ob - renal and urinary tract disorders

7/25/2019 Ob - Renal and Urinary Tract Disorders

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OBSTETRICS RENAL AND URINARY TRACT DISORDERS

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TRANSCOM|CLINGY,MD 1

URINARY TRACT DILATATION

Kidneys become larger

Dilatation of structures and pelvis as well as ureter

o Before 14 weeks due to hormonal relaxation of

muscular layers of urinary tract

o Hormone responsible: PROGESTERONE

Marked dilatation is apparent beginning in midpregnancy

because of ureteral compressiono More prominent on the right

(+) vesicuureteral reflux

Increased risk of upper urinary infection

o Important consequence

Secondary to hormonal or mechanically obstructive factors

FUNCTIONAL RENAL HYPERTROPHY

o apparent soon after conception

o Glomeruli are larger, but the cell numbers do not

increase

o Pregnancy-induced intrarenal vasodilatation

both afferent and efferent resistance

decreasesleads to increased effective

renal plasma flow and glomerular filtration

o

at 12 weeks gestation\

o GFR increased by 20 percent above

nonpregnant values

o plasma flow and glomerular filtration

increase by 40 and 65 percent, respectively

o serum concentrations of creatinine and urea decrease

substantively across pregnancy

o Other alterations include those related to

o maintaining normal acid-base homeostasis

o osmoregulation

o fluid and electrolyte retention

ASSESSMENT OF RENAL DISEASE IN PREGNANCY

URINALYSIS

o

Recommended as early as 1st TRIMESTER to assess

any signs of infection

o unchanged during pregnancy, except for occasional

glucosuria

o protein excretion normally is increased

o IDIOPATHIC HEMATURIA (3%)

1+ or greater blood on urine dipstick when

screened before 20 weeks

2x risk of preeclampsia

o PROTEINURIA

>300 mg/day

considered abnormal

500 mg/day

important with gestationalhypertension

SERUM CREATININE

o If >0.9 mg/dl(75 mol/l)

Intrinsic renal disease should be suspected

ULTRASOUND

o imaging of renal size, relative consistency, and

elements of obstruction

IV PYELOGRAPHY

o Not done routinely

o injection of contrast media with one or two

abdominal radiographs may be indicated by the

clinical situation

Cystoscopy

Renal Biopsy (usually postponed until pregnancy is completed)

URINARY TRACT INFECTION

Most common infection encountered during pregnancyo Asymptomatic bacteriuria (most common)

o Systemic cystitis

o Pyelonephritis

Involves renal calyces, pelvis & parenchyma

Organisms that cause urinary infection

o Those from normal perineal flora about 90% o

strains are E. Coli

cause nonobstructive pyelonephritis

o (+)adhesions (P- and S-fimbriae)

cell-surface protein structures that enhance

bacterial adherence and thereby, virulence

adhesins promote binding to vaginal and

uroepithelial cells through expression of the

PapG gene that encodes the P-fimbriae tip pregnant women have more severe sequelae from urosepsis

maternal deaths have been attributed to E coli bearing Dr+ and

P adhesins

Predisposing factors:

o urinary stasis

o vesicoureteral reflux

o diabetes

In the puerperium, risk factors that predispose a woman to

urinary infections.

o Bladder sensitivity to intravesical fluid tension is

decreased as a consequence of labor trauma or

conduction analgesia

o Sensation of bladder distention can also be diminished

by discomfort caused by an episiotomy, periurethra

lacerations, or vaginal wall hematomas

o Normal postpartum diuresis may worsen bladde

overdistention

o catheterization to relieve retention commonly leads to

urinary infection

DIAGNOSIS

o Urinalysismost cost effective

o Urine culture gold standard for asymptomatic

bacteriuria

ASYMPTOMATIC BACTERIURIA

Persistent, actively multiplying bacteria within urinary tract in

women who have no symptoms

typically present at the first prenatal visit

o recommened screening during 1st

prenatal visit

highest incidence in African-American multiparas with sickle-cel

trait & lowest incidence in affluent white women of low parity

covert bacteriuria has been associated with preterm or low-

birthweight infants

INCIDENCE

o Varies from 2-7%

o Depends on parity, race and socioeconomic status


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DIAGNOSIS

o Clean-voided specimen containing >100,000

organisms per mL

Diagnostic

considered as evidenced of infection

o Importance of correct diagnosis if untreated can

lead to: acute pyelonephritis and symptomatic UTI

o

Esterase-nitrite dipstick Dipstick culture technique

excellent positive & negative predictive

values

Most common organismstill E.coli

Urine culturenot requested routinely

TREATMENT

o 3-day course

o May be treated empirically by antimicrobial agents

like: (please refer to the table)

Nitrofurantoinideal, most sensitive

Quinolonesreserved to prevent resistance

of microorganisms

CYSTITIS AND URETHRITIS

Cystitisdysuria, urgency and frequency

o Few associated systemic findings

Usually there is pyuria as well as bacteriuria

Microscopic hematuriacommon

Gross hematuriaoccasionally from hemorrhagic cystitis

Usually uncomplicated, involvement of upper urinary tract by

ascending infection

Mucupurulent cervicitisusually coexists

C. trachomatiscommon pathogen of gastrourinary tract

o Can cause lower urinary tract symptoms with pyuria

accompanied by a sterile urine culture may be from

urethritis

DIAGNOSISo Frequency, urgency, dysuria and pyuria accompanied

by urine culture with no growth

TREATMENT:

o Erythromycin therapy

safe in pregnancy, also DOC in PROM

NECROTIZING ENTEROCOLITIS

o complication of giving too much strong antibiotics

ACUTE PYELONEPHRITIS

Most common serious complication of pregnancy (renal infxn)

o Which usually develops during 2nd

trimester (during

this period no workup performed in pt)

leading cause of septic shock during pregnancy

urosepsis is related to increased incidence of cerebral palsy in

preterm infants

no serious longterm maternal sequelae ASSOCIATED RISK FACTORS:

o Nulliparity

o Young age

DIFFERENTIAL DIAGNOSIS

o Labor

o Chorioamnionitis

o Appendicitis

o Placental abruption

o Infected myoma

o Puerperium for metritis with pelvic cellulites

Almost all clinical findings are ultimately caused by

endotoxemia(bacteriuria -> endotoxemia -> urosepsis)

CLINICAL FINDINGS

o

Pyelonephritis is unilateral (>1/2) and right-sided

Bilateral in a fourth

o Anorexia, nausea and vomiting

o abrupt onset of fever, shaking chills and aching pain

in one or both lumbar regions

Fever of variable degrees is always present

can be as high s 40 degrees Celsius

o Tenderness usually can be elicited by percussion to

one or both costovertebral angle (kidney punch)

o Urinary sediment frequently contains many

leukocytes in clumps seen on urinalysis

o Bacteremia in 15 to 20% of women

o Organisms that are commonly isolated:

E coli (from urine or blood (70 to 80%)

Klebsiella pneumoniae (3 to 5%)

Enterobacter or Proteus species (3 to 5%)

gram-positive group B Streptococcus and S

aureus (up to 10%)

MANAGEMENT (IV hydration to ensure urinary output: corner stone)

MANAGEMENT FOR NON RESPONDERS

o Sonography

If there is no clinical improvement by 48-72

hrs


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to look for urinary tract obstructionalways

rule out if patient doesnt respond to

treatment

search is made for abnormal ureteral

pyocalyceal dilatation

OUTPATIENT MANAGEMENT

o for women w/uncomplicated pyelonephritis

o

Women with pyelonephritis were given CeftriaxoneIM two 1g doses 24hrs apart in the hospital

At this point only third were considered

candidates for outpatient therapy

Surveillance

o risk of recurrent infection (30-40%)

CHRONIC PYELONEPHRITIS

TYPES

Chronic Interstitial Nephritis

Nephrolitiasis

CHRONIC INTERSTITIAL NEPHRITIS

Frequently not symptomatic

Advance casessymptomatic, those of renal insufficiency

Obstructionpromote chronicity

NEPHROLITIASIS

- CALCIUM SALTS

o make up 80% of renal stones

o Half of affected women have polygenic familial

idiopathic hypercalciuria (most common

predisposing factors)

- STRUVITE STONES

o associated with Staghorn calculi; often seen with

Klebsiella

- Kidney stones develop in 7% with an average age of onset

in the third decade- calcium oxalate stones in young nonpregnant women are

most common

- most stones in pregnancy65 to 75%are calcium

phosphate or hydroxyapatite

-

a low-calcium diet promotes stone formation

- Prevention of recurrences with hydration and a diet low in

sodium and protein

- Thiazide diuretics also diminish stone formation

- INDICATIONS OF STONE REMOVAL

o Obstruction

o Infection

o intractable pain

o heavy bleeding

Removal by a flexible basket viacystoscopy

nonpregnant patients, stone

destruction by lithotripsy

COMMON PRESENTING SYMPTOM

o Infection -60%

o Flank and abdominal pain

o Hematuria

DIAGNOSIS

o More than 90% -present with pain

o Gross hematuria presenting symptom in 23% o

pregnant patients

IMAGING

o Sonography

to visualize stones, many are not detected

because hydronephrosis

o one-shot pyelogram

o

If there is abnormal dilatation without stonevisualization

o Transabdominal color Doppler sonography

to detect presence or absence of ureteral

jets of urine into the bladde

o Helical computed tomography (CT) scanning

the imaging method of choice for

nonpregnant individuals

avoided during pregnancy

o MR imaging

Recommended as the second-line test

following nondiagnosticsonography

MANAGEMENT

o Treatment depends on symptom and duration of

pregnancy (gestational age)o IV hydration and analgesics are always given

o 2/3 symptomatic with conservative treatment and

stone usually passes spontaneously

o invasive procedure

ureteral stenting

ureteroscopy

percutaneous nephrostomy

transurethral laser lithotripsy

basket extraction

o persistent pyelonephritis should prompt a search fo

obstruction due to nephrolithiasis

o fluoroscopy limits the utility of percutaneous

nephrolithotomy

o

extracorporeal shock-wave lithotripsy iscontraindicated in pregnancy

o ureteroscopic removal is also safe in pregnancy.

GLOMERULAR

ACUTE GLUMERULONEPHRITIS

Abrupt onset of hematuria and proteinuria associated with

varying degrees of renal insufficiency and salt and wate

retention

CAN CAUSE:

o Edema

o Hypertension


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o Circulatory congestion symptoms of end spectrum

of disease (pulmonary congestion or pulmonary

edema)

Acute post streptococcal glumerulonephritis prototypical in

diagnosis

DIAGNOSIS

o Renal biopsy may be necessary in determining

etiology as well as direct management DIFFERENTIAL DIAGNOSIS

o Severe preeclampsia

no hematuria

hypertension evident after 20 weeks

EFFECTS OF GLUMERULONEPHRITIS IN PREGNANCY

(Very Important!)

Most common lesions on biopsy

o Membranous Glumerulonephritis

o IgA GN

o Diffuse Mesangial GN

Acute GNprofound effect on pregnancy outcome

Overall fetal loss was 25% and perinatal morbidity after 28weeks was 80/1,000 live births

About half of these women developed hypertension and fourth

did so before 32 weeks (in preeclampsia hypertension develops

after 20wks)

Worst perinatal outcome

o Women w/ impaired renal function

o Early or severe HPN

o Nephrotic-range proteinuria

RAPIDLY PROGRESSIVE GLUMERULONEPHRITIS

If acute GN doesnt resolve and rapidly progressive GN leads to

end stage renal failure within weeks to months

Patient with this feature may have (+) test for antineutrophil

cytoplasmic antibody (ACA)

CHRONIC GLUMERULONEPHRITIS

Many cases with unknown cause

Characterized by progressive renal destruction over years or

decades eventually producing ESRD

Gradual decline in renal function

o Persistent proteinuria

o Hematuria

MICRO

o Renal lesion categorized as proliferative, sclerosing or

membranous

Some women with typical preeclampsia-eclampsia does not

resolve post partum and found to have Chronic GN DIAGNOSIS

o Renal biopsyestablished prognosis

NEPHROTIC SYNDROME

CHARACTERIZED BY:

o Heavy proteinuria >3g/day (HALLMARK)

o Hypoalbuminema

o Hyperlipidemia

o Edema

Others:

o Hypertension

o Albumin nephrotoxicity

o renal insufficiency

DIAGNOSIS

o 24hr urine collection

Proteinuria of 300 mg/dL (cut-off value) o

even 500 mg/dL (in Williams daw sabi nDoc)

serum creatinine level > 1.4 mg/dL

Defects of barrier are glomerular capillary wall that alters

excessive filtration of plasma protein are caused by:

o Primary glomerular disease

o Haematological or toxic injury

o Metabolic vascular disease

Differential diagnosis: Preeclampsia

MANAGEMENT

o Depends on etiology

o Edema managed cautiously during pregnancy

o Normal amounts of dietary protein of high biologica

value are encouraged

POLYCYSTIC KIDNEY DISEASE

Usually autosomal dominant systemic disease that primarily

affects kidney Usually uncommon

85% are due to PKD1 gene mutations on chromosome 16

15% to PKD2 mutations on chromosome 4

Prenatal diagnosis is available if the mutation has been

identified in a family member or if linkage has been established

in the family

Renal complications are more common in men than in women

Hypertension develops in 75%

progression to renal failure is a major problem

Symptoms usually appear during third or fourth decade

FINDINGS:

o Flank pain

o Hematuria

o

Nocturia

o Proteinuria

o abdominal masses

o calculi

o infection

o

10% die due to ruptured of associated intracranial berry

aneurysm

Others have

o cardiac valvular lesions


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mitral valve prolapsed

mitral, aortic, and tricuspid valvular

incompetence

Pregnancy Outcomes

The prognosis depends on the degree of associated

hypertension and renal insufficiency

Urinary tract infections are common

Pre-eclampsia

CHRONIC RENAL DISEASE

pathophysiological process that can progress to end-stage renal

disease

Subclinical loss of function

Mild impairment -3mg/dL

It progresses from stage 0GFR > 90 mL/min/1.73 m2to stage

5GFR < 15mL/min/1.73 m2

Diabetes and Hypertension

o Most common causes of ESRD

CATEGORIES OF RENAL FUNCTION

o normal or mild impairment

o serum creatinine < 1.5 mg/dL

o moderate impairment

o serum creatinine 1.5 to 3.0 mg/dL

o severe renal insufficiencydefined as a serum

creatinine > 3.0 mg/dL

MANAGEMENT

o Frequent prenatal visits to determine BP trends

o Screened and treated

Serial serum creatine

Protein excretin

Bacteriuria is treated to decrease risk of

pyelonephritiso CHON restricted diet is not recommended

o Anemia d/t CRI responds to erythropoietin

o S/E: HPN

ACUTE RENAL FAILURE

AKA: Acute kidney injury

sudden impairment of kidney function with retention of

nitrogenous and other waste products normally excreted by the

kidneys(sudden decrease in GFR

Most common associated with severe preeclampsia and

eclampsia

Accompanied by serum creatinine level of10.7 mg/dL

Oliguriaimportant sign of acute impaired renal function

CAUSES AND ASSOCIATED FACTORS

o Preeclampsia-eclampsia

o HELLP syndrome

o

Obstetrical hemorrhage Placental abruption

Postpartum

abruption

o Septicemia

o Acute fatty liver

o Hyperemesis gravidarum

PREVENTION OF ACUTE TUBULAR NECROSIS BY:

Acute kidney injury in obstetrics is most often due to acute

blood loss, especially that associated with preeclampsia

o Prompt and vigorous replacement of blood in

instances of massive hemorrhage such as placenta

abruption and placental previa (blood loss is a very

important predisposing factor in developing ARF)o Avoidance of vasoconstrictors, treat hypertension

(Never give Methergine in pregnancy ->furthe

vasoconstriction)

o Termination of pregnancy complicated by severe

preeclampsia and eclampsia wth careful blood

replacement

o Preserve health status of mother

o Avoid potent diuretics

DIAGNOSIS AND MANAGEMENT

o An acute increase in serum creatinine is most often

due to renal ischemia

o obstetrical cases, both prerenal and intrarenal factors

are commonly operative

o

evident azotemia and severe oliguria

o Early dialysis appears to reduce the mortality rate

IDIOPATHIC POSTPARTUM RENAL FAILURE

Believed to be a new syndrome of acute irreversible rena

failure that developed within first 6 weeks postpartum

Pathological changes identified by renal biopsy

o Necrosis and endothelial proliferation in glomeruli

o Plus necrosis, thrombosis and intimal thickening o

arterioles

MORPHOLOGY

o Erythrocytes consistent with microangiopathic

hemolysis and thrombocytopenia

Microangiopathic hemolysis will give very high level of lactatedehydrogenase (>600 is significant), thrombocytopenia and also

decreased platelet count

SGPT is also elevated, >60 level

- Italicized- from boo

- yung hindi, from ppt/lectur

-According to Doc, expect cases on platings and exam

Believeyou can and youre halfway there. Believe God can and the race is

won.

ob - renal and urinary tract disorders

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