Renal (3) Flashcards
Fluid/Volume homeostasis numbers (we should know this by now)
Osmolar homeostasis:
- Mediated by osmolality-sensors in anterior hypothalamus
- stimulates thirst
- causes pituitary release of vasopressin
- Cardiac atria releases ANP
Volume homeostasis:
- Mediated by juxtaglomerular apparatus
- JGA senses change in volume - this triggers RAAS
What’s the difference in osmolar and volume homeostasis?
Osmolar is mediated by osmolality sensors in anterior hypothalamus; Volume is mediated by JGA
What percent of hospitalized patients are hyponatremic?
What are the common causes?
15%
Over fluid resuscitation and increased endogenous vasopressin
Hyponatremia algorithm:
Neurologial S/S of hyponatremia:
The most severe consequences of hyponatremia include:
Seizure, coma and death
Treatment for hyponatremia:
- treat underlying cause
- hypertonic/3% NaCl: 80 ml/hr over 15 hours
- slow and steady correction
Na+ correction should not exceed ___ mEq/L/hr
1.5
What can happen from rapid correction of hyponatremia (>6 mEq/L in 24 hours)?
Osmotic Demyelination Syndrome (often permanent neuro damage)
Treatment for hyponatremic seizures:
medical emergency
3-5 ml/kg of 3% over 20 minutes, until seizures resolve
Common causes of hypernatremia:
- excessive evaporation
- poor oral intake (very young, very old, ams)
- overcorrection of hyponatremia
- diabetes insipidus
- GI losses
- excessive sodium bicarb (treating acidosis)
Hypernatremia algorithm:
Symptoms of hypernatremia:
- orthostasis
- restlessness
- lethargy
- tremor, muscle twitching, spasticity
- seizures
- death
Treatment for hypernatremia:
- Route cause, assess volume status
- Hypovolemic = normal saline
- Euvolemic = water replacement (PO or D5W)
- Hypervolemic = diuretics
How fast do you want to reduce sodium in hypernatremic patients and why?
≤0.5 mmol/L/hr and≤ 10 mmol/L per day to avoid cerebral edema, seizures and neurological damage
What percentage of potassium is in the ECF?
<1.5%
Serum K reflects ____ K+ regulation more than ____ ____ K+
transmembrane; total body
What causes the distal nephron to secrete K+ (and reabsorb Na+)
Aldosterone
What happens to K+ excretion in renal failure?
K+ excretion declines - excretion shifts towards the GI system
Common causes of hypokalemia?
- Renal loss: diuretics, hyperaldosteronism
- GI loss: N/V/D, malabsorption
- Intracellular shift: alkalosis, B agonists, insulin
- DKA (osmotic diuresis)
- HCTZ
- Excessive licorice
3 major categories for cause of hypokalemia:
Renal loss, GI loss, transcellular shift
Symptoms of hypokalemia:
Generally cardiac and neuromuscular
- muscle weakness/cramps
- ileus
- dysrhythmias, U wave
Treatment for hypokalemia:
- Treat underlying cause
- Potassium PO > IV
- K given @ 10-20 mEq/L/hr IV
- avoid excessive insulin, beta agonists, bicarb, hyperventilation
How much does 10 meq IV K+ increase serum?
Each 10 meq increases serum K+ by ~0.1 mmol/L
Causes of hyperkalemia:
- Renal failure
- Hypoaldosteronism
- Drugs that inhibit RAAS
- Drugs that inhibit K+ excretion
- Depolarizing NMB (sux)
- Acidosis (respiratory/metabolic)
- Cell death (trauma, tourniquet)
- Massive blood transfusion
How much does succinylcholine increase serum K+?
0.5-1 mEq/L
Symptoms of hyperkalemia:
- Chronic may be minimally symptomatic (malaise, GI upset)
- Skeletal muscle paralysis, decreased fine motor
- Cardiac dysrhythmias
EKG progression in hyperkalemia:
- peaked T wave
- P wave disappearance
- prolonged QRS complex
- sine waves
- asystole
Treatment for hyperkalemia:
- dialyze within 24h prior to surgery
- 1st initial treatment = calcium (stabilize cell membrane)
- hyperventilation
- Insulin +/- glucose
- Bicarb
- Loop diuretics
- Kayexalate (hours to days)
*avoid sux, hypoventilation, LR and K containing fluids
How does hyperventilation affect potassium levels?
Increase in pH by 0.1 will decrease K+ by 0.4-1.5 mmol/L
Where is calcium stored?
Only 1% of body’s calcium is in ECF; 99% is stored in bone
Why do we look at ionized calcium instead of serum?
60% of plasma calcium is protein bound to albumin and is rendered inactive - only ionized calcium is physiologically active
What is a normal iCa+?
1.2-1.38 mmol/L
What two things affect ionized calcium levels?
Albumin levels and pH
↑pH/Alkalosis = ↑Ca++ binding to albumin (therefore ↓iCa++)
What hormones regulate Ca++?
How do they work?
- Parathyroid hormone: increase GI absorption, renal absorption, and regulates bone/bloodstream levels
- Vitamin D: augments intestinal Ca++ absorption
- Calcitonin: promotes storage of Ca++ in bone
Causes of hypocalcemia:
- decreased PTH secretion
- Magnesium deficiency
- Low vitamin D or disorder of vitamin D metabolism
- Renal failure (kidneys don’t respond to PTH)
- Massive blood transfusion
What causes AKI and what is the time frame for development?
- Deterioration over hours- days
- Caused by failure to excrete nitrogenous waste products or maintain fluid/e- homeostasis
AKI effects ____% of hospitalized patients and ___% of ICU patients
20%
50%
What is a hallmark of AKI?
Azotemia: Build up of nitrogenous waste products (urea, Creatinine)
What is the build up of nitrogenous waste products like urea and creatinine?
Azotemia
Is AKI reversible?
Yes, with timely interventions
What is the mortality rate of AKI with multisystem organ failure requiring dialysis?
50% mortality
What are the risk factors for developing AKI?
- Pre-exisiting renal disease
- Advanced age
- CHF
- PVD
- DM
- Sepsis (hypotension)
- Jaundice
- Major operative procedures
- IV contrast
What is the AKI diagnostic criteria?
- Increase Cr by 0.3 mg/dL in 48 hrs
- INcrease Cr by 50% within 7 days
- Decrease Creatinine clearance by 50%
- Abrupt oliguria (not always present)
What are physical symptoms of AKI?
*Asymptomatic
*Malaise
*Hypotension
*Hypovolemia/ hypervolemia
Differentiate pre-renal, renal, and postrenal AKI:
Prerenal: decreased renal perfusion
Renal: Nephron injury
Postrenal: Outflow obstruction (easiest to treat)
What are causes of pre, renal and postrenal azotemia
What is the most common form of AKI?
Pre-renal azotemia (1/2 of hospital acquired AKI cases)
What is usually the cause of pre-renal azotemia? What will labs look like?
Usually a volume issue (reversible)
*still reabsorbing Na+ and H2O)
Bun:Cr >20:1
What is the treatment for pre-renal azotemia?
Restore RBF: Fluids, mannitol, diuretics, maintain MAP
Can use vasopressors if needed (vasopressin)
How do anesthesia meds affect the kidneys?
Reduce renal blood flow
What are lab changes associated with renal azotemia?
- Decrease GFR (late sign)
- Decrease urea reabsorption in proximal tubule (Decrease BUN)
- Decrease creatinine filtration (increase creatinine)
- BUN:Cr <15:1
What is the cause of post renal azotemia? How can renal ultrasounds be useful for this?
Outflow obstruction: U/S shows hydronephrosis
Increased nephron tubular hydrostatic pressure
Is post renal azotemia reversible? What is the treatment?
Depends on duration of injury→ persistent obstruction damages tubular epithelium
TX: remove obstruction
What causes the neurological complications of AKI? What are some of the neurologic complications of AKI?
Protein/amino acid build up in the blood
Uremic encephalopathy
- Mobility disorders
- Myopathies
- Seizures
- Stroke
- Neuropathies
How does AKI impact CV system?
In order of incidence:
* HTN
* LVH
* CHF
* Ischemic heart disease
* Arrhythmias
* Pulmonary edema
* Uremic cardiomyopathy
What are hematologic complications of AKI?
Anemia:
* Decreased EPO, RBC production, RBC survival
* Platelet dysfunction
* vWF disrupted by uremia
What can be given in preop to increase vWF and factor 8?
Prophylactic DDAVP if you think procedure has potential for increased blood loss
Tachyphylaxis with DDAVP
What are metabolic complications associated with AKI?
- Hyperkalemia
- Water/sodium imbalances
- Hypoalbuminemia
- Metabolic acidosis
- Malnutrition
- Hyperparathyroidism (over drive trying to stimulate kidney to reabsorb Ca++)
What vasopressor is the best option when treating hypotension in pt with AKI?
Vasopressin: Constricts efferent arteriole (better than alpha agonist for maintaining RBF)
What are anesthesia implications with AKI?
- Correct fluid/e- imbalances
- Volume with NS (No K+)
- Careful with colloids (albumin better)
- Maintain MAP
- Prophylactic NaHCO3
- Avoid drugs with active metabolites, decreases RBF and renal toxins
- Recent labs (K+)
- Dialysis preop (may need postop)
What are the benefits of prophylactic sodium bicarb in patients with AKI?
- Decreases formation of free radicals
- Prevents ATN from causing renal failure
How is CKD different from AKI?
CKD is progressive and irreversible
What are the leading causes of CKD?
DM and HTN
What are the common surgeries for patients with CKD?
- HD access
- Toe/foot debridement and amputations
- Non-healing wounds
How many stages of CKD are there? What is the GFR associated with each stage?
5
How does CKD impact CV system?
- Systemic hypertension (retaining sodium and water)
- Activation of RAAS (HTN)
- Dyslipidemia
- predisposed to silent MI
What is the 1st line treatment for HTN from CKD?
Thiazide diuretics
(many need ACE-i/ ARB–often used in CKD)
Why dont we like ACE-inhibitors and ARBs?
- Decrease systemic BP
want to hold on day of surgery to reduce risk of profound hypotension (have all pressors ready if either of these meds are on board)
Which patients are high risk for silent MI?
women/DM
Dyslipidemia with CKD often causes TG >_____ and LDL >______
TG >500
LDL >100
How does CKD affect hematologic system?
Anemia
- EPO to target hgb 10
- Platelet dysfunction (platelets dont survive in uremic environment)
- Transfusion (excess hgb leads to sluggish circulation)
Why are potential transfusion risks in patients with CKD?
- sluggish circulation with increased hgb
- Acidosis
- Hyperkalemia
When should dialysis be considered?
- Volume overload
- Severe hyperkalemia
- Metabolic acidosis
- Symptomatic uremia (encephalopathy)
- Failure to clear meds
Which is more efficient: HD or PD?
HD more efficient: PD is slower so less likely to cause hypotension
What is the leading cause of death in HD patients?
Infection (impaired immune system/healing)
Anesthesia concerns for patients with CKD:
- Stability of ESRD
- Body weight pre/post HD (within 24 hrs of surgery)
- BP
- glucose (A1C)
- Aspiration precautions (gastric u/s)
- Pressors
- Uremic bleeding
Which pressors are less effective in a patient with CKD?
Neo and ephedrine
What is the peak and duration of desmopressin?
P: 2-4 hours
D: 6-8 hours
What is the best NMB for renal patients? (Not dependent on renal elimination)
Nimbex (metabolized by plasma esterases)
Which meds are known to have active metabolites and should be avoided with renal patients?
- Morphine
- Demerol
What is renal dosing based on?
GFR
Which meds are lipid insoluble and are eliminated unchanged in urine?
Thiazide diuretics
Loop diuretics
Dig
ABX
prolonged duration of action–need renal dosing
What are some meds that rely on renal excretion? What might be a better NMB reversal for kidney patients?
Suggamedex
Morphine is ___% cleared through urine. Its active metabolites put renal patients at high risk of _______ _______.
40%
Respiratory depression (life threatening)
What is the main adverse effect of Demerol? How does normeperidine E1/2T compare to Demerol?
Neurotoxicity (tremor, nervousness, muscle twitches, seizures) → Need HD
Normeperidine half time 15-30 hours compared to demerol 1/2 time 2-4 hours
What are some preop concerns/considerations for patients with renal issues?
- K+ <5.5 mEq/L on elective surgery
- HD patients should be dialyzed within 24 hours of elective procedure
- Aspiration prophylaxis
- Decrease in RBF from anesthesia
- Blood loss activates baroreceptors (increase SNS)
- Catecholamine constrict afferent arteriole (decrease RBF)
- Long periods of hypotension decrease RBF
Majority of pts with hypercalcemia have ____ or ____.
Hyperparathyroid; cancer
- Hyperparathyroid serum Ca++ <11
- Cancer serum Ca++ >13
Less common causes of hypercalcemia:
- Vitamin D intoxication
- Milk-alkali syndrome (excessive GI Ca++ absorption)
- Granulomatous disease (sarcoidosis)
S/S of hypercalcemia:
- Confusion, lethargy
- Hypotonia,↓DTR
- Abd pain
- N/V
- Short QT interval
*Chronic ↑Ca++→ Hypercalciuria & nephrolithiasis
S/S of hypocalcemia:
- Paresthesias
- Irritability
- Hypotension
- Seizures
- Myocardial depression
- Prolonged QT interval
**life threatening complication = post-parathyroidectomy hypocalcemia induced laryngospasm
Causes of Hypo-magnesium:
- Low dietary intake or absorption
- Renal wasting
S/S of hypomagnesium
- Muscle weakness or excitation
- Seizures
- Ventricular dysrhythmia (polymorphic V-tach/torsades)
Treatment of hypomagnesium:
- Depends on severity of symptoms
- Slower infusions for less severe
- Torsades/seizure = 2g mag sulfate
Causes of hypermagnesium:
- very uncommon
- generally due to over treatment (Pre-eclampsia/eclampsia, pheochromocytoma)
S/S of hypermagnesium:
- 4-5 mEq/L = lethargy, N/V, flushing
- > 6 mEq/L: hypotension,↓DTR
- > 10 mEq/L: paralysis, apnea, heart blocks, cardiac arrest
Treatment for hypermagnesium:
- Diuresis
- IV calcium (stabilize cell membrane)
- Dialysis
What is the primary “functional/structural unit” of the kidney?
How many does each kidney have?
Nephron; each kidney has 1 million nephrons
Where are the kidneys located?
How is the right different?
Retroperitoneal between T12 and L4
- Right slightly caudal to left to accommodate liver
How much cardiac output do the kidneys receive?
20% or 1-1.25 L/min
What part receives majority of renal blood flow?
The outer layer/cortex - receives 85-90%
Which part of the nephron is vulnerable to necrosis from hypotension?
Loop of henle in the inner layer/medulla
Primary functions of the kidney:
- Regulates EC volume, osmolarity, composition
- Regulates BP (RAAS, ANP)
- Excretes toxins/metabolites
- Maintain acid/base balance
- Produces hormones
- Blood glucose homeostasis
What two things regulate volume and BP?
- RAAS→↑Na+/H20 reabsorption
- ANP→↑Na+/H20 reabsorption
What hormones are produced by the kidney?
Renin, erythropoietin, calcitriol, prostaglandins
What is the best measure for renal function over time?
Normal values?
Glomerular filtration rate; 125-140 mL/min
*heavily influences by hydration status
What is the most reliable measure of GFR?
Normal values?
Creatinine clearance;
110-140 mL/min
*creatinine freely filtered, not reabsorbed
Which lab value is good for acute monitoring and correlates with muscle mass?
Normal values?
Serum creatinine; 0.6-1.3 mg/dL
*can be influenced by high protein diet, supplements, muscle breakdown
In acute cases, double serum creatinine can mean drop in GFR by ___.
50%
Renal function lab: BUN
Normal values 10-20 mg/dL
- Urea is reabsorbed into blood
- BUN is affected by diet, intravascular volume
- Low BUN could mean malnourished or volume diluted
- high could mean high protein diet, dehydrates, GI bleed, trauma, muscle wasting
Renal function lab: BUN:creatinine ratio
Normal: 10:1
- BUN (reabsorbed) to creatinine (not reabsorbed)
- good measure of hydration status
Renal function lab: Proteinuria
Normal: <150 mg/dL
- >750 mg/day could suggest glomerular injury or UTI
Renal function lab: Specific gravity
Normal: 1.001-1.035
- comparing 1ml urine to 1ml distilled water
- measures nephron’s ability to concentrate urine
Volume status assessment:
*look at big picture for hydration status
- history and physical exam
- orthostatic pressure changes
-↓BE (wtf is this?)
-↑Lactate
- Drop in UOP is a late sign of volume loss
- UOP 30ml/hr; 0.5 ml/kg/hr
- Oliguria: <500mL in 24 hours
How to monitor volume status?
- US to assess IVC
- CVP, RAP
- LAP, PCWP
- PAP
- SVV
Considerations when using SVV to monitor fluid status
- Compares inspiratory vs. expiratory pressure
- Assumes ventilated patient
- Assumes sinus rhythm
