Renal Assessment-Assessment Exam 3 Flashcards
1
Q
Fluid compartment picture
A
2
Q
____ is more immediately altered by kidneys
A
ECF
3
Q
Increased muscle means increased what?
Increased fat means less what?
A
Water (for both)
4
Q
What does ADH do?
A
Sodium and water retention
5
Q
What is osmolar homeostasis mainly mediated by?
A
osmolality-sensors in anterior hypothalamus
6
Q
What does osmolar homeostasis cause?
A
- Sensors Stimulate thirst
- Cause Pituitary Release of Vasopressin (ADH)
- Cardiac atria releases ANP→act on kidney to ↓Na+/H20 reabsorption
7
Q
What is volume homeostasis mediated by?
A
juxtaglomerular apparatus
8
Q
What does volume homeostasis cause?
A
- JGA senses changes in volume
- ↓Vol @ JGA triggers Renin-Angiotensinogen-Aldosterone system (RAAS)→Na+/H20 reabsorption
9
Q
Hyponatremia diagnosis algorithm
A
10
Q
What percent of hospitalized pts are hyponatremic?
Why?
A
15%
- over fluid-resuscitation
- ↑endog vasopressin
11
Q
What can cause hyponatremia in a hypovolemic pt?
A
diuretics, gi loss, burns, trauma
12
Q
What can cause hyponatremia in a euvolemic pt?
A
salt restriction, endocrine related -Hypothyroid, SIADH (holding on to H20 >Na+)
13
Q
What can cause hyponatremia in a hypervolemic pt?
A
ARF/CKD
heart failure
14
Q
What is the upper and lower cutoff for sodium to need correction prior to surgery?
A
125
155
15
Q
Once sodium is less than ____, you will start to see more pronounced symptoms
A
130
16
Q
Hyponatremia s/s chart
A
17
Q
Treatment of hyponatremia
A
- Treat underlying cause (look at volume status)
- Electrolyte drinks
- NS
- Diuretics
- Hypertonic/3%
18
Q
What is the rate for 3% NaCl?
na+ correction should not exceed _____. Why?
A
80 ml/hr over 15 hr
1.5 meq/L/hr- too rapid of correction can cause osmotic demyelination syndrome
19
Q
What is considered rapid correction in treatment of hyponatremia?
A
> 6 meq/L in 24 hr
20
Q
What do you give for hyponatremic seizures?
A
3-5ml/kg of 3% over 20 min, until seizures resolve
21
Q
How often should you check sodium when replacing it?
A
q4 hours
22
Q
Common causes of hypernatremia
A
- Excessive evaporation
- Poor oral intake (very young, very old, altered mental status)
- Overcorrection of hyponatremia (ex. 3% NS treatment)
- Diabetes insipidus → b/c patients have copious diluted urine
- GI losses
- Excessive sodium bicarb (when treating acidosis)
23
Q
Hypernatremia diagnostic algorithm chart
A
24
Q
What can cause hypernatremia in a hypovolemic pt?
A
Renal or GI loss
25
What can cause hypernatremia in a euvolemic pt?
DI, insensible loss (skin, respiratory)
26
What can cause hypernatremia in a hypervolemic pt?
Increases Na intake
Hyperaldosteronism
Cushings
27
Symptoms of hypernatremia
Orthostasis
Restlessness
Lethargy
Tremor/Muscle twitching/spasticity
Seizures
Death
28
Treatment of hypernatremia
Address Root cause, Assess volume status (VS, UOP, Turgor, CVP)
- Hypovolemic: normal saline
- Euvolemic: water replacement (po or D5W)
- Hypervolemic: diuretics
29
What is the goal Na+ reduction rate in hypernatremia?
What is this avoiding?
≤0.5 mmol/L/hr, and ≤ 10 mmol/L per day
Cerebral edema, seizures, neuro damage
30
If more than 50% of major veins collapse, what does this indicate?
Volume depletion
31
Potassium is a major (ICF/ECF?) cation
ICF
- < 1.5% in ECF; majority of it is in cell
32
Does serum or total K+ reflect transmembrane K+ regulation more?
Serum
33
____ causes the distal nephron to secrete K+ (and reabsorb Na+)
Aldosterone
34
In renal failure, K+ excretion _____
declines
35
Causes of hypokalemia chart
36
Common causes of hypokalemia
What are the 3 major categories?
Categories: renal loss, GI loss, transcellular shift
Renal loss- Diuretics, Hyperaldosteronism
GI loss – N/V/D, malabsorption
Intracellular shift- Alkalosis, β-Ag’s, Insulin
DKA (osmotic diuresis)
HCTZ (in BP meds)
Excessive licorice
37
S/S of hypokalemia
Generally cardiac and neuromuscular
- Muscle weakness/Cramps
- Ileus
- Dysrhythmias, U wave
38
Treatment of hypokalemia
Underlying cause
Potassium PO > IV (CVC); IV may require days
- Generally, K+ given @ 10-20mEq/L/hr IV
- Each 10 meq IV K+→↑Serum K+ by ~0.1 mmol/L
Avoid excessive insulin, β-agonists, bicarb, hyperventilation, diuretics
39
Causes of hyperkalemia
Renal failure
Hypoaldosteronism
Drugs that inhibit RAAS
Drugs that inhibit K+ excretion
Depolarizing NMB (Succs)
Acidosis (Respiratory/Metabolic)
Cell death (trauma, tourniquet)
Massive blood transfusion
40
Symptoms of hyperkalemia
Chronic may be minimally symptomatic (malaise, GI upset)
Skeletal muscle paralysis,↓fine motor
Cardiac dysrhythmias
41
EKG progression of hyperkalemia
peaked T wave
P wave disappearance
prolonged QRS complex
sine waves
asystole
42
Succs increases serum K+ by _____ meq/L
0.5-1
43
Hyperkalemia treatment
- Dialyze within 24h prior to surgery
- Calcium- 1st initial treatment (quickly stabilize cell membrane)
- Hyperventilation (↑pH by 0.1 →↓K+ by 0.4-1.5 mmol/L)
- Insulin +/- glucose (10u IV: 25g D50) * works in 10-20 min
- Bicarb
- Loop Diuretics
- Kayexalate (hrs to days)
*Avoid Succs, hypoventilation, LR & K+ containing IV fluids
44
Only 1% of body's Ca++ is in _____. The other 99% is stored where?
ECF
Bone
45
What percent of plasma Ca++ is protein bound to albumin?
What does this mean?
60%
It's rendered inactive
46
Only ____ Ca++ is physiologically active
ionized
47
Normal iCa++
1.2-1.38 mmol/L
48
What 2 things affect ionized Ca++ levels?
Albumin levels
pH
↑pH/Alkalosis→↑Ca++ binding to albumin (therefore ↓iCa++)
49
Causes of hypocalcemia
- ↓Parathyroid hormone (PTH) secretion
*complication of thyroid/PT surgery, can lead to laryngospasm
- Magnesium deficiency
- Low Vit D or disorder of Vit D metabolism
- Renal failure (kidneys not responding to PTH)
- Massive blood transfusion (citrate preservative binds Ca++)
50
PTH acts on what 3 things to increase Ca++ absorption?
Bones
Kidneys
GI
51
Majority of pts with hypercalcemia have what?
What are usually the Ca++ levels in these?
Hyper-parathyroid: <11
cancer >13
52
Less common causes of hypercalcemia
Vit D intoxication
Milk-alkali syndrome (excessive GI Ca++ absorption)
Granulomatous diseases (sarcoidosis)
53
S/S chart for hyper/hypocalcemia
54
Causes of hypo-magnesium
Low dietary intake or absorption
Renal wasting
55
Symptoms of hypo-magnesium
Muscle weakness or excitation
Seizures
Ventricular dysrhythmia (Polymorphic V-tack/Torsades De Pointes)
56
Treatment of hypo-magnesium
Depends on severity of sx
Slower infusions for less severe
Torsade's/seizures→ 2g Mag Sulfate
57
What is hypermagnesemia usually caused by?
Who do you see this in the most?
Over treatment of mag (mag gtts)
- Pre-eclampsia/Eclampsia→ only real treatment is delivery of baby; common to have them on mag gtt and emergency c-section
- Pheochromocytoma→ excessive catecholamine release ; magnesium helps with BP; true treatment is removal of tumor
58
Symptoms of hypermagnesemia (with perspective levels)
4-5 mEq/L: Lethargy, N/V, Flushing→ common in OB patients
>6 mEq/L: hypotension, ↓DTR
>10 mEq/L: Paralysis, apnea, heart blocks, cardiac arrest
59
Treatment of hypermagnesemia
Diuresis, IV calcium, dialysis
60
How often should you check a mag level in hypermagnesemia?
q4 hours
61
Where are the kidneys located?
- Located retroperitoneal between T12-L4
- Right slightly caudal to left to accommodate liver
62
What is the primary/functional unit of the kidney?
Nephron
63
Each kidney has ____ nephrons
approx. 1 million
64
What does the nephron consist of?
Glomerulus
Tubular system
- Bowman capsule
- Proximal Tubule (PCT)
- Loop of Henle
- Distal Tubule (DCT)
- Collecting duct
65
Kidneys receive __% of CO which is equal to about ___ L/min
20%
1-1.25 L/min
66
The outer layer of the kidney is the ___ and it receives ___% of RBF
Cortex
85-90%
67
The inner layer of the kidney is the ____. The ____ is particularly vulnerable for developing necrosis in response to hypotension
Medulla
Loop of henle
68
69
Primary functions of the kidneys
Regulates ECF volume, osmolarity, composition
Regulate BP (intermediately & Long term) →through RAAS & ANP
Excrete toxins/metabolites
Maintain acid/base balance
- pH regulated by reabsorption & excretion of HCO- & H+
Produce hormones (Renin, Erythropoietin, Calcitriol, Prostaglandins)
Blood glucose homeostasis
70
What 2 things help regulate volume/BP in the kidneys?
RAAS
ANP
71
What maintains serum Ca++?
Calcitriol
72
What are the renal functions labs?
GFR
Creatinine Clearance
Serum creatinine
BUN
BUN:creatinine ratio
Proteinuria
Specific gravity
73
Normal GFR and considerations
125-140 ml/min
- Best measure renal function over time
- Heavily influenced hydration status
- So if patient dehydrated, you wont get accurate picture of GFR
74
Normal creatinine clearance and considerations
110-150 mL/min
- Creatinine freely filtered, not reabsorbed
- To check this have to do 24 hour urine test
- Most reliable measure of GFR
75
Normal serum creatinine and considerations
0.6-1.3 mg/dL (correlates with muscle mass, so a little higher in males)
- Can be influenced by high protein diet, supplements (ex. creatine), muscle breakdown
- Good for acute monitoring; Having a baseline is critical to assess for trends
- Serum creatinine inversely related to GFR
- In acute case, double Serum creatinine can mean drop in GFR by 50% → indicates AKI
76
____ is better for trending kidney uses, while ___ is better for detecting an acute change
GFR
Creatinine
77
GFR drops by ___ ml/min per decade after age ___
10 ml/min
20 y/o
78
Normal BUN and considerations
10-20 mg/dL
- Urea is reabsorbed into blood
- BUN affected by diet, intravascular volume
- Low BUN could mean malnourished or volume diluted
- High could mean ↑protein diet, dehydrated, GI bleed, trauma, muscle wasting
- Obviously high BUN can indicate poor renal function
79
Normal BUN:creatinine ratio and considerations
10:1--> BUN should be 10x higher than creat.
- BUN (reabsorbed) to Creatinine (not reabsorbed)
- Good measure of hydration status
80
Normal proteinuria level and considerations
<150 mg/dL
- >750mg/day could suggest glomerular injury or UTI
81
Normal urine specific gravity and considerations
1.001-1.035
- Comparing 1ml urine to 1ml distilled water
- measures nephron’s ability to concentrate urine
82
What are you looking for when assessing volume status? (renal assessment)
Look at big picture for hydration status
History and physical exam
Signs the patient is dry / volume depleted
83
What are the signs that a pt is dry/depleted?
- Orthostatic pressure changes
- ↓BE (base excess)
- ↑Lactate
- Drop in UOP is a late sign of volume loss
- UOP- 30 ml/hr; 0.5-1ml/kg/hr
- Oliguria: <500mL in 24h
84
What are the volume monitors?
- US to assess IVC
- CVP, RAP
- LAP, PCWP (Powerful stimuli for renal vasoconstriction)
- PAP
SVV (stroke volume variation)
- Compares inspiratory vs expiratory pressure
- Assumes patient is ventilated
- Also Assumes sinus rhythm
85
>__% collapse in ___ indicates fluid deficit
50%
IVC
86
What is passive leg raise?
Determine fluid responsiveness
- Lay them flat, and lift up legs, and it allows you to determine if they would be responsive to fluid challenge
87
What is an acute kidney injury>
- Deterioration over hours-days
- Failure to excrete nitrogenous waste products or maintain fluid/electrolyte homeostasis
88
AKI affects ___% of hospitalized pts and ___% of ICU pts
20%
50%
89
AKI is usually caused by what?
Hypotension/hypovolemia
Nephrotoxins
90
What is azotemia?
buildup of nitrogenous products s/a urea, creatinine
- hallmark of AKI
91
What is the mortality of an AKI w/ multi system organ failure requiring dialysis?
>50%
92
Risk factors of AKI
Pre-existing renal disease
Advanced age
CHF
PVD (peripheral vascular disease)
Diabetes
Sepsis ( b/c of hypotension)
Jaundice
Major operative procedures
IV Contrast
93
AKI diagnostic criteria
- ↑Serum Cr by 0.3 mg/dL within 48 h
- ↑Serum Cr by 50% within 7 days
- ↓Creatinine clearance by 50%
- Abrupt oliguria *although not always seen in AKI
94
Physical symptoms of AKI
Asymptomatic
Malaise
Hypotension
Hypovolemic or hypervolemic
95
AKI causes chart
96
What is the most common form of AKI?
Pre-renal azotemia
97
___ of hospital acquired AKI cases are pre-renal
Half
98
Causes of AKI in OR?
Keep MAP within ___% of baseline
Anesthesia meds + volume & blood loss →↓RBF
20%
99
In pre-renal AKI, BUN:CR is usually what?
>20:1
100
T/F
Pre-renal is reversible
True!
- Most common cause of ATN iis pre-renal azotemia if not reversed in time
- In Pre-renal azotemia, they are still reabsorbing Na+ & H20
101
What is the treatment for pre-renal azotemia?
Restore RBF
Fluids, Mannitol, Diuretics, maintain MAP, Pressors are questionable
- Ideally you can maintain MAP with crytsalloids and colloids and not have them as deep during anesthesia
- You dont want to over constrict with pressors and damage the kidneys this way; but if pressors is last resort then need to do so
- Vasopressin is pressor of choice!
102
Renal azotemia is an ___ renal disease and it potentially ____
Intrinsic
Reversible
103
S/S of renal azotemia
- ↓GFR(late sx)
- ↓urea reabsorption in prox tubule →↓BUN
- ↓Creatinine filtration→↑blood creatinine
- BUN:Cr often < 15:1
104
What is post renal azotemia?
Outflow obstruction
↑Nephron tubular hydrostatic pressure
105
____ is used to diagnose post-renal azotemia
Renal ultrasonography
106
In post renal azotemia, the reversibility is inversely related to what?
Duration
- The longer this issue has existed, the less reversible it is
107
Treatment of post renal azotemia
Remove obstruction
- persistent obstruction damages tubular epithelium
108
AKI chart
109
Neurological complications of AKI
Symptoms are Related to protein/amino acids buildup in blood
Uremic Encephalopathy (dialysis can improve this)
Mobility disorders
Neuropathies
Myopathies
Seizures
Stroke
110
CV complications of AKI
Systemic hypertension
Left ventricular hypertrophy
CHF
Pulmonary edema- late sign
Uremic cardiomyopathy - late sign
Arrhythmias r/t build up of electrolytes
111
Hematological complications of AKI
Anemia
↓ EPO (erythropoietin) production
↓ red cell production
↓ red cell survival
Platelet dysfunction (plt function assay or TEG are valuable)
vWF disrupted by uremia
- Prophylactic DDAVP is good treatment!
- ↑VWF & Factor VIII to improve coagulation
112
Metabolic complications of AKI
Hyperkalemia
Water/sodium imbalances
Hypoalbuminemia (kidneys allowing albumin to escape)
Metabolic acidosis
Malnutrition
Hyperparathyroidism
- Parathyroid in overdrive to in attempt to stimulate kidney to reabsorb Ca++
113
114
AKI anesthesia implications
Correct fluid, electrolyte, acid/base status
Volume- NS preferred for renal (no K+)
Careful w/colloids- albumin preferred; synthetic colloids less desired
MAP maintained (20% of baseline)!!!
Vasopressors→ Vasopressin & alpha agonists
- Vasopressin is pressor of choice over alpha agonists b/c vasopressin preferentially constricts efferent arteriole vs alpha agonists
Prophylactic sodium bicarb
- Decreases formation of free-radicals
Prevents ATN from causing renal failure
115
CKD is ____ and _____
Progressive and irreversible
116
Leading causes of CKD
Diabetes, HTN
117
Presentation of CKD
Often getting surgery for dialysis access
DM, toe/foot debridement's & amputations
Non-healing wounds
Often frequent flyers
118
In CKD, GFR decreases by ____ per decade starting from age ___
10
20
119
CKD staging chart
120
What is the GFR equation?
186 x (SCr)-1.154x (age)-0.203x (0.742 if female) x (1.210 if African American)
121
CKD CV effects
Systemic hypertension
Dyslipidemia
Predisposed to silent MI
122
What is the 1st line treatment for CKD HTN?
Thiazide diuretics
- May need ACE-I/ARB
- We do not like ACE’s and ARB’s b/c we see profound hypotension that is difficult to treat
123
Side note about ACEs and ARBs for CKD pts
Often used in CKD b/c:
- ↓systemic BP and glomerular pressure
- ↓proteinuria by reducing glomerular hyperfiltration
- ↓glomerulosclerosis
124
CKD systemic HTN considerations
-HTN is both a Cause and consequence
- Retention of sodium and water
- Chronic Activation of renin-angiotensin-aldosterone system
125
What are typical lipid levels in CKD?
Triglycerides often > 500
LDL often > 100
126
Populations that are high risk for silent MI
Women and diabetics
127
CKD hematologic effects
Anemia
- Responsive to exogenous erythropoietin
- Target Hbg 10
- Platelet dysfunction b/c platelets dont survive well in uremic environment
- Blood Transfusions → consider the Risks vs benefits, b/c excess hgb leads to sluggish circulation
128
Indications to consider dialysis
Volume overload
Severe hyperkalemia
Metabolic acidosis
Symptomatic uremia
Failure to clear medications
129
What is the leading cause of death in dialysis pts?
Infection
130
Anesthesia concerns of CKD
- Assess stability of ESRD
- Body weight pre/post dialysis (we base doses of meds on body weight)--> want a weight within 24 h of surgery
- Want to know if they have Well-controlled BP, and if Meds were continued.. Especially know if on ace’s or arbs
- Need to know Glucose management; good to know A1C b/c allows you to know they are unmanaged
- Aspiration precautions in these patients (DM, obesity)--> slowed GI motility → can do ultrasound of gastric area to make sure its empty
- Pressors for these patients→ not as responsive to noepi b/c of constant high catecholamines
- Uremic bleeding
131
What are considerations with uremic bleeding?
- normal platelet count/PT/PTT. Assess plt function.
- Consider Cryo, F VIII, vWF to optimize clotting
Desmopressin (DDAVP)
- Give early due to : Peak 2-4h; lasts 6-8h
- Can be given prophylactically if expecting blood loss
- Tachyphylaxis – so cant give today and tomorrow and expect same effect - need to pick surgery you expect the most blood loss
132
Many anesthetic agents are ___ soluble and reabsorbed by ______
Lipid
Renal tubular cells
133
What is the best NMB on nonRSI kidney pts?
Nimbex (metabolized in plasma)
134
For CKD pts, it's important to avoid ___ metabolites. These include what?
Active
morphine, demerol
135
What is important with lipid insoluble drugs?
Eliminated unchanged in urine, prolonged duration of action due to decreased kidney function
- Renal dosing, based on GFR
136
What are lipid insoluble drugs that we need to renally dose?
Thiazides
Loop diuretics
Digoxin
Many abx
137
Renal excretion drug chart
Liver will eventually metabolize these
138
Morphine is ___% cleared through urine by what metabolites?
40%
morphine-3 glucuronide
morphine-6 glucuronide
139
What is the metabolite of demerol?
Normeperidine
140
Considerations of demerol for kidneys
- Analgesic and CNS effects
- main adverse effect is neurotoxicity (nervousness, tremors, muscle twitches, seizures)
- Multiple doses of meperidine result in accumulation of normeperidine due to its long elimination half-life (15-30 h) as compared with the meperidine (2-4 h).
141
K+ < ___ on an elective surgery is a concern
5.5
142
Dialysis pts should be dialyzed within ____ preceding elective sx
24 hrs
143
Blood loss activates ____. What does this mean?
Baroreceptors
- ↑SNS outflow and increase in circulating catecholamines and they constrict afferent arteries which further decrease RBF
144
Catecholamines active ___. What does this mean?
α1-Rs
- ↑afferent arteriole constriction→↓RBF
145
Hormones that regulate Ca++
- Parathyroid hormone: ↑’s GI absorption, renal reabsorption, and regulates bone/bloodstream levels
- Vitamin D: augments intestinal Ca++ absorption
- Calcitonin: promotes storage of Ca++ in bone
