Acute Renal Failure

 characterized by sudden loss of the ability of the kidneys to excrete wastes, concentrate
urine, conserve electrolytes, and maintain fluid balance, is a frequent clinical problem,
particularly in the intensive care unit, where it is associated with a mortality of between
50% and 80%.
 Renal failure results when the kidneys cannot remove the body’s metabolic wastes or
perform their regulatory functions.

Pathophysiology

 Underlying problems. There are underlying problems that cause the development of
ARF such as hypovolemia, hypotension, reduced cardiac output and failure, and
obstruction of the kidney.
 Blood flow. As these underlying problems affect the body, the blood flow to the kidneys
reduces.
 Decreased kidney function. With inadequate blood flow to the kidney, there is impaired
kidney function.
 Failure. If the underlying conditions are not treated and corrected, they can lead to
permanent damage of the kidneys.

Categories
Prerenal

 Prerenal failure is caused by interference with renal perfusion (e.g., blood volume
depletion, volume shifts [“third-space” sequestration of fluid], or excessive/too-rapid
volume expansion), manifested by decreased glomerular filtration rate (GFR).
 Disorders that lead to prerenal failure include cardiogenic shock, heart
failure (HF), myocardial infarction (MI), burns, trauma, hemorrhage, septic
or anaphylactic shock, and renal artery obstruction.
Renal (or intrarenal)

 Intrarenal causes for renal failure are associated with parenchymal changes caused
by ischemia or nephrotoxic substances.
 Acute tubular necrosis (ATN) accounts for 90% of cases of acute oliguria.
 Destruction of tubular epithelial cells results from (1) ischemia/hypoperfusion (similar
to prerenal hypoperfusion except that correction of the causative factor may be
followed by continued oliguria for up to 30 days) and/or (2) direct damage from
nephrotoxins.
Postrenal

 Postrenal failure occurs as the result of an obstruction in the urinary tract anywhere
from the tubules to the urethral meatus.
 Obstruction most commonly occurs with stones in the ureters, bladder, or urethra;
however, trauma, edema associated with infection, prostate enlargement, and
strictures also cause postrenal failure.
Clinical Manifestations

 Lethargy. Since waste products cannot be filtered, it slowly accumulates in the different
parts of the body.
 Dryness. The skin and mucous membrane are dry from dehydration.
 Central nervous system symptoms. This include drowsiness,
headache, muscle twitching, and seizures.
 Increased creatinine. All phases of ARF exhibit an increase in creatinine.

Prevention

Preventing renal failure involves the following:

 Hydration. Provide adequate hydration to patients at risk for dehydration.

 Shock. Prevent and treat shock promptly with blood and fluid replacement.
 Close monitoring. Monitor central venous and arterial pressures and hourly urine
output of critically ill patients to detect the onset of renal failure as early as possible.
 Blood administration. Take precautions to ensure that the appropriate blood is
administered to the correct patient in order to avoid severe transfusion reactions.
 Infections. Prevent and treat infections promptly because they can produce progressive
renal damage.
 Toxic drug effects. To prevent toxic drug effects, closely monitor dosage, duration of
use, and blood levels of all medications metabolized or excreted by the kidneys.

Complications

Depending on the duration and severity of ARF, a wide range of potentially life-threatening
complications can occur.

 Metabolic acidosis. Waste products could not be eliminated by the kidneys and they
can contribute to metabolic acidosis.
 Fluid and electrolyte imbalances. Imbalances may occur due to hemorrhage, renal
losses, and gastrointestinal losses.

Assessment and Diagnostic findings

Urine

 Volume: Usually less than 100 mL/24 hr (anuric phase) or 400 mL/24 hr (oliguric
phase), which occurs within 24–48 hr after renal insult.
 Color: Dirty, brown sediment indicates the presence of RBCs, hemoglobin,
myoglobin, porphyrins.
 Specific gravity: Less than 1.020 reflects kidney disease,
e.g., glomerulonephritis, pyelonephritis with loss of ability to concentrate; fixed at
1.010 reflects severe renal damage.
  pH: Greater than 7 found in urinary tract infections (UTIs), renal tubular necrosis,
and chronic renal failure (CRF).
 Osmolality: Less than 350 mOsm/kg is indicative of tubular damage, and
urine/serum ratio is often 1:1.
 Creatinine (Cr) clearance: Renal function may be significantly decreased before
blood urea nitrogen (BUN) and serum Cr show significant elevation.
 Sodium: Usually increased if ATN is cause for ARF, more than 40 mEq/L if a kidney
is not able to resorb sodium, although it may be decreased in other causes of
prerenal failure.
 Fractional sodium (FeNa): Ratio of sodium excreted to total sodium filtered by the
kidneys reveals the inability of tubules to reabsorb sodium. Readings of less than 1%
indicate prerenal problems, higher than 1% reflect intrarenal disorders.
 Bicarbonate: Elevated if metabolic acidosis is present.
 Red blood cells (RBCs): May be present because of infection,
stones, trauma, tumor, or altered glomerular filtration (GF).
 Protein: High-grade proteinuria (3–4+) strongly indicates glomerular damage when
RBCs and casts are also present. Low-grade proteinuria (1–2+) and white blood
cells (WBCs) may be indicative of infection or interstitial nephritis. In ATN, proteinuria
is usually minimal.
 Casts: Usually signal renal disease or infection. Cellular casts with brownish
pigments and numerous renal tubular epithelial cells are diagnostic of ATN. Red
casts suggest acute glomerular nephritis.
Blood

 BUN/Cr: Elevated and usually rise in proportion with ratio of 10:1 or higher.
 Complete blood count (CBC): Hemoglobin (Hb) decreased in presence of anemia.
RBCs often decreased because of increased fragility/decreased survival.
 Arterial blood gases (ABGs): Metabolic acidosis (pH less than 7.2) may develop
because of decreased renal ability to excrete hydrogen and end products of
metabolism. Bicarbonate decreased.
 Sodium: Usually increased, but may vary.
 Potassium: Elevated related to retention and cellular shifts (acidosis) or tissue
release (red cell hemolysis).
 Chloride, phosphorus, and magnesium: Usually elevated.
 Calcium: Decreased.
 Serum osmolality: More than 285 mOsm/kg; often equal to urine.
 Protein: Decreased serum level may reflect protein loss via urine, fluid shifts,
decreased intake, or decreased synthesis because of lack of essential amino acids.
 Radionuclide imaging: May reveal calicectasis, hydronephrosis, narrowing, and
delayed filling or emptying as a cause of ARF.
 Kidney, ureter, bladder (KUB) x-ray: Demonstrates size of kidneys/ureters/bladder,
presence of cysts, tumors, ad kidney displacement or obstruction (stones).
 Retrograde pyelogram: Outlines abnormalities of renal pelvis and ureters.
 Renal arteriogram: Assesses renal circulation and identifies extravascularities,
masses.
 Voiding cystoureterogram: Shows bladder size, reflux into ureters, retention.
 Renal ultrasound: Determines kidney size and presence of masses, cysts,
obstruction in upper urinary tract.
 Nonnuclear computed tomography (CT) scan: Cross-sectional view of kidney and
urinary tract detects presence/extent of disease.
  Magnetic resonance imaging (MRI): Provides information about soft tissue
damage.
 Excretory urography (intravenous urogram or pyelogram): Radiopaque contrast
concentrates in urine and facilitates visualization of KUB.
 Endourology: Direct visualization may be done of urethra, bladder, ureters, and
kidney to diagnose problems, biopsy, and remove small lesions and/or calculi.
 Electrocardiogram (ECG): May be abnormal, reflecting electrolyte and acid-base
imbalances.
Urine tests

 Urinalysis: Analysis of the urine affords enormous insight into the function of the
kidneys.
 Twenty–four–hour urine tests: This test requires you to collect all of your urine for
24 consecutive hours. The urine may be analyzed for protein and waste products
(urea nitrogen and creatinine). The presence of protein in the urine indicates kidney
damage. The amount of creatinine and urea excreted in the urine can be used to
calculate the level of kidney function and the glomerular filtration rate (GFR).
 Glomerular filtration rate (GFR): The GFR is a standard means of expressing
overall kidney function. As kidney disease progresses, GFR falls. The normal GFR is
about 100–140 mL/min in men and 85–115 mL/min in women. It decreases in most
people with age. The GFR may be calculated from the amount of waste products in
the 24–hour urine or by using special markers administered intravenously. Patients
are divided into five stages of chronic kidney disease based on their GFR.
 Urine Specific Gravity: This is a measure of how concentrated a urine sample is. A
concentrated urine sample would have a specific gravity over 1.030 or 1.040
Blood tests

 Creatinine and urea (BUN) in the blood: Blood urea nitrogen and serum creatinine
are the most commonly used blood tests to screen for, and monitor renal disease.
 Creatinine is a breakdown product of normal muscle breakdown.
 Urea is the waste product of breakdown of protein.
 The level of these substances rises in the blood as kidney function worsens.
 Electrolyte levels and acid–base balance: Kidney dysfunction causes imbalances
in electrolytes, especially potassium, phosphorus, and calcium.
 High potassium (hyperkalemia) is a particular concern.
 The acid–base balance of the blood is usually disrupted as well.
 Decreased production of the active form of vitamin D can cause low levels of
calcium in the blood. Inability to excrete phosphorus by failing kidneys causes its
levels in the blood to rise.
 Blood cell counts: Because kidney disease disrupts blood cell production and
shortens the survival of red cells, the red blood cell count and hemoglobin may be
low (anemia). Some patients may also have iron deficiency due to blood loss in
their gastrointestinal system. Other nutritional deficiencies may also impair the
production of red cells.
Other tests

 Ultrasound: Ultrasound is often used in the diagnosis of kidney disease. An

ultrasound is a noninvasive type of test.
  In general, kidneys are shrunken in size in chronic kidney disease, although
they may be normal or even large in size in cases caused by adult polycystic
kidney disease, diabetic nephropathy, and amyloidosis.
 Biopsy: A sample of the kidney tissue (biopsy) is sometimes required in cases in
which the cause of the kidney disease is unclear. Usually, a biopsy can be collected
with local anesthesia only by introducing a needle through the skin into the kidney.

Medical Management

The objectives of treatment of ARF are to restore normal chemical balance and prevent
complications until repair of renal tissue and restoration of renal function can occur.

 Pharmacologic therapy. Cation-exchange resins or Kayexalate can reduce elevated

potassium levels; IV dextrose 50%, insulin, and calcium replacement may be
administered to shift potassium back into cells; diuretic agents are often administered to
control fluid volume.
 Nutritional therapy. Replacement of dietary proteins is individualized to provide the
maximum benefit and minimize uremic symptoms; likewise, caloric requirements are met
with high-carbohydrate meals, because carbohydrates have a protein-sparing effect;
foods and fluids containing potassium or phosphorus are restricted; and
after diuretic phase, the patient is placed on a high-protein, high-calorie diet.

Nursing Management

Nursing Assessment

Assessment usually focuses on the characteristics of the urine.

 Assess urine output. Urine output varies from scanty to a normal volume.
 Assess blood in the urine. Hematuria may be present in patients with ARF.
 Assess laboratory results. Laboratory results may increase, decrease, or stabilize and
these may indicate each phase of ARF.
Nursing Diagnosis

 Electrolyte imbalance related to increased potassium levels.

 Risk for deficient volume related to increased in urine output.
Nursing Care Planning & Goals

The goals for a patient with ARF are:

 Improve nutritional intake.

 Restore fluid balance.
 Reduce metabolic rate.
 Promote pulmonary function.
 Prevent infection.
Nursing Interventions

Nursing interventions are aimed at restoring renal function and reducing potential causes of
increased renal injury.

 Monitor fluid and electrolyte balance. The nurse monitors the patient’s fluid and
electrolyte levels and physical indicators of potential complications during all phases pf
the disorder.
 Reducing metabolic rate. Bed rest is encouraged and fever and infection are
prevented or treated promptly.
 Promoting pulmonary function. The patient is assisted to turn, cough, and take deep
breaths frequently to prevent atelectasis and respiratory tract infection.
 Preventing infection. Asepsis is essential with invasive lines and catheters to minimize
the risk of infection and increased metabolism.
 Providing skin care. Bathing the patient with cool water, frequent turning, and keeping
the skin clean and well moisturized and keeping the fingernails trimmed to avoid
excoriation are often comforting and prevent skin breakdown.
 Provide safety measures. Patient with CNS involvement may be dizzy or confused.
Evaluation

A successful nursing care plan has achieved the following:

 Improved nutritional intake.

 Restored fluid balance.
 Reduced metabolic rate.
 Promoted pulmonary function.
 Prevented infection.

Acute Pyelonephritis
 Sudden and severe inflammation of kidney due to bacterial infection
 Caused due to bacterial infection in the urinary tract
 Often treated with antibiotic, if untreated may lead to chronic pyelonephritis.
 E. coli most common causative of pyelonephritis but any blood stream infection
can also spread to the kidney

S/s:
Cloudy urine
Painful or burning urination pus or blood in urine
Fishy smelling urine,
Fever often higher than 103 F (39.4 C)
Nausea
Pain in the abdomen
Urgent or frequent urination
Fatigue
 Vital sign are usually normal but systolic blood pressure lower that 90 mmHg
suggest a more serious disease process and possible sepsis.

Diagnosis
 Urine test, deteremine if there is any infection, presence of blood or pus in urine.
 CBC, for leukocytosis and laboratory signs of sepsis.
 X ray and ultrasound, to check for any cyst or obstruction or tumor in the urinary
tract.
 CT scan, check any collection or structural abnormality.

Treatment
Antibiotic, prescribed initially for one week or two and symptom should subside
within two to three days of antibiotics.

Ceftriaxone is generally a good choice for initial empiric parenteral therapy of

pyelonephritis.

Carbapenems should generally be reserved for the most critically ill patients or when no
other agents are appropriate.

Appropriate empiric antibiotics for inpatients with acute pyelonephritis include:

 An antipseudomonal carbapenem (imipenem or meropenem) plus vancomycin
(for the most critically ill)
 Ceftriaxone (usually preferred for most cases)
 Fluoroquinolone (depending on local resistance)
 Piperacillin-tazobactam (preferred for suspected Enterococcus or Pseudomonas)
 Cefepime (not for Extended Spectrum Beta Lactamase)
 Cefotaxime
 Cefuroxime
 Ceftazidime
 Aztreonam
 Aminoglycosides (gentamicin, tobramycin, or amikacin)
 An antipseudomonal carbapenem (if a recent ESBL bacterial isolate is found)
PLUS
 Add vancomycin or linezolid if a Gram-positive organism is suspected

Complication
 ureteral obstruction

Recurrent kidney infection

Kidney scar

Prevention
 Drink plenty of water, to wash off any infection and toxins from the body.
 Avoid using cream and lotions in genital areas
 Foods to avoid: alcohol, artificial sweetener, black tea, canned soup, broth
powder, and bullion, carbonated drinks
 Intake food contain a low amount of soduim

Carcinoma with papillary features and psammoma bodies

o Psammoma bodies can be found in organs such as
the thyroid, ovaries, endometrium, and the lining of the central nervous system.
They are involved in both cancerous and benign tumors, and can also be a sign of
chronic inflammation. Specifically, some non-cancerous conditions in
which psammoma bodies can be found include benign ovarian tumors, cervical
polyps, or growths on the cervical canal connecting the uterus and vagina. Thi
can be detected after biopsy of the mass is taken and stained with haematoxylin
and eosin
o Papillary tyroid carcinoma, epithelial malignancy showing evidence of follicular
cell differentiation and a set of distinctive nuclear features. The tumor usually
appears as an irregular solid mass, but it may have cystic features in rare cases.

Etiology
o Radiation exposure
o Genetic, Familial PTC cases have been reported in 5% of all patients with PTC and may
portend a more aggressive disease course.
o There is a higher incidence of PTC in regions with high dietary iodine intake and patients
with preexisting benign thyroid disease

Epidemiology

Papillary thyroid carcinoma occurs predominantly in middle-aged adults with a 3 to 1 female-to-

male ratio, and the median age at presentation is 50 years. Even though rare in children, PTC is
still the most common pediatric thyroid malignancy. It affects Whites more commonly than
Blacks
Fine Needle Aspiration (FNA)

Fine-needle aspiration specimens from conventional PTC are usually cellular and may show
papillary structures, monolayer sheets, and 3D groups in a background of watery or thick so-
called ropy colloid, nuclear or calcific debris, macrophages, and stromal fragments.

Radiographic Features

o On thyroid scans, PTCs typically appear as cold (hypo-functioning) nodules but rarely can
appear as hot (hyperfunctioning) nodules.
o Ultrasound examination is the imaging modality of choice for PTC.
o Sonographic features include a hypoechoic or isoechoic solid nodule with irregular or
poorly defined margins, micro-calcifications, taller-than-wide shape, and disorganized
internal vascularity.
o Ultrasound findings are also invaluable for guiding fine-needle aspiration biopsy of
abnormal nodes.
o Microcalcifications are highly specific for this type of cancer.
o Other imaging modalities, including CT, MRI, and FDG-PET/CT, may be needed to assess
the extent of extra-thyroidal extension, evaluate the presence of substernal masses,
detect recurrent tumors, and improve diagnostic accuracy.

Treatment / management

o Surgery. Choices depend on the location and extent of identifiable disease and the
risk that unidentifiable disease foci are also present.
 lobectomy is an option for unifocal tumors smaller than 4 cm with
no evidence of extrathyroidal extension or lymph node metastasis.
 Prophylactic central-compartment neck dissection (ipsilateral or
bilateral) should be a consideration in patients with PTC with
clinically uninvolved central neck lymph nodes (cN0) who have
advanced primary tumors (T3 or T4) or clinically involved lateral
neck nodes (cN1b), or if the information will be used to plan further
steps in therapy.

o Adjuvant Radioiodine Therapy. radioiodine is the therapy of choice in patients with

PTC to ablate residual normal thyroid tissue. Radioactive iodine therapy is given 4 to
6 weeks after surgery
o Potential adverse effects of radioactive iodine include:
 Sialoadenitis
 Transient thyrotoxicosis
  Pulmonary fibrosis
 Emesis
 Brain edema (can be prevented with the use of corticosteroids)
 Infertility
 Small risk of leukemia, breast or bladder cancer
o Thyroid Hormone Treatment
After thyroidectomy, patients require lifelong thyroid hormone therapy, usually
as monotherapy with levothyroxine (LT4).
o Chemotherapy

reserved for patients with recurrent or excessive remnant disease after the
initial surgical treatment and radioactive iodine ablation.

Differential diagnosis

primary differential diagnoses of PTC are:

 Reactive changes following fine-needle aspiration.[40] This condition
characteristically shows nuclear enlargement, chromatin clearing, and micro-
nucleoli similar to the nuclei of PTC.
 Severe chronic lymphocytic thyroiditis, where the reactive atypia attributed to
inflammation results in nuclear morphology similar to that of PTC.[41]
 Adenomatoid nodules
 Diffuse hyperplasia
 Dyshormonogenetic goiter
 Follicular adenoma
 Follicular thyroid carcinoma
 Medullary thyroid carcinoma
 Metastatic tumors
Complications
Extra thyroid extension
Local or regional recurrence
Distant metastases