SURGERY III  Non-contrast and contrast CT scan of abdomen

Dr. Baviera – Renal Stones and pelvis

Case History  What is you final diagnosis?

A 38 yr. old woman complains of acute onset of
right flank pain, with periodic increases in intensity.
She has also experienced chills, nausea and
vomiting soon after the onset of pain. The patient
denies voiding problems and hematuria. She has
been working as a cook in a fastfood restaurant
and is otherwise healthy.
Physical Exam
V/S:
Temp: 38.4oC
CR: 88 bpm
RR: 16 cpm
BP: 150/70 mmHg
Abdomen: soft, moderate right sided tenderness
with right costovertebral angle tenderness, no
peritoneal signs
Genitourinary: normal
Rectal: normal
What are you DDx?
What is you working diagnosis?
Things to know:
 Pathogenesis/ physiochemical properties
 Etiologic factors of specific stone types
 Clinical features of some disease
 Evaluation of patients with stone
 Management of stone patient
Laboratory findings
 Electrolytes, BUN, creatinine: normal
 WBC: 16,000 with left shift
 Urinalysis: pH 5.0, leukocyte esterase positive,
nitrite negative, 5-10 WBC/hpf, >25 RBC/hpf
Imaging Studies
 Abdominal radiograph
 UTZ of the abdomen
-pelvocaliectasia, right
-unremarkable finding of the left kidney and
urinary bladder
-incidental finding of ovarian cyst, left measuring
4.9x5.3cm
 Do you need other laboratories to confirm your
diagnosis? If yes, please enumerat6e and explain
the significance of the laboratory result.
 What are the different imaging tools you can use
in localizing the problem?
UROLITHIASIS
 Presence of stones in the urinary tract (pelvis
to the urethra)
 1 ½ length of the whole urinary system
 12% of all individuals will experience stone
disease
Specific stone incidence
 Calcium oxalate – 30-35% (MOST COMMON
d/t lifestyle change)
 Mixed calcium oxalate and phosphate – 0-
35%
 Mg ammonium phosphate – 15-20%
(associated with infection)
 Uric acid – 5-10%
 Cystine – 2% (not common; hereditary;
without any obvious reasons of food
preferences; very radioopaque in imaging,
can be seen clearly)
 Xanthine, silicates, dihydroxyadenosine, and
drug metabolites are rare
Factors influencing stone formation
 Genetic (enzymatic disorders) – cystinuria
RTA, decrease renal activity of aldolase,
abnormal purine metabolism; first dx because
of the components)
 Environmental – intake of too much of
everything (milk, internal organs, etc.)
 Diet (animal fat: uric acid, leafy vegetables;
oxalate)
* >1,000 mg – calcium is excreted in the urine
* We must drink fluids enough to produce 2L of
urine/day
Physical and chemical parameters
 Supersaturation – spontaneous nucleation
of crystals begins at a certain concentration
  Epitaxy – oriented overgrowth of one type of
crystal on the surface of a pre-existing crystal
of a different type (i.e. uric acid with calcium
oxalate overgrowth)
 Urinary inhibitors – citrate, pyrophosphate,
zinc, alanine, glycosaminoglycans
 Matrix – group of antigenically distinct protein
found in urine of stone formers. Appears to
bind calcium more readily than the
mucoprotein of nonstone former
 Renal anatomy – diverticulas, strictures
Etiologic factors of some stones
1. Calcium stones
a. Urinary supersaturation with calcium due to
intestinal hyperabsorption of calcium
(hyperparathyroidism, Vit. D intoxication and
sarcoidosis)
b. Renal hypercalciuria due to impaired tubular
absorption of calcium which stimulates
parathyroid function and Vit. D synthesis
leading to increase intestinal calcium
absorption
c. Resorptive hypercalciuria – due to
immobilization and hyperparathyroidism
d. Calcium oxalate stone formation associated
with hyperoxaluria due to intestinal
hyperabsorption of oxalate secondary to fat
malabsorption, intestinal bypass surgery,
dietary sources (leafy vegetables, Vit. C,
peanuts, tea)
2. not able to take picture gadali si doc bavy
3. Cystine calculi
a. Associated with cystinuria, an inherited
renal tubular absorption defect of cysteine,
ornithine, lysine, arginine (COLA)
4. Struvite stones
a. Found in all alkaline urine with associated
infection with bacteria having urease activity
b. Urea is split into ammonia which raises the
pH, causing a decrease in the solubility of
magnesium ammonium phosphate leading
to precipitation of stones
Signs/Symptoms
 Pain (most common)– renal, ureteral, bladder
or urethral calculi  no pain)
 Hematuria (most common)– gross or
microscopic
 Nausea/ vomiting
 Fever and chills
 No symptoms (asymptomatic) – not blocking
the water drainage
1 cm – do something because spontaneous
passage is low
What is technique is the best option for
management?
- Some factors: Metabolic stone studies
- Anatomic urinary tract factors
- Extraordinary tract factors
MGT: ESWL  PCNL (puncture)  Ureteroscopy
 Open surgery
Clinical features of stone disease
1. Pain
2. Hematuria
a. Generally patients have gross or
microscopic hematuria
b. There maybe no RBCs in the urine if the
calculus is either causing complete
obstruction or is not moving
3. Nausea and vomiting
a. Ureteral colic occurs because of increase
intraluminal pressure, local distention of the
ureteral wall, spasm secondary to irritation,
local ischemia
b. The shared segmental innervation between
the intestine and the ureter suggest that the
disordered intestinal motility seen during
ureteral colic is due to viscera-visceral
reflexes.
Management of acute episode
1. Pain medication after diagnosis assured
2. IV fluid – it is important not to overhydrate
as this will increase distention and may
make peristalsis less effective and pain
worse.
Indications for admission
1. Intractable pain
2. Nausea and vomiting such that oral pain
medications are not kept down
3. High grade obstruction
 4. Infection
5. Solitary kidney with any degree of
obstruction or infection

Outcome of stones in the ureter

 Most calculi pass spontaneously especially if
present in distal ureter (4mm stone = 90%
chance of spontaneous passage; 8mm stone
= 20% chance of spontaneous passage)

Surgical management of urolithiasis

1. Extracorporeal shock wave lithotripsy
(ESWL)
2. Percutaneous nephrolithiasis (PCNL)
3. Ureteroscopy
4. Combination treatment
5. Open surgical intervention

Medical evaluation for urolithiasis

A. Metabolic work-up
1. Urinalysis – hematuria is almost always
present; proteinuria is often seen because
of blood breakdown products; pH >7
suggest urease splitting organism; pH <6
favors uric acid and cysteine calculi crystals
may have characteristic appearance and in
reality are rarely seen
2. Specific urine testing
a. Nitroprusside test for cystinuria
b. Quantitative analysis of 24 hour urine
specimen
 Calcium: normal <300mg
 Uric acid: normal <600mg
 Cystine: normal 50-180mg
 Magnesium: normal 6.0-8.5
mEq/24hrs.
3. not able to take picture paspas si doc bavy
4. Oral calcium tolerance test
a. Aids in the differentiation of
hypercalciuria due to
hyperparathyroidism, absorptive
hypercalciuria, renal tubular leak
b. May be performed on an outpatient
basis
c. Uses calcium loading and abstinence to
determine the mechanism of
hypercalciuria and thus direct
appropriate treatment