Aki hypertension contributes to load-induceI.pdf

phr21005 90 views 24 slides Sep 26, 2024
Slide 1
Slide 1 of 24
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24

About This Presentation

Aki


Slide Content

ACUTE KIDNEY
INJURY
5th stage

´INTRODUCTION
´Acute kidney injury (AKI) is a potentially life-threatening syndrome that
occurs primarily in hospitalized patients and frequently complicates the
course of those who are critically ill.
´It is characterized by a rapid decrease in glomerular filtration rate (GFR)
and the resultant accumulation of nitrogenous waste products (eg,
creatinine), with or without a decrease in urine output. AKI often coexists
with other clinical syndromes such as shock and sepsis.

´AKIis defined as an increase in serum creatinine (SCr) of at least
0.3 mg/dL (27 μmol/L) within 48 hours, a 50% increase in baseline
SCrwithin 7 days, or a urine output of less than 0.5 mL/kg/h for at
least 6 hours. ( normal values of above??)

Etiology

´The KDIGO definition is based on either an increase in SCror a decrease
in urineoutput.
´Stage 1 includes either a 1.5 to 1.9 increase in SCrfrom baseline within 7
days or
´an absolute increase in SCrof 0.3 mg/dL (27 μmol/L) over 48 hours.
´Thus, even small increases in SCrindicate AKI, and this highlights the
importance of early detection.

Diagnosis
´Decreased urination or
increased
´Nausea vomiting, and fatigue
´Concentrated urin (orange)
´Weight loss and also weight
gain
´Brown urin
´Flank pain origion
´Symptoms of volume overload
´Urinalysis showed change in
osmolarity
´Change in Na conc.
´U/S helps in differentiation
AKI from CRF

Desired outcome
´A primary goal in caring for patients with AKI is ameliorating
identifiable underlying causes of AKI such as hypovolemia,
nephrotoxic
drugs, or ureter obstruction.
´Prerenal and postrenal AKI can be reversed if the underlying
problem is promptly identified and corrected, whereas treatment of
intrinsic renal failure is primarily supportive until kidney function
recovers.

Pharmacologic Therapy
´Hydration in Patients with
Hypovolemia
´Isotonic crystalloid solutions such
as 0.9% normal saline and
balanced crystalloid solutions (eg,
Lactated Ringer’s,
´There is colloid fluids and
crystalloid. In case of
replacement, crystalloid is
preferred
´It is important to be careful about
the sodium level and chloride

´Caution must be taken with hydration because overzealous fluid
resuscitation can result in ----------------
´Blood transfusions may be indicated when there is acute blood loss.
´Besides fluids replacement, vasopressors like norepinephrine may
be needed to restore organ perfusion

´Loop Diuretics in Patients with Volume Overload
´Most studies evaluating loop diuretics (eg, furosemide, bumetanide) for
preventing or treating AKI demonstrated improved urine output but no
improvement in survival or need for dialysis.
´There are some reports that loop diuretics may worsen kidney
function and may be harmful if given for prevention of AKI.
´all loop diuretics are equally effective in fluid removal when given in
equipotent IV doses (40 mg furosemide = 10−20 mg torsemide = 1 mg
bumetanide

Importants notes about diuretics
´It is important to take care from the side effects of loop diuretics,
which may be associated with the wrong adminstration.
´In AKI, there is a need for large doses of loop diuretics
´What is the ceiling effect of loop diuretics?
´Loop diuretics are the diuretics of choice for management volume
overload in AKI (how can this be assessed??). The usual starting
dose of IV furosemide for treatment of AKI ranges from 40 to 80
mg

Cont.
´Low dose of dopamin acting as vasodilation and enhance renal
blood flow
, this effect confirmed in healthy individuals but no efficacy recorded
in AKI patient

Renal Replacement Therapy
´It indicated in:
•• Anuria or severe oliguria
• Potassium greater than 6.5 mEq/L (mmol/L)
•• Metabolic acidosis with a pH less than 7.2
• Pronounced elevations in BUN and SCr
• Symptoms of uremia
• Diuretic-resistant fluid overload

´Two types of RRT modalities are used in AKI:
´Intermittent hemodialysis (IHD) ( the preferable and effective in
controlling AKI)
´continuous renal replacement therapy (CRRT). (it is the desired
method for patients cannot tolerate rapid volume removal), but there
is no. of disadvantages, like --------

Supportive therapy
´Adequate nutrition
´Correction of electrolyte imbalance
´Fluid management
´Correction any hematological abnormalities, like treating infections,
GI problems, Cardio-vascular conditions

Prevention of AKI
´Avoidance of nephrotoxic drugs, like
´Aminoglycoside: Risk factors for aminoglycoside-induced AKI
include high cumulative drug expo-sure, prolonged course of
therapy (typically after 7–10 days), preexisting CKD, increased age,
and concurrent administration of other nephrotoxic drugs.
´NSAIDs: cause prerenal AKI through inhibition of prostaglandin-
mediated renal vasodilation.

´Amphotericin B: 12-53% toxicity with the conventional
formulation
´Cumulative dose, high daily dose, dehydration. All increase the risk
of nephrotoxicity
´To overcome this problem, lipid-base formula had developed

´Radiocontrast agents
´Contrast agents are water-soluble, triiodinated, benzoic acid salts.
´Nephrotoxicity results from both ischemia and direct proximal
tubule toxicity, with a resultant decrease in GFR and increased SCr
within 24 to 48 hours of the damage
´Well hydration is very important to overcome this problem
´Mention extra methods for reduction toxicity of contrast media?

ACE-I and ARBs
´ACE-I and ARBs

´A 62-year-old man presents to the clinic with complaints of pain in the back of his
left leg. In addition, he has increased dizziness and drowsiness and has “generally
not been feeling well” over the past week. He has a past medical history
´of stage 2 chronic kidney disease (CKD) with proteinuria (baseline SCr1.3 mg/dL
[115 μmol/L]), hypertension, depression, and obesity. He reports that he has been
tryingtomake lifestyle changes to better manage his medical problems, including
dieting, vigorous walking to lose weight, and using a pill organizer to ensure he
doesn’t miss doses of his medications. He went to a walk-in urgent care medical
clinic 1 week ago for left leg pain. He was diagnosed with Achilles tendonitis
secondary to power walking. He received a boot to immobilize his left foot and
was started on naproxen for pain and inflammation. Today, he states that his left
foot feels better in the boot after wearing it for 7 days, but he

´has little energy, he has been going to the bathroom less often, and
his urine is dark. His weight is usually 220 pounds (100 kg), and
today he weighs 215 lb(97.5 kg). His blood pressure was 115/60
and heart rate was 118 beats per minute.

´Current Medications:
´Losartan 100 mg orally once daily
´Furosemide 40 mg orally twice daily
´Simvastatin 40 mg orally daily in the evening
´Metformin 500 mg orally twice daily
´Glyburide 5 mg orally daily
´Metoprolol 25 mg orally twice daily
´Paroxetine 20 mg orally daily
´Naproxen 275 mg orally every 8 hours as needed for pain and inflammation

´What information is suggestive of acute kidney injury (AKI)? What
risk factors does he have for developing AKI?
´What additional laboratory information do you need to fully assess
the patient?
´What additional information would you elicit from him regarding
his pharmacotherapy before creating a treatment plan?