Nursing Care of Individual Experiencing a Renal Disorder: Vascular Disorders Renal Trauma Acute Kidney Injury - PowerPoint PPT Presentation


PPT – Nursing Care of Individual Experiencing a Renal Disorder: Vascular Disorders Renal Trauma Acute Kidney Injury PowerPoint presentation | free to download - id: 43cafe-YzZjN


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation

Nursing Care of Individual Experiencing a Renal Disorder: Vascular Disorders Renal Trauma Acute Kidney Injury


Nursing Care of Individual Experiencing a Renal Disorder: Vascular Disorders Renal Trauma Acute Kidney Injury Renal A & P -excellent site- renal pathophysiology – PowerPoint PPT presentation

Number of Views:501
Avg rating:3.0/5.0
Slides: 58
Provided by: caroly60
Learn more at:


Write a Comment
User Comments (0)
Transcript and Presenter's Notes

Title: Nursing Care of Individual Experiencing a Renal Disorder: Vascular Disorders Renal Trauma Acute Kidney Injury

Nursing Care of Individual Experiencing a Renal
DisorderVascular DisordersRenal TraumaAcute
Kidney Injury
Renal A P -excellent site- renal
I. AP of the Kidney- (locate structures)
  • Fibrous capsule
  • Renal cortex
  • Renal medulla
  • Pyramids
  • Papillae
  • Minor calyx
  • Major calyx
  • Renal pelvis
  • Ureter

II. Functions of the Kidneys
  • Regulates ______ _________ of extracellular
  • Regulates fluid electrolyte balance thru
  • processes of glomerular__________,
    tubular _________, and tubular _____________.
  • Name some of the F Es regulated by kidneys

volume and composition
filtration, reabsorption, secretion
Na, K, HCO3, H,
Functions of the Kidneys (cont)
  • Regulates acid-base balance through
  • Hormonal functions (BP control), multisytem
    effect through gt

HCO3 and H
Renin Release
RAAS Renin-Angiotensin-Aldosterone-System
How the RAAS Pathway Works (Know this)
Click here- Renin-Angiotensin-Aldosterone Pathway
The Song!
Valerie Kolmer 2006
Quick Quiz
  • Pick the correct pathway of the RAAS
  • 1. Renin Angiotensin II ACE ADH
  • 2. Renin Angiotensin I Aldosterone ADH ACE
  • 3. Renin-Angiotensin 1-ACE-Angiotensin

Functions of the Kidneys (cont)
  • Erythropoietin Release
  • If a patient has chronic renal failure, what
    condition will occur/WHY???

Anemia from impaired erythropoietin
production and platelet abnormalities gt
bleeding risk
Functions of the Kidneys (cont)
  • Activated Vitamin D
  • Necessary to absorb Calcium in the GI
  • tract.
  • If a patient has renal failure, what will happen
    to the patients serum calcium level?

Low serum calcium level/elevated phosphate-
inability kidneys to activate vit D-
hypocalcemia gt parathyroid gland gt secretes PTH
gt stimulates bone demineralization gt release
calcium from bones!
Review Functions of the Kidneys
  • Regulate
  • 1.___________
  • 2.___________
  • 3.___________
  • 4.___________
  • Release of ________________
  • Activation of _______________

1. volume 2. composition extrcellular fluid 3.
fluid 4. electrolyte balance
1. renin 2. activation Vit D
III. Nephron- functional unit of Kidney!
  • How the Nephron Works! Click-watch YouTube video!

Identify the Nephrons Parts
  • Glomerulus
  • Bowmans
  • capsule
  • Proximal tubule
  • Loop of Henle
  • Distal tubule
  • Collecting duct

Click here for Nephron AP Games too!
Renal Trauma (click- view renal trauma slides)
  • Etiology
  • Blunt force from falls, MVA, sports injuries,
    knife/gunshot wounds, impalement, rib fractures
  • Common Manifestations
  • Microscopic to gross hematuria
  • Flank or abdominal pain
  • Oliguria or anuria
  • Localized swelling, tenderness, ecchymosis flank
  • area (Turners signbluish discoloration
    flank area
  • due to retroperitoneal bleeding)
  • ( Cullen's sign -periumbilical
    ecchymosis figure A Grey-Turner's sign
  • on the abdominal flank
    figure B ) and ascites. )
  • Sign/Symptoms depend upon severity injury
  • Severe blood loss/signs shock

Renal Trauma

Major injury to the renal hilar vessels with
devascularization of the kidney is a grade V
Renal Trauma
  • What are common diagnostic tests used in renal

UA (hematuria)- H H (decreasing values) CT,
MRI, IVP with cystography Ultrasound maybe
renal arteriogram
CT-determine if peritoneal violation and predict
need for laparotomy-here initially see
extravasation and fluid in paracolic gutters
(peritoneal violation) and also a hematoma in
perirenal space
Renal Trauma-Interventions
  • Minor or Major?
  • Conservative
  • Bedrest and close observation.
  • Monitor for S S of ?

Bleeding, potential Shock!! (Hypovolemic) Monitor
Renal Trauma-Interventions
  • Surgical-
  • Surgical repair, maybe nephrectomy
  • Percutaneous arterial embolization during
  • Nursing management
  • Accurate assessment
  • Monitor H H levels
  • Bedrest close observation evaluate S S of
  • Fluid mgt
  • Prevent complications/monitor I O
  • Manage drainage tubes
  • Daily weights

Renal Surgery-Nephrectomy
  • Indications for Nephrectomy
  • Renal tumor
  • Massive Trauma
  • Polycystic Kidney Disease
  • Donating a Healthy kidney

Renal Surgery-Nephrectomy
  • Post Op Nursing Management
  • Strict I O
  • Urine output should be at least _____.
  • What should u.o. be if patient had bilateral
    nephrectomy? ______.
  • Observe urine
  • TCDB incentive spirometry
  • Incision in flank area, 12th rib removed
  • Medicate for pain as ordered

30 ml/hr
I hope you said 0
Renal Vascular ProblemsPatho of
  • Development of arterio sclerotic lesions in the
    arterioles and glomerular capillaries
  • ?
  • Decreased blood flow which leads to ischemia and
    patchy necrosis
  • ?
  • Destruction of glomeruli
  • ?
  • Decrease in GFR

Vascular Disorders of the KidneyRenal Artery
  • Definition Narrowing of one or both renal
    arteries due to atherosclerosis or structural
  • Common Manifestation!
  • Uncontrollable HTN-
  • Why?

Think pathophysiology of HTN!
Vascular Disorders of the KidneyRenal Artery
  • Treatment/Collaborative Care
  • Diagnostic Tests
  • Renal arteriogram-most definitive
  • Management
  • Conservative-antihypertensive meds
  • Percutaneous Transluminal Angioplasy
  • Surgical re-vacularization (Graft)
  • ?Nephrectomy

Vascular Disorders of the KidneyRenal Artery
  • Treatment/Collaborative Care

What type of procedure is this? What are some
post procedure nursing care interventions?
Vascular Disorders of the Kidney
  • Renal Vein Stenosis
  • Definition Partial occlusion in one or both
    renal arteries due to atherosclerosis or
    structural abnormalities in vein by a thrombus.
  • Risk Factors
  • Nephrotic syndrome
  • Use of Birth control pills
  • Certain Malignancies

Vascular Disorders of the KidneyRenal Vein
  • Pathophysiology/etiology
  • Cause unclear-thrombus forms in renal vein
  • Associated with trauma, nephrotic syndrome
  • deterioration of renal function
  • Common Manifestations/Complications
  • Decreased GFR
  • Signs of Renal Failure
  • Complication ---Pulmonary Embolus

Vascular Disorders of the KidneyRenal Vein
  • Treatment/Collaborative Care
  • Diagnosis- Renal venography
  • Management
  • Thrombolytic drugs-
  • streptokinase or tPA
  • Anticoagulant therapy to prevent
  • further clot formation

Acute Kidney Injury
  • Definition
  • Rapid decline in renal function- leads to
    accumulation of nitrogenous wastes (azotemia)
  • Kidneys unable to remove urea from blood-become
    uremic (multiple body symptoms affected)

Click here-MD lecture on AKI YouTube 8 min!
Acute Kidney Injury
  • Etiology of AKI
  • Pre-renal
  • Intra-renal
  • Post renal

Etiology of Acute Kidney InjuryPre-renal (most
common cause AKI!)
  • Causes of pre-renal AKI failure-all related to
    dec. blood flow to kidneys!
  • Hypovolemia dehydration, shock, burns
  • Decreased cardiac output CHF, MI, arrythmias
  • Dec. vascular resistance (septic shock, etc)
  • Renal vascular obstruction renal artery
  • stenosis, thrombus.

Etiology of Acute Kidney InjuryIntra-renal
  • Direct injury to the kidneys/nephrons
  • Due to renal tissue causing damage to renal
    tissue (parenchyma)
  • Causes of intra renal AKI failure
  • Acute ischemia (prolonged pre-renal)
  • ATN (acute tubular necrosis)
  • Destruction of tubular epithelial cells,
    slough, plug
  • tubules- abrupt decline in renal
  • possible if basement membrane remains
    intact tubular
  • epithelium regenerates)

Causes of Intrarenal Failure
  • Hemolytic blood transfusion (ATN)
  • Trauma (crush injuries gt release myoglobin
  • muscle tissue gt blocks tubules
  • (ATN)
  • Nephrotoxic drugs/chemicals (ATN)
  • Aminoglycosides
  • Radiographic contrast agents
  • Arsenic, lead, carbon tetachloride
  • Acute glomerulonephritis/pyelonephritis
  • Systemic lupus

Causes of Acute Kidney Injury (ATN)
  • Renal ischemia
  • Disruption basement membranedestruction tubular
  • Nephrotoxic agents
  • Necrosis tubular epithelium plug tubules
    basement membrane intact.
  • Potentially reversible IF
  • Basement not destroyed and tubular epithelium

Renal ischemia
Nephrotoxic agents
Etiology of Acute Kidney Injury Post-renal
  • Causes of post-renal failure (mechanical
    obstruction of urinary outflow urine backs up
    into renal pelvis)
  • BPH (Benign Prostatic Hypertrophy)
  • Calculi
  • Trauma
  • Prostate cancer

Diagnostic Tests in Acute Kidney Injury
  • BUN (blood urea nitrogen)
  • Normal 8-20 mg/dl measurement of
  • amt of urea in blood
  • What is urea?
  • BUN fluctuates
  • BUN elevated in?
  • BUN increased when?

Nitrogenous waste product from breakdown of
(protein) amino acids by liver -
Excessive protein intake, GI bleeding,
Overhydration, primary liver disease (synthesis
of urea depends upon liver), kidney disease
  • Which urinary symptoms is the most common initial
    manifestations of AKI?
  • a- dysuria
  • b- anuria
  • c- hematuria
  • d- oliguria

Oliguria-dec. GFR, less than 400 ml/24 hr
  • The clients BUN is elevated in AKI. What is the
    likely cause of this finding?
  • a- fluid retention
  • b- hemolysis of red blood cells
  • c- below normal protein intake
  • d- reduced renal blood flow

Elevated BUN reflects impairment of renal
function, thus indicates reduced renal blood
flow- normal blood flow is needed for adequate
GFR. Also-Hemolysis of Red blood cells will
obstruct renal tubules can also cause an elevated
Diagnostic Tests in Acute Kidney Injury
  • Serum Creatinine end product of muscle and
    protein metabolism excreted by the kidneys at a
    constant rate
  • Normal 0.6-1.2 mg/dl
  • Directly related to GFR
  • 2 X normal (2.4) 50 nephron fx loss
  • 10 X normal (12) 90 nephron fx loss
  • BUN Creatinine ratio Normal 101
  • BUN Creatinine
  • 16 1.6
  • 12 1.2
  • 8 0.8

Diagnostic Tests in Acute Kidney Injury
  • Creatinine clearance
  • Most accurate indicator of Renal Function
  • Reflects GFR
  • Involves a 24 hr urine/serum creatinine
  • Formula
  • Amount of urine creatinine X urine V
  • serum creatinine
  • Normal 100-135ml/minute

Diagnostic Tests in Acute Kidney Injury
  • Urine Specific Gravity
  • Normal 1.003-1.030
  • Fixed sp. Gravity- 1.010 usually in AKI
  • kidneys lose ability to concentrate urine
  • Serum Electrolytes
  • 1- Serum Sodium Normal 135-145meq/L
  • May be high, low, or normal
  • High in Volume deficit (dehydration)
  • Low due to damaged tubules not conserving
  • sodium

Diagnostic Tests in Acute Kidney Injury
  • Serum Electrolytes
  • 2- Serum K Normal 3.5-5.5 meq/l
  • Almost always increased
  • WHY?
  • Kidneys excrete 80-90 of our K
  • If Kgt 6.0 treatment initiated to prevent?

gt inability kidneys to excrete potassium
acidosis worsens hyperkalmeia hydrogen ions
enter cells potassium driven out of cells!!
Fatal dysrhythmias!
Diagnostic Tests in Acute Kidney Injury
  • Serum Electrolytes
  • 3- Serum Calcium
  • Normal 9-11mg/dl
  • due to production of
  • activated Vitamin D needed to
  • calcium from GI tract
  • What other process is occurring to
  • decrease serum calcium???

Hypocalcemia causes PTH to be released gt bone
demineralization gt more phosphate be released
from bone phosphate already high, calcium
binds with phosphates
Diagnostic Tests in Acute Kidney Injury
  • Serum Electrolytes
  • 4- Serum Phosphorus
  • Normal 2.0-4.5mg/dl
  • Phosphorus- product of protein
  • breakdown excreted by the kidneys
  • What other process is occurring to
    increase serum phosphorus?

Parathyroid gland secretes PTH because calcium
is low, causes phosphorus also to be released
from bone gt phosphorus
Diagnostic Tests in Acute Kidney Injury
  • ABGs
  • pH
  • Metabolic acidosis due to ability
  • kidneys to excrete acid metabolites
  • (uric acid, ammonia) so the pH will be
  • __________.
  • Also, bicarb levels due to bicarb being
  • used up to buffer excess H ions.

Stages of Acute Kidney Injury
  • Oliguric Phase
  • Usually appears 1-7 days of initiating event
  • Diuretic Phase
  • Start varies, usually within10-12 days of onset
    oliguric phase
  • Recovery
  • Usually within a month, recovery takes up to 12

Oliguric Phase of AKI
  • Signs and Symptoms to Anticipate? (similar to
  • Urine less that 400 ml in 24 hours
  • Specific gravity fixed at 1.010 in oliguria in
    intra renal failure
  • Fluid overload
  • Urine with RBCs, casts, WBCs
  • K likely elevated
  • Oliguric Phase
  • Onset 1-7 days
  • Duration 10-14 days
  • Urine output Less than 400 ml/24 hours in 50 of

Acute Kidney Injury Oliguric
  • Metabolic acidosis
  • kidneys unable to synthesize NH3, need H
    excretion, or excrete acid metabolites serum
    bicarbonate, dec. used to buffer H (Kussmaul
  • Ca deficit phosphate excess
  • dec. GI absorption Ca (lack of active vitamin D)
    not significant in AKI
  • Nitrogenous product accumulation
  • unable to eliminate urea and creatinine gt
    elevated BUN, serum creatinine

Diuretic Phase of AKI
  • Onset days to weeks
  • Duration 10 days (1-3 weeks)
  • Urine output1-3 liters/day
  • Signs and Symptoms to Anticipate?
  • Fluid Volume Overload or Fluid Volume Deficit
  • Elevated BUN and serum creatinine (continue)
  • K likely to be elevated or decreased???
  • Hyponatremia and hypotension

Recovery Phase of AKI
  • Recovery Phase
  • Onset When BUN and Creatinine are stablized
  • Duration 4-12 months
  • Urine output Normal
  • Signs and Symptoms to Anticipate?
  • Continue to monitor for signs and symptoms of
  • F E imbalances
  • All body systems for effects of fluid volume

Initial Treatment-Oliguric Phase
  • Fluid Challenge/Diuretics
  • Done to r/o dehydration as cause of AKI and
    blast out tubules if ATN.
  • 250-500cc NS given I.V. over 15 minutes
  • Mannitol (osmotic diuretic) 25gm I.V. given
  • Lasix 80mg I.V. given
  • Should see what within 1-2 hours????

Urine- at least 30ml/hr!)
Treatment During OliguricPhase
  • If fluid challenge fails, fluid intake is
    usually limited and client is placed on fluid
  • Restriction is limited to 600ml u.o. past 24
  • Physician will specify in the orders how much.
  • Question
  • Patients u.o. on Tuesday300ml, what will be his
    fluid intake allowed on Wednesday? ________

900 ml (600 300)
Acute Kidney Injury Management of.
  • 1- Treat primary disease/condition whether
  • it is pre-intra-or post renal problem.
  • 2-Prevention
  • Frequent monitoring for early signs of AKI in at
    risk patients
  • What can the nurse assess for at this point?
  • 3-Assess for Fluid V deficit vs Fluid V overload
  • Strict I O
  • Daily weights 500ml-1 lb. (1kg approx 1000ml
  • Monitor lab valueswhich ones? _______

Acute Kidney Injury Management of.
  • 4- Metabolic Acidosis
  • Administer NaHCO3 I.V. as ordered
  • 5-Hyperkalemia
  • What are the S S of hyperkalemia?
  • ___________________________________
  • Emergency Treatment- Hyperkalemia
  • Give insulin glucose I.V. Why?
  • K moves out of serum back into cells
  • with glucose in presence of

Irregular heartbeat, Fatigue,Weakness,Tingling,
numbness, other unusual sensations, Paralysis,
Difficulty breathing think musles!!
Acute Kidney Injury Management of Potassium
  • Emergency Treatment- Hyperkalemia
  • Sodium Bicarbonate I.V.
  • Correct acidosis get potassium into cells
  • Kayexalate po or enema
  • Sodium exchanged for potassium in GI tract
    gtosmotic diarrhea
  • Dialysis
  • Dietary Restrictions- Potassium
  • Avoid foods high in K
  • Name some of those foods ________________

Avoid- Bananas, oranges, milk, spinach,
chocolate, dried beans peas (limit milk, fruits
Acute Kidney Injury Management of.
  • 6- Calcium Imbalance
  • Administer calcium supplements as ordered
  • (Phoslo, Oscal) Serve also as excellent
    phosphate binders-with meals as binders!
  • 7-Phosphorus Imbalance (Click for Davita
    dialysis for more information)
  • Administer phosphate binders Amphogel
    Basaljel, Renagel
  • Cautious use of aluminun-based phosphate
  • 8- Treat Hypertension (HTN)
  • Lasix, Procardia, Vasotec as ordered

Acute Kidney Injury Management of.
  • 9- Assess for anemia
  • Administer Epogen/Procrit as ordered
  • PRBCs as ordered
  • 10-Diet (Nutritional considerations)
  • Fluid restriction as ordered
  • Low K diet, Low Na diet
  • Low protein diet Why? _________
  • 11- Emergency Dialysis/CRRT indicated when
  • K gt 6.0, Fluid V overload, uremia
  • Metabolic acidosis lt15 HCO3

  • CRRT- a method of continuous dialysis that
    removes volume and solutes slowly.
  • Hemodynamically unstable patient may be better
    able to tolerate CRRT's slow, gradual removal
    process than the rapid changes associated with
  • CRRT has two primary goals to correct the
    electrolyte and metabolic abnormalities
    associated with renal dysfunction, including
    hyperkalemia, hyperphosphatemia, hypocalcemia,
    and metabolic acidosis, and to maintain optimal
    fluid balance.
  • Ideally, CRRT is in progress 24 hours a day until
    renal function returns or the patient can
    tolerate hemodialysis.
  • CRRT also allows for the administration of high
    volumes of selected fluids without causing volume
  • From CRRT- Help for Acute Kidney Injury

A patient develops Acute Kidney Injury after
being on Amphotericin for 1 week
  • The patients AKI is primarily related to
  • A. spasms of the renal arteries
  • B. blood clots in the loops of Henle
  • C. low cardiac output
  • D. acute tubular necrosis

D- Side effect- risk of renal tubular acidosis
permanent renal impairment!
A patients K level is elevated. The physician
orders Kayexalate because it
  • A. increases sodium excretion from colon
    B. exchanges hydrogen ions for sodium ions
  • C. increases calcium absorption in the colon
  • D. exchanges sodium for potassium in colon

D-serves as exchange to reduce K level