Acute Renal Failure
Download
Report
Transcript Acute Renal Failure
Objectives
Anatomy
Function
Chronic Renal Failure (CRF)
Causes
Symptoms
Dialysis
Anatomy and Physiology
The Kidneys
Hilum
Medulla
Pyramids
Papilla
Renal Pelvis
Anatomy
2 Kidneys
2 Ureters
Bladder
Urethra
Kidney Function
Detoxify blood
Increase calcium absorption
calcitriol
Stimulate RBC production
erythropoietin
Regulate blood pressure and
electrolyte balance
renin
Formation of Urine
Glomerular Filtration
GFR
Reabsorption and Secretion
Simple diffusion and osmosis
Facilitated diffusion
Active transport
Azotemia: elevated blood
urea nitrogen not from an intrinsic
renal disease
Oliguria:
urine output less than
500cc/24hr.
Nonoliguria: urine output greater than
500cc/24hr.
Anuria: urine output less than
50cc/24hr.
Acute Versus Chronic
Acute
sudden onset
rapid reduction in urine output
Usually reversible
Tubular cell death and regeneration
Chronic
Progressive
Not reversible
Nephron loss
75% of function can be lost before its
noticeable
ARF versus CRF
Neuropathy
Renal osteodystrophy
Small size Kidney
Past history of CKD
Broad cast
Chronic renal failure
Chronic renal failure: slowly
progressive and non- reversible loss of
kidney function
Uraemia: metabolic outcome of chronic
renal failure
End-stage renal disease: requirement
for renal replacement therapy
ETIOLOGY
Diabetes mellitus (28%)
Hypertension (25%)
Glomerulonephritis (21%)
Polycystic Kidney Diease (4%)
Other (23%): Obstruction, infection,
etc.
Progression of chronic renal failure
Factors causing progression
sustaining primary disease
systemic hypertension
Intraglomerular hypertension
Proteinuria
Nephrocalcinosis
Dyslipidaemia
Imbalance between renal energy demands
and supply
Slowing the Progression of
Chronic Renal Failure
Control BP to <130 /80
Diet
Anaemia
Calcium and Phosphate
Dyslipidaemia
Obesity
Smoking Cessation
Old Chinese saying…….
Good doctor relieve disease
Better doctor cure disease
Superior doctor prevent disease
Symptoms of chronic renal failure
Many are symptom free until 2/3 of
renal mass lost. Often no physical
examination findings or history.
Several common modes of
presentation:
progressive lethargy, anorexia, (and
later vomiting)
hypertension, and /or heart failure
unexplained anaemia
serendipitous findings on biochemistry
The Medical Burden Of
Chronic Renal Failure
Prevention of ESRD may prevent
other co-morbid conditions from
developing
In particular, there is a high
prevalence of Cardiovascular diseases
in patients with Chronic kidney
disease
CHRONIC RENAL FAILURE:
CLINICAL MANIFESTATIONS
Sodium and water retention
Hyperkalemia
Metabolic Acidosis
Mineral and Bone metabolism
Cardiovascular and Pulmonary Disorders
Hematologic Abnormalities
Neuromuscular Abnormalities
Gastrointestinal Abnormalities
Endocrine Abnormalities
Dermatologic Abnormalities
Sodium and Volume Balance
Sodium and water retention:
CHF, Hypertension, ascites, edema
Enhanced sensitivity to extra-renal sodium
and water loss
vomiting, diarrhea, fever, sweating
Symptoms: dry mouth, dizziness, tachycardia,
etc.
Recommendations
Avoid excess salt and water intake
Diuretics or dialysis
Potassium Balance
Hyperkalemia (GFR below 5 mL/min)
GFRs >5 mL/min: compensatory
aldosterone-mediated K transport in the
DCT
K-sparing diuretics, ACEis, beta-blockers
impair Aldosterone-mediated actions
Exacerbation of hyperkalenia:
Exogenous factors: K-rich diet, etc.
Endogenous factors: infection, trauma, etc.
Hyperkalemia & EKG
K > 5.5 -6
Tall, peaked T’s
Wide QRS
Prolong PR
Diminished P
Prolonged QT
QRS-T merge –
sine wave
Hyperkalemia Symptoms
Weakness
Lethargy
Muscle cramps
Paresthesias
Hypoactive DTRs
Dysrhythmias
Metabolic Acidosis
Decreased acid excretion and ability to
maintain physiologic buffering
capacity:
GFR < 20 mL/min: transient
moderate acidosis
Treat with oral sodium bicarbonate
Increased susceptibility to acidosis
Mineral and Bone
Bone disease (Figure 16-6) from:
Decreased Ca absorption from the gut
Over-production of PTH
Altered Vitamin D metabolism
Chronic metabolic acidosis
Cardiovascular and Pulmonary
Abnormalities
Volume and salt overload
CHF and pulmonary edema
Hypertension
Hyperreninemia: Hypertension
Pericarditis: Remic toxin accumulation
Accelerated atherosclerosis: linked to
factors above and metabolic
abnormalities (Ca alterations,
hyperlipidemia)
Hematological Abnormalities
Anemia: lack of erythropoietin production
Bone marrow suppression:
uremic poisons: leukocyte suppression infection
bone marrow fibrosis: elevated PTH an
aluminum toxicity from dialysis
Increased bruising, blood loss (surgery)
and hemorrhage
Lab Abnormalities: Prolonged bleeding
time, abnormal platelet aggregation
Neuromuscular Abnormalites
CNS Abnormalities:
Mild-Moderate: Sleep disorders, impaired
concentration and memory, irritability
Severe: Asterixis, myoclonus, stupor,
seizures and coma
Peripheral neuropathies:
“restless legs” syndrome
Hemodialysis-related neuropathies
Gastrointestinal Abnormalities
Peptic Ulcer disease: Secondary
hyperparathyrodism?
Uremic gastroenteritis: mucosal
alterations
Uremic Fetor: bad breath (ammonia)
Non-Specific abnormalities:
anorexia, nausea, vomiting,
diverticulosis, hiccoughs
Endocrine Abnormalities
Insulin: Prolonged half-life due to
reduced clearance (metabolism)
Amenorrhea and pregnancy failure:
low estrogen levels
Impotence, oligospermia and geminal
cell dysplasia: Low testosterone levels
Dermatologic Abnormalities
Pallor: anemia
Skin color changes: accumulation
of pigments
Ecchymoses and hematomas:
clotting abnormalities
Pruritus and Excoriations: Ca
deposits from secondary
hyperparathyroidism
Conclusion – chronic renal
failure
Progressive chronic disease leading to end-state renal
failure
Different primary disease can cause chronic renal
failure
Diabetic nephropathy is a frequent cause for chronic
renal failure
Symptoms can be very different and depend on
primary disease and stage of chronic renal failure
Stages of renal failure can be associated with a
progressive decrease of GFR
The consequences are complex according to the
different function of the kidney and involve many
organ systems
Pre-Dialysis Treatment
1. Maintain normal electrolytes
a. Potassium, calcium, phosphate are major
electrolytes affected in CRF
b. ACE inhibitors may be acceptable in many
patients with creatinine >3.0mg/dL
c. ACE inhibitors may slow the progression of
diabetic and non-diabetic renal disease [13]
d. Reduce or discontinue other renal toxins
(including NSAIDS)
e. Diuretics (eg. furosemide) may help
maintain potassium in normal range
f. Renal diet including high calcium and low
phosphate
1. Reduce protein intake to <0.6gm/kg body
weight
a. Appears to slow progression of diabetic
and non-diabetic kideny disease
b. In type 1 diabetes mellitus, protein
restriction reduced levels of albuminuria
c. Low protein diet did not slow progression
in children with CRF
1. Underlying Disease
a. Diabetic nephropathy should be treated
with ACE inhibitors until creatinine >2.53mg/dL
b. Hypertension should be aggressively
treated (ACE inhibitors are preferred)
Dialysis
½ of patients with CRF eventually
require dialysis
Diffuse harmful waste out of body
Control BP
Keep safe level of chemicals in body
2 types
Hemodialysis
Peritoneal dialysis
Hemodialysis
1.
a.
b.
c.
d.
e.
f.
Indications
Uremia - azotemia with symptoms and/or signs
Severe Hyperkalemia
Volume Overload - usually with congestive heart
failure (pulmonary edema)
Toxin Removal - ethylene glycol poisoning,
theophylline overdose, etc.
An arterio-venous fistula in the arm is created
surgically
Catheters are inserted into the fistula for blood flow
to dialysis machine
Hemodialysis
3-4 times a week
Takes 2-4 hours
Machine filters
blood and
returns it to
body
1. Procedure for Chronic Hemodialysis
a. Blood is run through a semi-permeable
filter membrane bathed in dialysate
b. Composition of the dialysate is altered to
adjust electrolyte parameters
c. Electrolytes and some toxins pass through
filter
d. By controlling flow rates (pressures),
patient's intravascular volume can be
reduced
e. Most chronic hemodialysis patients receive
3 hours dialysis 3 days per week
1. Efficacy
a. Some acids, BUN and creatinine are
reduced
b. Phosphate is dialyzed, but quickly
released from bone
c. Very effective at reducing
intravascular volume/potassium
d. Once dialysis is initiated, kidney
function is often reduced
e. Not all uremic toxins are removed
and patients generally do not feel
"normal"
f. Response of anemia to erythropoietin
is often suboptimal with hemodialysis
1. Chronic Hemodialysis Medications
a. Anti-hypertensives - labetolol, CCB, ACE
inhibitors
b. Eythropoietin (Epogen®) for anemia in
~80% dialysis pts
c. Vitamin D Analogs - calcitriol given
intravenously
d. Calcium carbonate or acetate to
phosphate and PTH
e. RenaGel, a non-adsorbed phosphate
binder, is being developed for
hyperphosphatemia
f. DDAVP may be effective for patients with
symptomatic platelet problems
Types of Access
Temporary site
AV fistula
Surgeon constructs by combining an
artery and a vein
3 to 6 months to mature
AV graft
Man-made tube inserted by a surgeon to
connect artery and vein
2 to 6 weeks to mature
Temporary Catheter
AV Fistula & Graft
Chronic Renal Failure
Long-Term
Management
Renal Dialysis
Hemodialysis
Common
complications
What This Means For You
No BP on same arm as fistula
Protect arm from injury
Control obvious hemorrhage
Bleeding will be arterial
Maintain direct pressure
No IV on same arm as fistula
A thrill will be felt – this is normal
Access Problems
AV graft thrombosis
AV fistula or graft bleeding
AV graft infection
Steal Phenomenon
Early post-op
Ischemic distally
Apply small amount of pressure to
reverse symptoms
Peritoneal Dialysis
Abdominal lining filters blood
3 types
Continuous ambulatory
Continuous cyclical
Intermittent
Considerations
Make sure the dressing remains intact
Do not push or pull on the catheter
Do not disconnect any of the
catheters
Always transport the patient and
bags/catheters as one piece
Never inject anything into catheter
Dialysis Related Problems
Lightheaded –give fluids
Hypotension
Dysrhythmias
Disequilibration Syndrome
At end of early sessions
Confusion, tremor, seizure
Due to decrease concentration of blood
versus brain leading to cerebral edema