Injuries to the Genitourinary Tract & Acute and chronic renal failure Lecture №5 Lecturer –...
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Transcript of Injuries to the Genitourinary Tract & Acute and chronic renal failure Lecture №5 Lecturer –...
Injuries to the Genitourinary Tract & Acute and chronic renal
failure
Lecture №5
Lecturer – Baralo Igor Vitalievich
EMERGENCY DIAGNOSIS & MANAGEMENT
About 10% of all injuries seen in the emergency room involve the genitourinary systemto some extent. Many of them are subtle and difficult to define and require greatdiagnostic expertise. Early diagnosis is essential to prevent serious complications.Initial assessment should include control of hemorrhage and shock along withresuscitation as required. Resuscitation may require intravenous lines and a urethralcatheter in seriously injured patients. In men, before the catheter is inserted, theurethral meatus should be examined carefully for the presence of blood.The history should include a detailed description of the accident. In cases involvinggunshot wounds, the type and caliber of the weapon should be determined, sincehigh-velocity projectiles cause much more extensive damage.The abdomen and genitalia should be examined for evidence of contusions orsubcutaneous hematomas, which might indicate deeper injuries to the retroperitoneumand pelvic structures. Fractures of the lower ribs are often associated with renal injuries,and pelvic fractures often accompany bladder and urethral injuries. Diffuse abdominaltenderness is consistent with perforated bowel, free intraperitoneal blood or urine, orretroperitoneal hematoma.Patients who do not have life-threatening injuries and whose blood pressure is stablecan undergo more deliberate radiographic studies. This provides more definitive stagingof the injury
Special Examinations
When genitourinary tract injury is suspected on the basis of the history and physical examination, additional studies are required to establish its extent.
Catheterization and Assessment of Injury
Assessment of the injury should be done in an orderly fashion so that accurate and
complete information is obtained. This process of defining the extent of injury is termed
1. Catheterization—Blood at the urethral meatus in men indicates urethral injury; catheterization should not be attempted if blood is present, but retrograde urethrography should be done immediately. If no blood is present at the meatus, a urethral catheter can be carefully passed to the bladder to recover urine; microscopic or gross hematuria indicates urinary system injury. If catheterization is traumatic despite the greatest care, the significance of hematuria cannot be determined, and other studies must be done to investigate the possibility of urinary system injury.
Catheterization and Assessment of Injury
2. Computed tomography (CT)—Abdominal CT with contrast media is the bestimaging study to detect and stage renal and retroperitoneal injuries. It can define thesize and extent of the retroperitoneal hematoma, renal lacerations, urinaryextravasation, and renal arterial and venous injuries; additionally, it can detectintra-abdominal injuries (liver, spleen, pancreas, bowel). Spiral CT scanning, nowcommon, is very rapid, but it may not detect renal parenchymal lacerations, urinaryextravasation, or ureteral and renal pelvic injuries. We recommend repeat scanning 10min after the initial study to aid the diagnosis of these conditions.
3. Retrograde cystography—Filling of the bladder with contrast material is essential toestablish whether bladder perforations exist. At least 300 mL of contrast medium shouldbe instilled for full vesical distention. A film should be obtained with the bladder filledand a second one after the bladder has emptied itself by gravity drainage. These 2 filmsestablish the degree of bladder injury as well as the size of the surrounding pelvichematomas.Cystography with CT is excellent for establishing bladder injury. At the time of scanning,this likewise must be done with retrograde filling of the bladder with 300 mL of contrastmedia to ensure adequate distention to detect injury.
Catheterization and Assessment of Injury
4. Urethrography—A small (12F) catheter can be inserted into the urethral meatus and3 mL of water placed in the balloon to hold the catheter in position. After retrogradeinjection of 20 mL of water-soluble contrast material, the urethra will be clearly outlinedon film, and extravasation in the deep bulbar area in case of straddle injury—or freeextravasation into the retropubic space in case of prostatomembranous disruption—willbe visualized.5. Arteriography—Arteriography may help define renal parenchymal and renalvascular injuries. It is also useful in the detection of persistent bleeding from pelvicfractures for purposes of embolization with Gelfoam or autologous clot.6. Intravenous urography—Intravenous urography can be used to detect renal andureteral injury. This is best done with high-dose bolus injection of contrast media (2.0mL/kg) followed by appropriate films.B. Cystoscopy and Retrograde UrographyCystoscopy and retrograde urography may be useful to detect ureteral injury, but areseldom necessary, since information can be obtained by less invasive techniques.C. Abdominal SonographyAbdominal sonography has not been shown to add substantial information during initialevaluation of severe abdominal trauma.
INJURIES TO THE KIDNEY
Renal injuries are the most common injuries of the urinary system. The kidney is well protected by heavy lumbar muscles, vertebral bodies, ribs, and the viscera anteriorly.
Fractured ribs and transverse vertebral processes may penetrate the renal parenchyma or vasculature. Most injuries occur from automobile accidents or sporting mishaps,chiefly in men and boys. Kidneys with existing pathologic conditions such as hydronephrosis or malignant tumors are more readily ruptured from mild trauma
INJURIES TO THE KIDNEY (Etiology )
Blunt trauma directly to the abdomen, flank, or back is the most common mechanism,accounting for 80-85% of all renal injuries. Trauma may result from motor vehicle accidents, fights, falls, and contact sports. Vehicle collisions at high speed may result in major renal trauma from rapid deceleration and cause major vascular injury. Gunshot and knife wounds cause most penetrating injuries to the kidney; any such wound in the flank area should be regarded as a cause of renal injury until proved otherwise. Associated abdominal visceral injuries are present in 80% of renal penetrating wounds.
INJURIES TO THE KIDNEY
(Pathology & Classification)
A - Grade 1 (the most common)—Renal contusion or bruising of the renal parenchyma. Microscopic hematuria is common, but gross hematuria can occur rarely.
B - Grade 2 Renal parenchymal laceration into the renal cortex. Perirenal hematoma is usually small
C - Grade 3 Renal parenchymal laceration extending through the cortexand into the renal medulla. Bleeding can be significant in the presence of large retroperitoneal hematoma
D - Grade 4 Renal parenchymal laceration extending into the renal collecting system; also, main renal artery thrombosis from blunt trauma, segmental renal vein, or both; or artery injury with contained bleeding.
INJURIES TO THE KIDNEY (Pathology & Classification)
Grade 5—Multiple Grade 4 parenchymal lacerations, renal pedicle avulsion, or both; main renal vein or artery injury from penetrating trauma.
INJURIES TO THE KIDNEY
(Late Pathologic Findings)
Late pathologic findings in renal trauma. Left: Ureteropelvic stenosis with hydronephrosis secondary to fibrosis from extravasation of blood and urine. Right: Atrophy of kidney caused by injury (stenosis) of arterial blood
INJURIES TO THE KIDNEY(Late Pathologic Findings)
1. Urinoma — Deep lacerations that are not repaired may result in persistent urinary extravasation and late complications of a large perinephric renal mass and, eventually,hydronephrosis and abscess formation.
2. Hydronephrosis — Large hematomas in the retroperitoneum and associated urinary extravasation may result in perinephric fibrosis engulfing the ureteropelvic junction, causing hydronephrosis. Follow-up excretory urography is indicated in all cases of major renal trauma.
3. Arteriovenous fistula — Arteriovenous fistulas may occur after penetrating injuries but are not common.
4. Renal vascular hypertension — The blood flow in tissue rendered nonviable by injury is compromised; this results in renal vascular hypertension in less than 1% of cases. Fibrosis from surrounding trauma has also been reported to constrict the renal artery and cause renal hypertension.
INJURIES TO THE KIDNEY Symptoms
There is usually visible evidence of abdominal trauma. Pain may be localized to one flank area or over the abdomen. Associated injuries such as ruptured abdominal viscera or multiple pelvic fractures also cause acute abdominal pain and may obscure the presence of renal injury. Catheterization usually reveals hematuria. Retroperitoneal bleeding may cause abdominal distention, ileus, and nausea and vomiting.
INJURIES TO THE KIDNEY Signs
Initially, shock or signs of a large loss of blood from heavy retroperitoneal bleeding may be noted. Ecchymosis in the flank or upper quadrants of the abdomen is often noted.
Lower rib fractures are frequently found. Diffuse abdominal tenderness may be found on palpation; an "acute abdomen" usually indicates free blood in the peritoneal cavity.
A palpable mass may represent a large retroperitoneal hematoma or perhaps urinary extravasation. If the retroperitoneum has been torn, free blood may be noted in the peritoneal cavity but no palpable mass will be evident. The abdomen may be distended and bowel sounds absent.
INJURIES TO THE KIDNEY Laboratory Findings
Microscopic or gross hematuria is usually present.
The hematocrit may be normal initially, but a drop may be found when serial studies are done.
This finding represents persistent retroperitoneal bleeding and development of a large retroperitoneal hematoma.
Persistent bleeding may necessitate operation.
INJURIES TO THE KIDNEY
X-Ray Findings
CT scan to determine whether renal vascular injury exists
INJURIES TO THE KIDNEY
X-Ray Findings
Intravenous urography
INJURIES TO THE KIDNEY X-Ray Findings
Arteriography defines major arterial and parenchymal injuries when previous studies have not fully done so. Arterial thrombosis and avulsion of the renal pedicle are best diagnosed by arteriography and are likely when the kidney is not visualized on imaging studies. The major causes of nonvisualization on an excretory urogram are total pedicle avulsion, arterial thrombosis, severe contusion causing vascular spasm, and absence of the kidney (either congenital or from operation)
INJURIES TO THE KIDNEY
Treatment
A. Emergency Measures The objectives of early management are prompt treatment of shock and hemorrhage, complete resuscitation, and evaluation of associated injuries. B. Surgical Measures 1. Blunt injuries—Minor renal injuries from blunt trauma account for 85% of cases and do not usually require operation. Bleeding stops spontaneously with bed rest and hydration. Cases in which operation is indicated include those associated with persistent retroperitoneal bleeding, urinary extravasation, evidence of nonviable renal parenchyma, and renal pedicle injuries (less than 5% of all renal injuries). Aggressive preoperative staging allows complete definition of injury before operation. 2. Penetrating injuries—Penetrating injuries should be surgically explored. A rare exception to this rule is when staging has been complete and only minor parenchymal injury, with no urinary extravasation, is noted. In 80% of cases of penetrating injury, associated organ injury requires operation; thus, renal exploration is only an extension of this procedure. C. Treatment of Complications Retroperitoneal urinoma or perinephric abscess demands prompt surgical drainage. Malignant hypertension requires vascular repair or nephrectomy. Hydronephrosis may require surgical correction or nephrectomy.
INJURIES TO THE KIDNEY surgical treatment
Nephrostomy Nephrectomy
INJURIES TO THE URETEREtiology
Ureteral injury is rare but may occur, usually during the course of a difficult pelvic surgical procedure or as a result of gunshot wounds. Rapid deceleration accidents may avulse the ureter from the renal pelvis. Endoscopic basket manipulation of ureteral calculi may result in injury.
INJURIES TO THE URETER Treatment
Prompt treatment of ureteral injuries is required. The best opportunity for successful repair is in the operating room when the injury occurs. If the injury is not recognized until 7-10 days after the event and no infection, abscess, or other complications exist, immediate reexploration and repair are indicated. Proximal urinary drainage by percutaneous nephrostomy or formal nephrostomy should be considered if the injury is recognized late or if the patient has significant complications that make immediate reconstruction unsatisfactory. The goals of ureteral repair are to achieve completedebridement, a tension-free spatulated anastomosis, watertight closure, ureteral stenting (in selected cases), and retroperitoneal drainage.
INJURIES TO THE BLADDER
Bladder injuries occur most often from external force and are often associated with pelvic fractures. (About 15% of all pelvic fractures are associated with concomitant bladder or urethral injuries.) Iatrogenic injury may result from gynecologic and other extensive pelvic procedures as well as from hernia repairs and transurethral operations
INJURIES TO THE BLADDER
Clinical Findings Pelvic fracture accompanies bladder rupture in 90%
of cases. The diagnosis of pelvic fracture can be made initially in the emergency room by lateral compression on the bony pelvis, since the fracture site will show crepitus and be painful to the touch.
Symptoms There is usually a history of lower abdominal trauma.
Blunt injury is the usual cause. Patients ordinarily are unable to urinate, but when spontaneous voiding occurs, gross hematuria is usually present. Most patients complain of pelvic or lower abdominal pain.
INJURIES TO THE BLADDER
SignsHeavy bleeding associated with pelvic fracture may result in hemorrhagic shock, usually from venous disruption of pelvic vessels. Evidence of external injury from a gunshot or stab wound in the lower abdomen should make one suspect bladder injury, manifested by marked tenderness of the suprapubic area and lower abdomen. An acute abdomen may occur with intraperitoneal bladder rupture. On rectal examination, landmarks may be indistinct because of a large pelvic hematoma.
INJURIES TO THE BLADDERLaboratory Findings
Catheterization usually is required in patients with pelvic trauma but not if bloody urethral discharge is noted. Bloody urethral discharge indicates urethral injury, and a urethrogram is necessary before catheterization.
When catheterization is done, gross or, less commonly, microscopic hematuria is usually present. Urine taken from the bladder at the initial catheterization should be cultured to determine whether infection is present
INJURIES TO THE BLADDER
X-Ray Findings Bladder disruption is shown on cystography. The bladder should be filled with 300 mL of contrast material and a plain film of the lower abdomen obtained. Contrast medium should be allowed to drain out completely, and a second film of the abdomen should be obtained. The drainage film is extremely important, because it demonstrates areas of extraperitoneal extravasation of blood and urine that may not appear on the filling film
INJURIES TO THE BLADDERX-Ray Findings
With intraperitoneal extravasation, free contrast medium is visualized in the abdomen, highlighting bowel loops
INJURIES TO THE BLADDER Complications
A pelvic abscess may develop from extraperitoneal bladder rupture; if the urine becomes infected, the pelvic hematoma becomes infected too.
Intraperitoneal bladder rupture with extravasation of urine into the abdominal cavity causes delayed peritonitis.
Partial incontinence may result from bladder injury when the laceration extends into the bladder neck. Meticulous repair may ensure normal urinary control.
INJURIES TO THE BLADDER Treatment
Surgical MeasuresA lower midline abdominal incision should be made. As the bladder is approached in the midline, a pelvic hematoma, which is usually lateral, should be avoided. Entering the pelvic hematoma can result in increased bleeding from release of tamponade and in infection of the hematoma, with subsequent pelvic abscess. The bladder should be opened in the midline and carefully inspected. After repair, a suprapubic cystostomy tube is usually left in place to ensure complete urinary drainage and control of bleeding.
Extraperitoneal bladder rupture
Extraperitoneal bladder rupture can be successfully managed with urethral catheter drainage only. (Typically 10 days will provide adequate healing time.) Large blood clots in the bladder or injuries involving the bladder neck should be managed surgically.As the bladder is opened in the midline, it should be carefully inspected and lacerations closed from within. Polyglycolic acid or chromic absorbable sutures should be used.
Extraperitoneal bladder lacerations occasionally extend into the bladder neck and should be repaired meticulously. Fine absorbable sutures should be used to ensure complete reconstruction so that the patient will have urinary control after injury. Such injuries are best managed with indwelling urethral catheterization and suprapubic diversion.
Intraperitoneal rupture
Intraperitoneal bladder ruptures should be repaired via a transperitoneal approach after careful transvesical inspection and closure of any other perforations. The peritoneum must be closed carefully over the area of injury. The bladder is then closed in separate layers by absorbable suture. All extravasated fluid from the peritoneal cavity should be removed before closure. At the time of closure, care should be taken that the suprapubic cystostomy is in the extraperitoneal position.
INJURIES TO THE BLADDER surgical treatment
Extraperitoneal bladder rupture Intraperitoneal rupture
INJURIES TO THE URETHRA
Urethral injuries are uncommon and occur most often in men, usually associated with pelvic fractures or straddle-type falls. They are rare in women. Various parts of the urethra may be lacerated, transected, or contused. Management varies according to the level of injury. The urethra can be separated into 2 broad anatomic divisions: the posterior urethra, consisting of the prostatic and membranous portions, and the anterior urethra, consisting of the bulbous and pendulous portions.
INJURIES TO THE URETHRA Clinical Findings
SymptomsPatients usually complain of lower abdominal pain and inability to urinate. A history of crushing injury to the pelvis is usually obtained.
SignsBlood at the urethral meatus is the single most important sign of urethral injury. The importance of this finding cannot be overemphasized, because an attempt to pass a urethral catheter may result in infection of the periprostatic and perivesical hematoma and conversion of an incomplete laceration to a complete one. The presence of blood at the external urethral meatus indicates that immediate urethrography is necessary to establish the diagnosis.
INJURIES TO THE URETHRA
X-Ray Findings
Fractures of the bony pelvis are usually present. A urethrogram (using 20-30 mL of water-soluble contrast material) shows the site of extravasation at the prostatomembranous junction. Ordinarily, there is free extravasation of contrast material into the perivesical space
INJURIES TO THE URETHRATreatment
Initial management should consist of suprapubic cystostomy to provide urinary drainage. A midline lower abdominal incision should be made, with care being taken to avoid the large pelvic hematoma. The bladder and prostate are usually elevated superiorly by large periprostatic and perivesical hematomas. The bladder often is distended by a large volume of urine accumulated during the period of resuscitation and operative preparation. The urine is often clear and free of blood, but gross hematuria may be present. The bladder should be opened inthe midline and carefully inspected for lacerations. If a laceration is present, the bladder should be closed with absorbable suture material and a cystostomy tube inserted for urinary drainage. This approach involves no urethral instrumentation or manipulation. The suprapubic cystostomy is maintained in place for about 3 months. This allows resolution of the pelvic hematoma, and the prostate and bladder will slowly return to their anatomic positions. Incomplete laceration of the posterior urethra heals spontaneously, and the suprapubic cystostomy can be removed within 2-3 weeks. The cystostomy tube should not be removed before voiding cystourethrography shows that no extravasation persists.
INJURIES TO THE URETHRAsurgical treatment
Primary suture of the urethra Cystostomy, dranage of the urohaematome
INJURIES TO THE PENIS
Disruption of the tunica albuginea of the penis (penile fracture) can occur during sexual intercourse. At presentation, the patient has penile pain and hematoma. This injury should be surgically corrected.
Acute renal insufficiency -
It is the acute process, when all function of the kidney are stopped.
Functions of the kidneys:
- excretory- incretory
Excretory functions of the kidneys
Excretion of urea Regulation of water-electrolyte balance Regulation of acid-base balance Excretion of drugs and toxins
Incretory functions of the kidneys
Regulation of arterial pressure Takes part in hematosis
Takes part in the metabolism of fats, lipids, minerals
Regulation of the calcium Regulation of the protein metabolism
(synthesis and hydrolysis of histidine)
Renal process
glomerular filtration canalicular absorption canalicular secretion diffusion osmotic concentration of the urine Synthetic process
Types of acute renal insufficiency
prerenalrenalpostrenalarenal
Stages of acute renal insufficiency
primary
oligo-anuric
diuretic
convalescence
polyuria
recover of the diuresis
Reasons of acute renal insufficiency prerenal forms (90% causes of ARI)Characterized by decreasing or stopping of arterial
flow into the kidney
Shok (oligemic, cardiogenic, bacteriemic)
Bleeding, burns, water loss and electrolytes due to vomiting, diarrhea, fistules of stomach, myocardial infarction, embolia of pulmonary artery; complicated forms of infection, peritonitis, acute intestinal obstruction
Reasons of acute renal insufficiency renal forms (5% causes of ARI)
I Nephrotoxycosis.
Poisoning: 1) mercury; 2) uranium; 3) cadmium; 4) chromium; 5) hydrogen tetrachloride; 6)chloroform; 7) phosphorus; 8) ethylene glycol; 9) acetic acid; 10) mushrooms
II Toxic-allergic actions.
1) sulfanilamides; 2) antibiotic; 3) barbiturate; 4)salicylates;5) colloidal gold ; 6) bismuth.
Reasons of acute renal insufficiency renal form (continuation)
III Infection1) Anaerobic (septic abortion); 2) Haemorragic fever; 3) Pyelonephritis; 4) Necrotic pappilitis; 5) Pneumonia; 6) Sepsis; 7) Acute anuric glomerulonephritis.
Reasons of acute renal insufficiency postrenal forms (5% causes of ARI) Obstruction of the ureter
- by stone - by thromb- by tumour
Pressure by the retroperitoneal space mass Obstruction of the urethrae
- Hyperplasia & cancer of the prostate- Tumour of the bladder’s neck - Stricture of the urethrae
Theories of the pathogenesis of acute renal insufficiency
1. Tubular obstruction
2. Interstitial oedema and passive regurgitation of glomerular filtrate on the level of tubules
3. Disorders of haemodynamics of the kidney
4. Disseminated intravascular clotting
Postrenal oliguria is the competence of urologists
Other types of ARI (prerenal oliguria and acute canalicular necrosis) is handled by the surgeon and trauma of urogenital organs.
Pathologic anatomia of ARI – main thing of morphologic changes – acute canalicular necrosis
Macroscopic: enlarged kidneys Histology:
- oedema of interstitial tissue- stasis of the renal blood vessels- necrosis of epithelium and basal membrane- focuses of inflammatory infiltration - detritus and myoglobin in the cavity of tubules- Late the regeneration of the epithelium
Diagnostics of ARI
First stage – starting- condition depends upon reason- to do test of hourly diuresis if patient’s grave condition
(<50 ml/hour must be done)Indications to catheterization of urinary bladder
(catheterization is necessary till difficult stage of the patient) - Important trauma- Shock, hypovolemic hypotension - Sepsis- Obstetrics complications, including septic abortion- Massive hemotransfusion - Operations by the patients, which inclined to renal diseases- Solid surgical operations in old patients- surgical operations on biliary tracts in patients with jaundice- Operations with artificial circulation of the blood & operations on the aorta
Diagnostics of ARI
Second stage: oligo-anuric (1-2 hours – 3-4 weaks)
clinic determine - disorders of fluid and electrolyte (hyperkaliemia etc.)- hyperazotemia- 50-90% of patients with infectious coplications
Ist та IIst stages of diagnostics- Central nervous system: sleepiness due to excessive hydration- Skin: dry, itching- Gastro-intestinal tract: anorexia, thirst, vomiting
diarrheadry tongue, coated, stomatitisgastroenterocolitisuremic pseudoperitonitis , pancreatitis,
paralytic ileus,
parotitis
Diagnostics of ARI
СVS: Arterial pressure (AP) is decreased due to hypovolemia, increased due to stenosis of renal artery, aneurism of aorta, myocardial dystrophy, myocarditis, dry pericarditis: increased pulsatium, AP decreased, cardiac fibrillation due to hyperkaliemia, venous pressure is increased.
Lungs: Dyspnoe, rough breath sounds, stagnant wheeze, fluid lung
Kidney: Pain in the lumbal regionWound healing: Is decreased due to proliferative and fibroblastic
process and late formation of granulatory tissueTemperature of body is normal and may be increased.
Diagnostics of ARI
IIIrd stage- Anemia due to decreased erythropoesis- ESR increased- Trombocytopenia- Leucocytosis- Hyperazotemia
Increased creatinine – endogenic end part of protein metabolism, which is excreted by kidneys according to level of glomerular filtration
it increases by 0,044-0,088 mmol/l for a day
(during infection and hematoma by 0,175 )
Urea – End product of protein metabolism is excreted by kidneys and give signals more reliable about the range of the catabolism
increases by 4,99-6,66 mmol/l daily
(during infection and hematoma by 16,65 )
Diagnostics of ARIhyperkaliemia
daily growth К in blood – 0,5 mmol/l(during sepsis, hematoma, crush syndrome – 1-2 mmol/l)
pH of blood is decreasedColor of urine is dark und due to the macrohaematuriaUrinal relative density
>1,015 due to prerenal oliguria<1,015 during disorder of canalicular function
Proteinuria due to parenchymatous nature of ARI (>3g/l daily), is absent during prerenal und subrenal oliguria
ErythrocyteurialeucocyturiaCylindruria
During acute canalicular necrosis epithelial and granular cylinders, free epithelial cells of canaliculus are brown,
that not be present during prerenal oliguriaDuring myo- and hemoglobinuria (incompatible blood
transfusion - pigmentary without or whith Erythrocytes)
Diagnostics of ARI
Sodium in the urine: during prerenal oliguria <10 mmol/l,
renal oliguria – 25 mmol/l and >Osmolarity of urine is more due to ARIIVth stageplain urography – kidney is increased in size, shadow of the
stone Intravenous urography – during prerenal ARI pelvic and
ureter is contrasted well, during acute canalicular necrosis only nephrogrames
arteriogram – during to occlusium of renal arteryCT
Diagnostics of ARI
Vth stage
Ultrasound diagnostic – is shown edema of the kidneys, hydronephrosis
MRT
ECG (electrocardiogram) – symptomes of the hyperpotassemia
plan X-ray film of lungs: “Fluid lung”
Peculiar features of subrenal ARI
1. Pathogenesis – is obstruction, but not shock and that is why clinical finding not such dramatic
2. Patient with subrenal anuria is forbear, but doctor have to perform urgent measures.
3. Urina is appeared not slow, but immediately polyuria has arised.
4. Before recoverying urinary flow stimulation of diuresis is contraindicated.
5. Treatment maybe:- palliative (drainage)- radical
Treatment’s principles of ARI
I. Primary stage1. Shock control and cardiac-vascular insufficiency control2. ARI prophylaxis (stimulation of diuresis )3. Etiological treatment
II. Oligo-anuric stage1. Stimulation of diuresis 2. Dilatation of glomerular vessels3. Reduction of protein catabolism and azotemia4. Eliminate disturbances of water-electrolyte balance and acid-
base balance5. Anemia control6. Maintenance liveral functions 7. Complication’s prophylaxis (infections, candidosis;
allergic reactions; therapy of cardiovascular disorders, common hygienic actions )
8. Treatment by hemodialysis
Treatment’s principles of ARI
III. Diuretic stage
1. Correction of azotic metabolism
2. Correction of disturbances water-electrolyte balance and acid-base
balance
- administration adequate fluid amount
- hypokaliemia control
IV. Stage of convalescence
1. Diet- hygienic regimen
Transcutaneus nephrostomy
Universal nephrostomy set (Bard-Angiomed), containing (1) coaxial
17.5-gauge needle/6F catheter system with obturator; (2) fine needle (22 gauge); (3)
0.035-in stiff guidewire with floppy J-tip; (4) coaxial 10F dilator/12F introducer catheter
system; and (5) 10F pigtail nephrostomy catheter.
Transcutaneus nephrostomy
Ultrasonically guided puncture of a dorsal lower calyx. Needle must be in
the scanning plane to be visualized.
Transcutaneus nephrostomy
Small-bore tract dilation and nephrostomy catheter insertion. A: J-guidewire inserted through the needle-catheter system and advanced with assistance of the catheter into the renal pelvis. B: Insertion of a coaxial dilator/introducer catheter system over the guidewire. Stiff proximal section of the guidewire prevents extrarenal kinking. C: After the dilator has entered the collecting system, the introducer catheter is advanced over its tip. D: Pigtail nephrostomy catheter is inserted into the renal pelvis over the guidewire and through the introducer catheter.
Chronic Renal Failure
In chronic renal failure, reduced clearance of certain solutes principally excreted by the kidney results in their retention in the body fluids. The solutes are end products of the metabolism of substances of exogenous origin (eg, food) or endogenous origin (eg, catabolism of tissue). The most commonly used indicators of renal failure are blood urea nitrogen and serum creatinine. The clearance of creatinine can be used as a reasonable measure of glomerular filtration rate (GFR).
Chronic Renal Failure
In individual cases, it is often difficult to establish the duration of renal failure. Historical clues such as preceding hypertension or radiologic findings such as small, shrunken kidneys tend to indicate a more chronic process. Acute renal failure may progress to irreversible chronic renal failure
Chronic Renal Failure
The incidence of severe chronic renal failure leading to end-stage renal disease is 280 cases per million population per year. These patients require chronic dialysis or renal transplantation. All age groups are affected. The severity and the rapidity of development of uremia are hard to predict. The use of dialysis and transplantation is expanding rapidly worldwide. Over 233,000 such patients in the United States are currently treated with dialysis. A trend toward increasingly older patients has been noted. At the present time, 94,000 patients have functioning kidney transplants
Chronic Renal Failure
Historical BackgroundThere are various causes of progressive renal dysfunction leading to end-stage or terminal renal failure. In the 1800s, Bright described several patients who presented with edema, hematuria, and proteinuria and ended in death. Chemical analyses of sera drew attention to retained nonprotein nitrogen (NPN) compounds, and an association was made between this and the clinical findings of uremia. Although the pathologic state of uremia was well described, long-term survival was not achieved until chronic renal dialysis and renal transplantation became available after 1960-1970. Significant improvements in patient survival have been made in the past 40 years
Chronic Renal Failure
Etiology
A variety of disorders are associated with end-stage renal disease. Either a primary renal process (eg, glomerulonephritis, pyelonephritis, congenital hypoplasia) or a secondary one (owing to a systemic process such as diabetes mellitus or lupus erythematosus) may be responsible. Superimposed physiologic alterations secondary to dehydration, infection, or hypertension often "tip the scale" and put a borderline patient into uncompensated chronic uremia
Chronic Renal Failure
Symptoms and SignsSymptoms such as pruritus, generalized malaise, lassitude, forgetfulness, loss of libido, nausea, and easy fatigability are frequent and nonfocal complaints in this chronic disorder. There is often a strong family history of renal disease. Growth failure is a primary complaint in preadolescent patients. Symptoms of a multisystem disorder (eg, systemic lupus erythematosus) may be present coincidentally. Most patients with renal failure have elevated blood pressure secondary to volume overload or from hyperreninemia. However, the blood pressure may be normal or low if patients have marked renal salt-losing tendencies (eg, medullary cystic disease). The pulse and respiratory rates are rapid as manifestations of anemia and metabolic acidosis. Clinical findings of uremic fetor, pericarditis, neurologic findings of asterixis, altered mentation, and peripheral neuropathy are often present. Palpable kidneys suggest polycystic disease. Ophthalmoscopic examination may show hypertensive or diabetic retinopathy. Alterations involving the cornea have been associated with metabolic disease (eg, Fabry disease, cystinosis, and Alport hereditary nephritis)
Chronic Renal Failure
Laboratory Findings1. Urine composition—The urine volume varies
depending on the type of renal disease. Quantitatively normal amounts of water and salt losses in urine can be associated with polycystic and interstitial forms of disease. Usually, however, urine volumes are quite low when the GFR falls below 5% of normal. Daily salt losses become more fixed, and, if they are low, a state of sodium retention occurs soon after. Proteinuria can be variable. Urinalysis examinations may reveal mononuclear white blood cells (leukocytes) and occasionally broad waxy casts, but usually the urinalysis is nonspecific and inactive.
Chronic Renal Failure
Laboratory Findings2. Blood studies—Anemia is the rule with normal platelet counts. Platelet
dysfunction or thrombasthenia is characterized by abnormal bleeding times. Several abnormalities in serum electrolytes and mineral metabolism become manifest when the GFR drops below 30 mL/min. Progressive reduction of body buffer stores and an inability to excrete titrable acids result in progressive acidosis characterized by reduced serum bicarbonate and compensatory respiratory hyperventilation. The metabolic acidosis of uremia is associated with a normal anion gap, hyperchloremia, and normokalemia. Hyperkalemia is not usually seen unless the GFR is below 5 mL/min. In patients with interstitial renal diseases, gouty nephropathy, or diabetic nephropathy, hyperchloremic metabolic acidosis with hyperkalemia (renal tubular acidosis, type IV) may develop. In these cases the acidosis and hyperkalemia are out of proportion to the degree of renal failure and are related to a decrease in renin and aldosterone secretion. Multiple factors lead to an increase in serum phosphate and a decrease in serum calcium. The hyperphosphatemia develops as a consequence of reduced phosphate clearance by the kidney. In addition, vitamin D activity is diminished because of reduced conversion of vitamin D2 to the active form of vitamin D3 in the kidney. These alterations lead to secondary hyperparathyroidism with skeletal changes of both osteomalacia and osteitis fibrosa cystica. Uric acid levels are frequently elevated but rarely lead to calculi or goutduring chronic uremia
Chronic Renal Failure
X-Ray Findings
Patients with reduced renal function should not be routinely subjected to contrast studies. Renal sonograms are helpful in determining renal size and cortical thickness and in localizing tissue for percutaneous renal biopsy. Bone x-rays may show retarded growth, osteomalacia (renal rickets), or osteitis fibrosa. Soft-tissue or vascular calcification may be present
Chronic Renal Failure
Renal Biopsy
Renal biopsies may not reveal much except nonspecific interstitial fibrosis and glomerulosclerosis. There may be pronounced vascular changes consisting of thickening of the media, fragmentation of elastic fibers, and intimal proliferation, which may be secondary to uremic hypertension or due to primary arteriolar nephrosclerosis. Percutaneous or open biopsies of end-stage shrunken kidneys are associated with a high morbidity rate, particularly bleeding
Chronic Renal Failure Treatment
I Conservative
II Surgical
- Chronic Peritoneal Dialysis
- Chronic Hemodialysis
- Renal Transplantation
Chronic Renal Failure Treatment
Management should be conservative until it becomes impossible for patients to continue their customary lifestyles. Conservative management includes restriction of dietary protein (0.5 g/kg/d), potassium, and phosphorus, as well as maintenance of close sodium balance in the diet so that patients become neither sodium-expanded nor-depleted. This is best done by the accurate and frequent monitoring of the patient's weight. Use of bicarbonate can be helpful when moderate acidemia occurs. Anemia can be treated with recombinant erythropoietin. Prevention of possible uremic osteodystrophy and secondary hyperparathyroidism requires close attention to calcium and phosphorus balance. Phosphate-retaining antacids and calcium or vitamin D supplements may be needed to maintain the balance
Chronic Renal Failure Treatment
Chronic Peritoneal DialysisChronic peritoneal dialysis is used electively or when circumstances (ie, no available vascular access) prohibit chronic hemodialysis. Improved soft catheters can be used for repetitive peritoneal lavages. In comparison to hemodialysis, small molecules (such as creatinine and urea) are cleared less effectively than larger molecules, but excellent treatment can be accomplished. Intermittent thrice-weekly treatment (IPPD), continuous cycler-assisted peritoneal dialysis (CCPD), or chronic ambulatory peritoneal dialysis (CAPD) is possible. With the latter, the patient performs 3-5 daily exchanges using 1-2 L of dialysate at each exchange. Bacterial contamination and peritonitis are becoming less common with improvements in technology
Chronic Renal Failure TreatmentChronic Hemodialysis
Chronic hemodialysis using semipermeable dialysis membranes is now widely performed. Access to the vascular system is provided by an arteriovenous fistula, vascular grafts (with saphenous vein or synthetic material), or by a subclavian permcatheter (placed either surgically or with interventional radiology). The actual dialyzers are of various geometries. Body solutes and excessive body fluids can be easily cleared by using dialysate fluids of known chemical composition. Newer, high-efficiency membranes (high/flux) are serving to reduce dialysis treatment time. Treatment is intermittent—usually 3-5 h 3 times weekly. Computer modeling, using measurements of urea kinetics, has provided more precise hemodialysis prescriptions. Treatments may be given in a kidney center, a satellite unit, or the home. Home dialysis is optimal because it provides greater scheduling flexibility and is generally more comfortable and convenient for the patient, but only 30% of dialysis patients meet the requirements for this type of therapy. More widespread use of dialytic techniques has permitted greater patient mobility. Treatment on vacations and business trips can be provided by prior arrangement. Common problems with either type of chronic dialysis include infection, bone symptoms, technical accidents, persistent anemia, and psychological disorders. The morbidity associated with atherosclerosis often occurs with long-term treatment. It is now recognized that chronically uremic patients, despite dialysis, can develop wasting syndrome, cardiomyopathy, polyneuropathy, and secondary dialysis-amyloidosis so that kidney transplant must be urgently done. Routine bilateral nephrectomy should be avoided because it increases the transfusion requirements of dialysis patients. Nephrectomy in dialysis patients should be performed in cases of refractory hypertension, reflux with infection, and polycystic disease with recurrent bleeding and pain. The dialysis patient can occasionally have acquired renal-cystic disease. Such patients need close monitoring for the development of in situ renal cell carcinoma. Yearly costs range from an average of $35,000 for patients who receive dialysis at home to as much as $35,000-60,000 for patients treated at dialysis centers, but much of this is absorbed under HR-1 (Medicare) legislation. If the patient has no other systemic problems (eg, diabetes), the mortality rates are 8-10%/year once maintenance dialysis therapy is instituted. Despite these medical, psychological, social, and financial difficulties, most patients lead productive lives while receiving dialysis treatment
Chronic Renal Failure Treatment
Renal TransplantationAfter immunosuppression techniques and genetic matching were developed, renal homotransplantation became an acceptable alternative to maintenance hemodialysis. Improved transplantation results are now noted owing to the development of newer immunosuppressant drugs. Currently employed post-transplant drugs include prednisone, azathioprine, mycophenolate mofetil, cyclosporine, and tacrolimus. The great advantage of transplantation is reestablishment of nearly normal constant body physiology and chemistry. Diet can be less restrictive. The disadvantages include bone marrow suppression, susceptibility to infection, cushingoid body habitus, and the psychological uncertainty of the homograft's future. Most of the disadvantages of transplantation are related to the medicines given to counteract the rejection. Later problems with transplantation include recurrent disease in the transplanted kidney and an increased incidence of cancer. Genitourinary infection appears to be of minor importance if structural urologic complications (eg, leaks) do not occur. Nephrology centers, with close cooperation between medical and surgical staff, attempt to use these treatment alternatives of dialysis and transplantation in an integrated fashion.
Indications to hemodialysis for patiens with ARI
During conservative treatment, if anuria is continued and levels urea and potassium promptly increases
Blood urea level 30 & > mmol/l Blood creatinine level 0,8 & > mmol/l Blood potassium 6,5-7 mecv/l Blood sodium < 120 mecv/l Acidosis Blood chlorine < 80 mecv/l Excessive hydration Grow progressively worse of general condition
(vomiting, adynamia, disorientation)