine is highly saturated solution containing large quantities of solutes,
these salts are not precipitated Because of the colloidal state mechanism in the urine.
This
protective
colloid
prevents
precipitation of solutes and convert the urine into a gel
Continue.. These colloids are efficient up to a point, but their capacity to maintain the solution may be overcome
by several abnormalities. The degree of super saturation is depend on:
Diet Feeding practice pH of the urine Amount of water intake
1. pH of the urine The pH of urine affects the solubility of some solutes: Examples 1.
Phosphate and carbonate calculi being more readily formed in an alkaline than an acid medium.
Why we add ammonium chloride to the ration?
Ammonium chloride or phosphoric acid added to the rations of steers increases the acidity of the urine and reduces the incidence of calculi. The mechanism is uncertain but is probably related to the effect of pH on the stability of the
urinary colloids or the effect of diuresis.
Continue……. However, dietary supplementation with ammonium chloride does not consistently prevent the formation of siliceous calculi. N.B
1. Feeding sodium chloride prevents the formation of silica calculi
2. Supplemental calcium in the diet helps prevent calculus formation when phosphate or magnesium intake is high.
2. Diet/Ration of the animal Silica Oxalic acid
Magnesium
Ration
Phosphorus
Vitamin D
3. Feeding practices Can influence the function of the kidney and may contribute to calculus formation. Example…………. In sheep fed grain in a few large meals, there is
a marked reduction in urine volume and a marked increase in urine concentration and calcium excretion at the time of feeding.
4. Water intake Obstructive urolithiasis occurs mostly in
winter season and reduced water intake leads
to
increase
crystalloids in the urine.
concentration
of
III. Factors favoring concretion
Most calculi, and siliceous calculi in particular, are composed of organic matter named as mucoprotein particularly its mucopolysaccharide fraction.
The mucopolysaccharide acts as a cementing agent and favors the formation of calculi when precipitates are present.
The mucoprotein content of the urine is increased when:
1.
High concentrate ration with low roughage
2.
High Phosphorus content in the diet
3.
Implantation with diethylstilbestrol in
fattening steers
Occurrence Urethral obstruction may occur at any site but is most common at the sigmoid flexure in steers, uretheral
process in rams Urolithiasis is as common in females as in males, but obstruction rarely if ever occurs in females because of the shortness and large diameter of the urethra.
Clinical findings (depends on site of obstruction)
1. Calculi in the renal pelvis or ureters are
not usually diagnosed ante-mortem although obstruction of a ureter may be detectable on
rectal examination, especially if it is accompanied by hydronephrosis.
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If the renal pelvis is suddenly blocked then,
acute distension of renal pelvis is occurred resulting in acute pain, accompanied by
stiffness of the gait and pain on pressure over the loins.
Continue… 2. If the calculi obstruct the UB distension of the UB, signs of abdominal pain !!!, frequent attempt to urinate, uretheral pusation, RE reveled distended UB Rupture is usually occurred within 2 days resulting in uroabdomen, depression Signs of abdominal pain is disappeared, and signs of uremia is mostly prevalent.
Continue……….. 3. Obstruction of the urethra by a calculus
A. Incomplete obstruction B. Complete obstruction
A. Incomplete obstruction of the urethra
1.
Signs of abdominal pain !!!!!
2.
Dribbling of blood stained urine (Dribblers)
3.
Occasionally a small stream of urine will be
voided followed by a complete blockage.
B. Complete obstruction of the urethra 1.
Abdominal pain including
kicking at the belly treading with the hind feet swishing of the tail. Repeated twitching of the penis, sufficient to shake the prepuce, is often observed The animal may make strenuous efforts to urinate, accompanied by straining, grunting and grating of the teeth
Continue……… 2. Frequent attempt to urinate 3. Urethral pulsation 4. RE reveals distended UB 5.HR, RR may increased during the attack. Site of obstruction in Rams and bucks are mainly at the uretheralprocess
Rupture of urethra (water belly) Rupture of the UB (uroabdomen) The rupture usually within 2 days With urethral rupture: The urine leaks into the connective tissue of the ventral abdominal wall and prepuce and causes an obvious fluid swelling, which may spread as far as the thorax. This results in a severe cellulitis and toxemia. The skin over the swollen area may slough.
Continue………… When the bladder ruptures there is an immediate relief from discomfort but anorexia and depression
develop as uremia develops.
Two types of bladder rupture have been described: 1. Multiple pinpoint perforations in areas of necrosis or discrete tears in the bladder wall.
2. Rupture at the dorsal aspect of the UB
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A fluid wave is detectable on tactile percussion and the abdomen soon becomes distended. The animal may continue in
this state for as long as 2-3 days before death occurs.
Fibrin deposition around the dorsal surface of the bladder may be palpated per rectum in steers.
In rare cases death occurs soon after rupture of the bladder as a result of severe internal hemorrhage.
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Abdominocentesis and needle aspirate of
subcutaneous tissue
Warming the fluid may facilitate detection of
the urine odor, although this is a subjective and poorly sensitive diagnostic test.
Clinical pathology Urinalysis
Sands
Crystals RBCs, Epithelial cells
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Serum 1. Elevations of BUN, Cr even before rupture. 2. (When UB is ruptured) urine has a markedly low sodium and chloride concentration and high osmolality relative to plasma Resulting in hyponatremia, hypochloremia, hyperphosphatemia, and hypo-osmolality in serum. Serum K levels are, however, still in normal levels
Treatment A.
The treatment of obstructive urolithiasis is primarily surgical.
B.
If the animal near the end of their feedlot feeding period and close to being marketed, slaughtering is mostly preferable.
C.
In cases of Incomplete obstruction, administer muscle relaxant (aminopromazine, 0.7 mg/kg of BW), however,
field efficacy of using any muscle relaxant is not effective.!!!!!!
Continue…….. A more rational treatment is infiltration of local anesthetic agent around the origin of the retractor penile muscles or a pudendal nerve block, which would relax the retractor penis muscle and straighten the sigmoid flexure, thereby creating a wider and straighter urethral passage way.
Continue.. Normograde hydropulsion is only occasionally successful (intermittent injection of 0.9% Na Cl through urethral catheter
into the urethra in an attempt to flush out the calculi) However, Normograde hydropulsion may pack small crystals
more tightly into the urethra and might cause urethral trauma with resultant urethral stricture Surgical treatment includes perineal urethrostomy to relieve bladder pressure and for the removal of calculi.
Prevention 1. Adequate balance of calcium and phosphorus to avoid precipitation of excess phosphorus in the urine
(1.2:1.0) is ok, but 2:1.0 is highly recommended.
2. Addition of Table salt at 4% is highly recommended (Increase water intake, prevent deposition of magnesium and phosphate around the nidus of calculi)
Continue 3. Feeding the animal on 300 g Salt /day completely eliminate siliceous calculi. 4. Feeding of ammonium chloride as urine acidifier (45 g/d to steers and 10 g daily to sheep) may prevent urolithiasis due to phosphate. N.B An alkaline urine (pH > 7.0) favors the formation of phosphate-based stones (struvite, apatite) and calcium carbonate based stones.
Best wishes for you all Dr. Maged El-Ashker Associate Professor of Internal Medicine
