1
Q
List steps of water purification for dialysis
A
- Pretreatment
- Filtration, softening, pH neutralization
- Sediment filter – removes particulate matter such as clay, sand, sediment, contains multiple layers with variable pore sizes
- Carbon filter – removes chlorine, sediment, volatile organic compounds via adsorption
- Water softener – removes calcium and magnesium
- Filtration, softening, pH neutralization
- Purification – removes inorganic solute and bacteria and endotoxins
- Reverse osmosis
- Deionization
- Safety standards and monitoring – endotoxin retaining filter – reduce levels of bacterial fragments and endotoxins
- Distribution
2
Q
What are the types of PD membrane failure?
A
- UF Failure – transition to high transporter
- due to increase in membrane vascularity and effective surface area (as a result of glucose exposure, bioincompatible PD solutions, peritonitis episodes, systemic inflammation with uremia
- Loss of aquaporin
- Loss of membrane surface area
- due to adhesions and scarring after severe peritonitis or other intra-abdominal complication or peritoneal sclerosis
- Lymphatic reabsorption of dialysate
3
Q
Management of restless legs in dialysis patients
A
- Exercise, stretching
- Reduce caffeine intake
- Reduce/avoid meds associated with RLS (SSRIs, antidepressants)
- Treat iron deficiency
- Increase dialysis
- Dopamine agonists - pramipexole, ropinerole
- Alpha 2 delta calcium channel ligands - gabapentin, pregabalin
- Levodopa
- Benzodiazepines
4
Q
What are biocompatible PD solutions?
List 3 reasons for and 2 reasons against the use of these solutions
A
Neutral pH, low glucose degradation product (GDP) solutions
For: preservation of kidney fxn, preserve urine output, help with inflow pain assoc with low pH solutions for some patients(?)
Against: No effect on technique survival, no effect on mortality, increased cost
5
Q
What are the differences in clinical presentation and physical exam findings for inflow stenosis, outflow stenosis, and central vein stenosis?
A
See attached.
Also:
- Augmentation test - poor in inflow stenosis, good in outflow stenosis
- Arm elevation test: normal or accentuated collapse in inflow stenosis, no colapse in outflow stenosis
6
Q
Risk factors for DDS?
A
Extremes of age
First run
High urea >60
Pre-existing neurologic diseases (head trauma, stroke, seizure disorder)
Concomitant presence of other conditions that could be associated with cerebral edema (such as hyponatremia, hepatic encephalopathy, or hypertensive emergency)
Concomitant presence of another condition associated with increased permeability of the blood-brain barrier (such as sepsis, vasculitis, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, encephalitis, or meningitis)
7
Q
What did the IDEAL trial show?
A
- Early vs. late start HD (NEJM 2010)
- 828 adults randomized to start HD when GFR 10-14 or 5-7.
- No difference in survival or clinical outcomes between the groups.
8
Q
Mechanical vs. non-mechanical complications in PD
A
- A)Mechanical
- Clot
- Omental wrap
- Leak
- B) Non-mechanical
- Infection
- Eosinophilic allergic reaction
9
Q
How do you perform a PET test?
A
- Night dwell must be 8-12 hours. At start of test, drain night dwell over 20 minutes while sitting. Then instill 2L 2.5% dextrose dialysate over 10 minutes while supine, rolling side to side every 2 minutes.
- Once infused, obtain time 0h dialysate samples for glucose, urea, and creatinine
- At 2h obtain dialysate AND plasma samples for glucose, urea, and creatinine
- At 4h, obtain dialysate samples for glucose, urea, and creatinine
- Drain out dialysate over 20 minutes while sitting
- Measure drain volume
- Calculate:
- D/P Cr and plot over time (T0, T2, T4)
- D/D0 Glucose and plot over time (T0, T2, T4)
10
Q
How do you interpret a PET test?
A
- High D/P Cr, high D/P urea, low D/D0 glucose):
- High transporter
- Low D/P Cr, low D/P urea, high D/D0 glucose)
- Low transporter
- D/PCr
- >0.83 - High
- 0.65-0.82 - High average
- 0.5-0.62 - Low average
- <0.5 - Low
11
Q
What is the modified PET test for UF failure
A
2L of 4.25% - if in 4 hours they don’t UF >400mL, they have UFF. (4/4/4 rule)
12
Q
DDx for bloody peritoneal dialysate?
A
- DDx bloody dialysate
- Menstrual bleeding
- Encapsulating peritoneal sclerosis (important not-to-miss, consider if >1 year PD)
- Intra-abdominal or retroperitoneal pathology
- Splenic rupture/infarct, liver carcinomatosis/rupture, iliopsoas hematoma, bleeding from outer uterine wall in a pregnant patient, spontaneous rectal sheath hematoma
- Renal tumors, renal cyst rupture, retroperitoneal hematoma
- Catheter-related post-insertion
13
Q
Management of bloody dialysate
A
- Investigate cause
- Instil heparin in the dialysate to prevent clotting in the peritoneal catheter (not systemically absorbed so it will not increase risk of bleeding).
- Perform 2-3 rapid exchanges with room temp dialysate to cause peritoneal vasoconstriction and decrease bleeding.
- Stop antiplatelet/anticoagulants if it’s reasonable to do so.
14
Q
DDx eosinophilic peritonitis
A
- Bacterial peritonitis
- Fungal/parasitic peritonitis
- Chemical peritonitis, allergic reaction to some component of the PD system (plastics in the catheter, additives like heparin, antibiotics or dialysis bag, dialysis fluid itself)
- Icodextrin
- Systemic eosinophilia/eosinophilia of effluent eg. hypereosinophilic syndrome
- Malignancy
- Pneumoperitoneum (laparoscopic surgeries)
15
Q
Risk factors for ESP
A
- Duration of peritoneal dialysis
- Severe peritonitis, or recurrent and fungal
- Higher dialysate glucose concentrations, use of acetate as dialysate buffer, bioincompatible dialysate?
- UF failure
- Drugs – Bb, CNIs
16
Q
Management of ESP
A
- Steroids in inflammatory phase (eg. pred 40 mg daily x 4 months then taper)
- Anti-fibrotic (tamoxifen)
- Rest the peritoneum (4-12 weeks, depending on symptoms)
- Transition to HD or dual-modality PD/HD (symptoms may worsen after stopping PD)
- Parenteral nutritional support
- Surgery (adhesion lysis and excision of peritoneum) if acute obstruction
17
Q
Problems for high transporter vs. low transporter
A
- Hyperglycemia, dyslipidemia, truncal obesity
- Ultrafiltration
- More exposure to glucose-based dialysate due to more frequent exchanges
- Higher dialysate protein losses (lower serum albumin)
- Poor phosphate clearance (requires longer dwell times)
18
Q
What are biocompatible PD solutions?
A
- Neutral pH, low glucose degradation product (GDP) solutions
19
Q
Possible pros and cons for biocompatible PD solutions?
A
- Pros: preservation of kidney fxn, preserve urine output, help with inflow pain assoc with low pH solutions for some patients(?)
- Cons: No effect on technique survival, no effect on mortality, increased cost
20
Q
List reasons/clinical findings you would want to intervene/investgate fistula
A
- Shiny skin
- Non-healing ulcer or eschar
- Prolonged bleeding post-dialysis
- Increasing pain
- Rapid expansion in size
- Steal syndrome
- High-output heart failure
21
Q
List strategies to preserve vascular access
A
- Avoid peripheral blood draws (use dorsum of the hand whenever possible)
- Avoid PICC lines and midline catheters
- Avoid central lines, especially subclavian lines
- Avoid arterial cannulation of radial and brachial arteries (use other sites if needed for cardiac and other endovascular interventions)
- Avoid cardiac implantable devices (can affect patency of the central veins, and increase longterm risk of infection). Consider epicardial or subcutaneous lead placement.
22
Q
How does ischemic monomelic neuropathy present?
Who is at risk?
A
- Immediate onset after the AVF creation (pain, numbness), due to axonal nerve injury from ischemia
- Significantly more likely to occur in patients who have vascular access creation with brachial artery inflow
23
Q
Ischemic monomelic neuropathy vs. steal?
A
- In contrast to typical steal, patients with IMN have profound motor and sensory deficits without other associated manifestations of tissue ischemia such as tissue loss.
24
Q
How to diagnose ischemic monomelic neuropathy and manage?
A
- In contrast to typical steal, patients with IMN have profound motor and sensory deficits without other associated manifestations of tissue ischemia such as tissue loss.
- Needs immediate ligation
25
Causes of hypercalcemia in dialysis patients (other than meds)
* Tertiary hyperparathyroidism
* High calcium dialysate bath
* Non-PTH mediated hypercalcemia
* Multiple myeloma
* Bone metastases/malignancy
* Sarcoidosis
* Lymphoma
* Endocrine – hyper/hypothyroid, adrenal insufficiency
26
Side effect of ESA
1. Access thrombosis
2. CV events (MI/stroke)
3. Hypertension
4. ?malignancy
27
What is a filtration fraction?
Fraction of plasma removed by ultrafiltration
**FF = (UF rate x 100) / Qp**
where Qp = filter plasma flow rate (ml/min)
**Qp = Qb x(1 - Hct)**
A filtration fraction of \<30% limits haemoconcentration. Increasing the blood pump speed (Qb) will reduce the filtration fraction (aim for 20-30%) and make filter clotting less likely.
28
What is an icodextrin solution?
* A polyglucose solution, iso-osmolar and induces ultrafiltration by itsoncotic effect.
* Absorption of polyglucose is by the **lymphatics** and so is much slower compared with glucose.
* The oncotic effect and the associated ultrafiltration are therefore more sustained than with glucose.
29
Advantages of icodextrin solutions
Indications to use icodextrin?
Advantages:
* Better UF
* Better glycemic control, less weight gain, less dyslipidemia
* Potential preservation of membrane (less glucose exposure)
Indications:
* Long dwell exchanges
* Type 1 UF failure
* Diabetics
* CHF
30
Advantages of short daily dialysis over conventional dialysis?
1. LVH regression
2. Better BP control
3. Better volume control and hemodynamic stability on HD
4. Better small molecule clearance
5. Quality of life
31
Components of CRRT orders
* Mode of CRRT - CVVHDF, CVVH
* Dialyzer choice - ST140
* Dose of dialysis - 25-30 mL/kg/hr
* Access
* Qb 150-180 mL/min
* Qd, Qr - split dose of dialysis, (mL/hr)
* % Pre-filter or post-filter
* Replacement fluid choice - choose K and Ca
* Fluid balance goal
* Anticoagulation - citrate (140-180mL/hr) with post-filter Ca infusion, or heparin (250-500 U/hr) per protocol
* Lab monitoring - q6h lytes and iCa, daily Mg, phos, Cr, urea, albumin
32
Causes of prolonged AVF bleeding after dialysis?
1. Outflow stenosis
2. Aneurysm
3. Anticoagulation
4. Underlying bleeding disorder
5. Uremia
6. Traumatic needling
33
Management of HIT in dialysis patient?
1. Stop heparin during dialysis
2. Note in chart to prevent heparin locks at end. Citrate lock instead.
3. Increase Qb
4. Saline flush during HD
5. Consider HDF with prefilter replacement
6. Evaluate for thrombosis
7. Argatroban or bivalirudin
34
Causes of intradialytic hypertension?
* Volume overload
* Hyperactive renin-angiotensin system in response to fluid removal
* ESA given during HD
* High sodium dialysate
* Removal of antihypertensives during dialysis
35
Treatment of intradialytic hypertension?
Optimize target weight
Clonidine or captopril post-HD if SBP \>180
36
List consequences of intradialytic hypotension
* Increased mortality
* Decreased cardiac function/myocardial stunning
* Vascular access thrombosis
* Decline in residual renal function
* Volume overload
* CVA, cognitive impairment
* GI hypoperfusion
* Symptoms- cramping, N/V
37
Pros and Cons of AVF
* Pros
* Less infection
* Associated with less mortality
* More reliable Qb
* Longer patency
* Cons
* Time to mature
* Not able to create in all patients
* High output HF
* Steal syndrome
38
Pros and Cons of CVC
* Pros
* Immediate use
* Ease of insertion
* May be only possible access
* Cons
* Increased risk of infection
* Associated with higher mortality
39
Why PD over HD?
* Maintain vascular access for the future
* May provide higher likelihood of preserved renal function
* Better hemodynamic stability (eg. cardiorenal)
* Less exposure to anticoagulation
* More independence, quality of life, easier to travel
* Improved LV mass
* Less dietary restrictions
40
How to increase AVF use in your dialysis program?
* Vascular access preservation strategies
* Early surgical referral
* Vascular mapping to optimize AVF maturation
* Proper maintenance care to prevent failure (eg. thrombosis)
41
Immediate management of type A dialyzer reaction
1. Do not return blood
2. Bolus fluid
3. Epi IM (0.5mg or 0.1mg IV)
4. Benadryl
5. Ranitidine
6. Steroids
42
Prevention of type A dialyzer reaction
* Avoid ethylene oxide to sterilize membrane
* Sterilization methods – gamma radiation, steam, electron beam
* Avoid AN69 with ACEi membrane
* Monitor dialysis solution
* Make sure it’s not contaminated
* Avoid heparin at HD
* Switch to a different membrane
* Rinse the circuit
43
Features of amyloidosis in a dialysis patient
* Carpal Tunnel
* Scapulohumeral periarthritis
* Flexor tenosynovitis
* Destructive spondyloarthropathy
* Bone cysts
* Visceral
* Especially GI tract
* Cardiac (Rare)
* Peripheral neuropathy
* Macroglossia and difficult swallowing
44
Risk factors for dialysis-related amyloidosis
* Dialysis vintage
* Low flux dialyzers
* Bioincompatible membranes
* Lack of residual renal function
45
Indications for PD catheter removal
Refractory peritonitis
Relapsing peritonitis
Fungal or mycobacterial
Peritonitis with intraabdominal process (abscess, perf, bowel infarct)
Culture-negative + persistent symptoms + peritoneal WBC
46
6 ways to help dialysis patient with GI bleeding
1. DDAVP
2. Dialysis
3. IV Conjugated estrogens
4. EPO and iron to Hb \> 100
5. TXA
6. Platelet transfusion
7. RBC Transfusion
47
4 benefits of ultrapure dialysate
1. Decreased HD associated **amyloid**
2. Less incidence of **reactions** on dialysis
3. Improved **anemia** and utilization of ESA’s
4. Improved **inflammatory** markers
48
Characteristics of dialyzable solute
1. Low Protein Binding (\< 80%)
2. Low volume of distribution (Vd)
3. Low Molecular Weight
4. Higher water solubility
5. Lower Charge
49
Metabolic complications of high glucose peritoneal dialysate
* Hyperglycemia, increased insulin req'ts
* Increased weight gain
* Increased dyslipidemia
50
Chest pain, back pain, SOB and hypotension few min into dialysis - DDx
1. Dialyzer reaction, type A
2. Air emoblism
3. Hemolysis
4. ACS
5. Pulmonary embolism
6. Arrhythmia
7. Pericardial tamponade/uremic
51
Managementof calciphylaxis
1. Increase HD frequency
2. Non-calcium based phosphate binders
3. Stop warfarin
4. Parathyroidectomy
5. Cinacalcet
6. +/- Thiosulfate
7. Low dialysate calcium
8. Hyperbaric oxygen
9. Renal transplant
52
When to refer for diagnostic angiography for AVF?
* **Physical findings** suggestive of stenosis (persistent arm swelling, prolonged bleeding after needle withdrawal, collateral veins, and altered features of the pulse or thrill).
* Unexplained, persistent**, decreased Kt/V (\>0.2 units)** on a fixed dialysis prescription.
* Directly measured access flow rate \<**400 to 500 mL/min.**
* Noninvasive evidence of AV fistula abnormality.
* (KDOQI 2019 update)
53
What are the three features on vascular mapping which predict a successful AVF creation?
1. vein lumen diameter **\>2.5mm**, arterial lumen diameter **\>2.0mm**
2. **vein dilation test**: proximal vein occluded; want avg increase in internal diameter of 50%
3. arterial dilation test: triphasic arterial pulse contour changes to biphasic pattern when clenched fish for 2 min then hand opened (shows capable of healthy dilation)
4. brachial artery flow \>80mL/min
5. Negative Allen's test (patent palmar arch)
6. mapping; cephalic and ulnar venous systems evaluated for **continuity** and **absence of strictures**
54
A 20 year old patient has dialysis through a central line. The kt/V single pool is 2.0. What are 4 reasons for increased kt/V?
1. Recovery of residual kidney function
2. Low body mass (low V)
3. High flux dialyzer
4. Sample taken too early (not enough time post-dialysis to re-equilibrate)
55
3 different ways to diagnose/investigate peritoneal leak
1. Thoracentesis – send for glucose, add provodine-iodine to PD fluid
2. CT with intra-peritoneal dye
1. Need to be upright
3. Technicium99 labelled albumin into peritoneal cavity scan
1. Need to be upright
56
Risk factors for access failure
1. Older age
2. Hx diabetes
3. Female
4. Obesity (deep veins)
5. Hx vascular disease/cardiac disease
6. Low Blood pressure
7. Qb \<600 in AVF, \<1000 in graft
57
Features of beta2 microglobulin amyloid
* Carpal tunnel syndrome (CTS)
* Scapulohumeral periarthritis ("shoulder pad sign")
* Flexor tenosynovitis
* Destructive spondyloarthropathy (C-spine)
* Bone cysts
* Visceral involvement, particularly the gastrointestinal tract
* Macroglossia
* misc: cardiac, pulmonary, and cutaneous may be involved (rare)
58
Risk factors for dialysis-related amyloidosis
* Dialysis vintage and age
* Low flux dialyzer
* BioINcompatible membrane(eg. cellulose)
* Lack of residual kidney function
59
Treatment for dialysis-related amyloid
* Symptomatic (heat, ROM, NSAIDS, steroid injections)
* High flux hemodialyzer, ultrapure dialysate, biocompatible, and avoiding dialyzer reuse
* **Transplantation = only proven way to help**
* Otherwise, palliative/symptom-directed
60
Complications of high Hb in dialysis patient
* hypertension (rapid rise in Hb is a risk factor)
* seizures (with rapidly increasing Hb)
* graft clotting from higher blood viscosity
* dialysis urea clearance may decrease slightly (diminished proportion of plasma to red cell volume)
* hyperkalemia
* difficulty with serum phosphorus balance (probably because appetite improved and more dietary intake of phosphate)
61
Mechanism of ultrafiltration and composition of ultrafiltrate?
Hydrostatic/transmembrane pressure causes fluid to move from high pressure compartment to low pressure compartment.
Fluid is “cell-free” and similar in composition to serum.
62
Definition of IDH?
SBP drop 20 or MAP drop 10 with clinical symptoms, or
SBP \<90 (this has been a/w mortality)
63
Management of IDH
1. Minimize intradialytic weight gain (target \<1 kg/day with salt reduction), Lasix
2. Extend the length of dialysis by 30 minutes or increase frequency
3. Avoid oral food/glucose during dialysis
4. Use sequential ultrafiltration or sodium profiling
5. Decrease dialysate temperature to 35.5 degrees as tolerated
6. Hold antihypertensive meds before HD
7. Midodrine
64
79 year old woman with CKD stage 4 has exertional dyspnea, JVP 1 cm, no edema, clear lung fields. BP 170/55, SEM radiating to neck, normal carotid upstroke, +S4. Name three findings you would expect on echocardiogram
LVH
Aortic sclerosis
Diastolic dysfunction
65
Define recirculation
Percent recirculation = ([P - A] ÷ [P - V]) x 100
where P=plasma [solute], A is arterial line [solute], V is venous line [solute]
So if P=A, then recirc would be 0%
66
Cardiopulmonary recirculation
* When dialyzed blood returns via venous line -\> right heart -\> lungs -\> left heart -\> AVF arterial line, instead of going to capillary beds.
* Central venous urea concentration drops as dialyzed blood returns and dilutes the systemic urea circulation.
* Occurs only with AV access and when dialyzer is fed from an arterial access
67
Techniques of measuring recirculation?
* **Ultrasound velocity dilution (recommended by KDOQI)**
* Thermal dilution
* Optical dilution
* Conductivity dilution
* Potassium dilution
* Urea dilution
68
Pure red cell aplasia - diagnostic tests and management
* BMBx (erythryoid hypoplasia) and anti-EPO antibodies by ELISA
* Tx
* Stop ESA
* Transfuse prn
* Immunosuppression
* Steroids and CYC (or CNI or MMF) for about 3-4 months
* IVIG
* Kidney transplant if not responding
69
Signs that a dialyzer membrane is bioincompatible?
* Cellulose membranes activate complement more readily than synthetic or reused membranes.
* 1) **Type B dialyzer reaction**: chest pain, back pain, nausea, vomiting, hypotension (onset at 15-30 minutes after starting dialysis…..
* 2) Dialysis associated **hypoxemia** during early part of dialysis due to neutrophil sequesteration in lungs and associated leukopenia (peaks at 30 min, resolves after 2 hours)
* 3) Early activation of cellular mechanisms causing **neutropenia and lymphocytosis**
* 4) Activation of **complement cascade** with elevated levels of C3a, C5a
* 5) Release of **cytokines** such as TNF and IL-1 which cause: tissue catabolism, increased risk of infection, increased beta2 microglobulin generation, rapid loss of residual renal function
70
Primary findings of the ADEMEX trial
* ~1000 Mexican CAPD patients, mean weekly **Kt/V 1.62,** CrCl 45 ml/min vs. weekly **Kt/V 2.12,** CrCl 55
* **No difference in technique, patient survival, or quality of life** between the two groups even when adjusted for factors known to be associated with survival (age, diabetes, serum albumin, nPNA, anuria)
71
Ways to increase adequacy?
1. Increase dialysis time
2. Increase dialysis frequency
3. Increase dialyzer KoA
4. Increase Qb via increasing needle diameter
5. Ensure adequate anticoagulation
6. Increase Qd
72
Management of PD-related hydrothorax
1. Stop peritoneal dialysis
2. Repair of diaphragmatic defect **surgically**
3. Obliteration of pleural space with **pleurodesis**
4. Continued peritoneal dialysis with **small volumes in supine** position (decreased IPP) can sometimes be carried out without recurrence
73
Clinical signs of dialysis-related uremic pericarditis?
1. Pulsus paradoxus
2. Muffled heart sounds
3. Pericardial friction rub
4. (Elevated JVP, hypotension, tachycardia)
Pulsus paradoxus = The difference between the systolic pressure at which the first Korotkoff sounds are heard during expiration and the pressure at which they are heard throughout the respiratory cycle quantifies pulsus paradoxus. (\>10 mmHb is abnormal.)
74
Dialyzer membrane characteristics that affect solute clearance?
1. Surface area
2. **Dialyzer reuse**
3. Pore size (flux: impacts permeability, less important for small molecules)
4. **Permeability constant** (Ko) which is a **function of the material** (synthetic non-cellulose membranes have highest Ko)
75
Incidence of gram negative PD peritonitis? gram positive? culture-negative?
15% gram neg
50% gram pos
20% culture neg
76
Ways to assess nutritional status in HD patients
1. Patient history: symptoms that point to specific cause, **changes in body weight**, review of food intake, calorie counts
2. **Subjective global assessment** [Reproducible, correlates with outcomes]
3. **Predialysis urea, serum albumin, prealbumin, phosphate, cholesterol panel**
4. nPNA (Normalized protein equivalent of total nitrogen appearance), to estimate protein intake [Clinical utility not clear]
5. **Bioimpedance analysis**, predicts total body water and total body mass [Correlates with anthropometry and serum albumin]
6. DEXA: measures bone density and body fat [No evidence that it correlates with outcomes]
77
5 features of aluminum toxicity
1. Microcytic anemia (and epo resistance)
2. Impaired bone mineralization and bone and muscle pain (osteomalacia)
3. Hypercalcemia
4. Acute neurotoxicity (typically due to contaminated dialysate): myoclonus, mental status changes, speech disturbance, hallucinations, seizures
5. Dementia
78
HD patient falls and has hip fracture - causes?
1. Osteitis fibrosa cystica (hyperparathyroidism)
2. Adynamic bone disease (suppression of PTH or parathyroidectomy)
3. Osteomalacia (vitamin D deficiency)
4. Dialysis-related amyloid
5. Osteoporosis
79
Kt/V for PD calculation
Peritoneal Kt= (Dialysate/Plasma urea) x 24 hr drain volume
Renal Kt = (Urine/Plasma urea) x 24hr urine volume
**Total daily Kt = Peritoneal Kt + Renal Kt**
**Multiply by 7 to get weekly Kt**
**Divide by V to get weekly Kt/V**
(where V=volume of distribution using Watson's formula and IBW)
80
Causes of low Kt/V and causes of volume overload in PD patients
Causes of low Kt/V:
* Non-adherance/not doing PD
* Not enough PD exchanges
* Loss of residual renal function
* Type 1 and 2 UF failure
* Change in transporter status
Causes of volume overload in general in PD patient:
* Non-adherance with dialysis
* Inappropriate dialysate selection
* Non-compliance with dietary salt and fluid restriction
* Inappropriate or inadequate dialysis prescription for body habitus and amount of residual renal function
* Loss of residual renal function
* Type I ultrafiltration failure
* Mechanical complications (catheter dysfunction, diaphragmatic leak)
* Poor glucose control in diabetics
81
Management of type 1 UF failure?
* Shorten dwell time
* Increase fill volume.
* If on APD, shorten dwell time to 1-1.5 hour dwells and increase number of exchanges
* If on CAPD, shorten/split the nocturnal dwell in CAPD or switch to APD
* Icodextrin for long day well in APD or nocturnal dwell in CAPD (to improve osmotic gradient and minimize glucose exposure)
* Rest the peritoneum by temporary switch to hemodialysis
* If significant residual renal function, high dose diuretics (may help to increase urine volume, but not solute clearance)
* Hemodialysis if unsuccessful
82
DDx cloudy dialysate
1. Infectious peritonitis (primary or secondary/enteric peritonitis)
2. Excess fibrin production (at initiation of PD or after recent peritonitis)
3. After prolonged dwell
4. Chemical peritonitis
5. Eosinophilic peritonitis
6. Chylous ascites (SVC syndrome or other impaired lymphatic drainage)
7. Malignancy
83
Management of PD peritonitis and duration of therapy
* Initial empiric:
* **Vancomycin** 30 mg/kg actual body weight (1.5-2 g IP) _6 hr dwell_ (or Cefazolin 20 mg/kg ABW IP if vanco allergy)
* **Gentamicin** 0.6 mg/kg actual body weight IP _6 h dwell (_or **Ceftazidime** 1-1.5 g IP, or cipro 500 mg po bid)
* Duration:
* MSSA, MRSA – 3 weeks
* CONS, strep, culture-negative – 2 weeks
* Pseudomonas, Stenotrophomonas – double cover, 3-4 weeks
* Other gram neg bacilli – 3 weeks
* Mixed – 3 weeks
* Adjuncts:
* **IP heparin** 1000U/L with each exchange until dialysate clear
* **Antifungal prophylaxis:** PO nystatin 500,000U QID or fluconazole until 1 week post antibiotics
* Repeat cell count and cultures q 3 days until effluent clear?
84
Diagnosis of ESP?
* Clinical features + CT findings (peritoneal calcification, bowel thickening, bowel tethering, bowel dilatation)
* Confirmed on laparotomy/laparoscopy
85
Factors contributing to malnutrition in PD
* Underdialysis
* Protein losses
* Decreased intake due to dietary restrictions
* Decreased intake due to bloating/gastroparesis
* Acidosis
* Volume overload
* Acute/chronic illness
86
Causes/mechanisms for peritonitis in PD patients
1. Intraluminal: Improper technique for connections
2. Periluminal: bacterial colonization on skin surface enter peritoneal cavity
3. Transmural: Intestinal bacterial migrate through bowel wall during diarrhea/hernia/instrumentation of colon
4. Hematogenous: seeding from distant infection
5. Transvaginal: ascending infection
87
Common DDx for abdominal pain in PD patients
1. Abdominal fullness from dialysate
2. Peritonitis
3. Incarcerated hernia
4. Tunnel infection
5. Drain pain, infusion pain (low pH solutions)
88
Explanations/reasons for high Kt/V?
1. Dialysis dose prescribed greater than necessary for body weight
2. UKM blood sample drawn from venous (rather than arterial) port
3. UKM blood sample diluted with injected saline or transfused blood
4. UKM blood sample drawn (inappropriately) from access affected by recirculation
5. Significant **residual urea clearance** (Kr) if Kr contributed to spKt/V
6. Low volume of distribution/weight
89
Advantages and disadvantages of reusing dialyzers?
* Advantages of dialyzer reuse:
* **Decreased cost:** allows more widespread use of costlier dialyzers and cost reduction
* **Decreased first use syndrome**: reduced exposure to residual sterilizing compounds used by manufacturer etc (type A reaction b), reduced incidence of intradialytic symptoms, enhanced dialyzer biocompatibility and reduced immune system activation (less type b reactions)
* Disadvantages of dialyzer reuse:
* Potential for exposure of patient and personnel to **sterilizing chemicals**
* Potential for **contamination** of dialyzer
* Potential for **loss of dialyzer mass transfer and ultrafiltration capacity**
* Potential **loss of beta-2 microglobulin clearanc**e with certain reuse techniques
90
How does midodrine work and give 2 indications for its use?
* Alpha1 agonist Intradialytic hypotension and HRS type 1
* Indications for midodrine:
* Refractory intradialytic hypotension
* Midodrine
* Contraindicated if active cardiac ischemia
* Hepatorenal syndrome
* Combined with octreotide, improves renal and systemic hemodynamics
91
How does blood volume monitoring work?
* Use of an ultrasonic or optimal sensor operating on the inflow blood line to **detect changes in hematocrit** during dialysis which correlate with blood volume
* As fluid is removed, the hematocrit will increase
* Possible use is to anticipate and prevent hypotensive episode by reducing ultrafiltration when a limiting increase in hematocrit during dialysis has occurred
* May also play a role in identifying patients with ‘occult’ volume overload, by absence of change in hematocrit despite fluid removal
* No evidence to support its use
92
Causes of hyperkalemia in dialysis
1. Dietary non-compliance
2. Dialysis non-compliance
3. Decreased dialysis adequacy (due to recirculation or other factors)
4. Loss of residual renal function
5. New medication
6. Increased recirculation
93
Risk factors for nephrogenic systemic fibrosis
1. Dose (and type) of gadolinium
2. Altered kidney function (HD, PD, Advanced CKD, Poorly functioning renal transplant)
3. Concurrent proinflammatory condition (systemic infection, surgery, thrombosis etc.)
4. Erythropoietin therapy (relationship incompletely understood)
94
Advantages and disadvantages of CRRT
* Advantages of CRRT
* 1) Slow modality therefore gentle solute and UF removal which may be better tolerated by hemodynamically unstable patients
* 2) Allows for greater and more continuous volume removal
* 3) Continuous and more precise electrolyte control
* **4) Middle molecule clearance**
* 5) Less impact on IC pressure
* 6) ‘virtual space’ for meds etc. that can be managed easily due to continuous fluid removal
* 7) Regional anticoagulation possible
* 8) Can by done by ICU staff so resources are more centralized (do not require hemodialysis nurses or dialysis techs)
* Disadvantages of CRRT
* 1) Increased cost
* **2) Low efficiency**, therefore not appropriate for intoxications
* 3) Limited mobility for tests etc. as attached to dialyzer 24 hours per day
* 4) Only possible in ICU setting
95
Prophylactic strategies for recurrent PD exit site infections
* Patient education
* Topical mupirocin
* Prompt Rx of exit and tunnel infections
* **Prophylactic Abx at time of insertion**
* **Prophylaxis before colonoscopies and gynecolonogical procedures**
* Flush before fill systems
96
Prophylactic strategies to prevent recurrent CVC infections
* Aseptic insertion and handling of the catheters
* Elimination of nasal carriage of Staphylococcus aureas
* Mupirocin treatment of the catheter exit site
* Use of a chlorhexidine gluconate-impregnated sponge in intravenous catheter dressings
97
Rule of 6's for maturation of AVF
* At 6 weeks:
* Vein diameter \>= 6 mm
* Vein \<= 6 mm from skin
* Straight segment \>=6 cm for cannulation
* Qb \>=600 mL/min
98
Risk factors for AV access thrombosis
1. Hypercoagulable state
2. Flow less than 600 in AV fistula and less than 1000 in graft
3. IDH
4. Reccurent needling- eg nocturnal or short daily associated with more access loss
5. Venous stenosis
6. Hemoglobin above target as a result of EPO
99
Management of suspected air embolism in HD patient
1. Clamp venous blood line
2. Stop blood pump
3. Left lateral decubitus, head down (trap air in the RV)
4. Cardiorespiratory support with 100% oxygen
5. CT scan to work-up PE if still suspected based on clinical situation
6. If necessary, consult cardiology or vascular surgery to aspirate air from the atrium or ventricle with a percutaneously inserted needle
100
Approach to screening for AVF access failure?
1. Regular monitoring with physical exan and clinical indicators on dialysis
1. Exam: Arm swelling, dilated veins, aneurysm, abnormal thrill/bruit, etc.
2. Dialysis: prolonged bleeding after needle withdraw, unexplained drop in clearance, high arterial presure, etc.
2. Not enough evidence for routine AVF/AVG surveillance by measuring access flow, pressure monitoring, or imaging for stenosis (KDOQI 2019)
3. If there are abormalities detected on clinical monitoring:
1. Direct access flow measurements (often done by ultrasound dilution=transonics)
2. Duplex ultrasound
3. Angiogram
101
How can you have normal venous pressures on HD even with outlet stenosis of AVF?
Blood can return to the venous system via collateral veins so venous pressures may not increase with outlet stenosis
102
Besides usual probing, what are 4 ways to determine a pt’s dry weight on dialysis?
* Clinical volume assessment
* Post HD JVP
* Not peripheral edema
* US of IVC and JVP
* Lung US
* Normalization of BP
* Bioimpedance
* Blood volume monitoring with sodium profiling
* BNP
103
List 5 patient-related reasons for malnutrition on dialysis.
* Protein-Energy Wasting Syndrome
* Poor appetite from uremia
* Dialysis associated catabolism
* Dietary restrictions of dialysis
* Comorbid conditions and inflammation
* Metabolic derangements
* Insulin resistance
* Medications (ex phosphate binders)
104
Old guy on dialysis with new afib. Started on warfarin. Previous duodenal ulcer. No stroke. Hard to keep inr in range.
Two reason for a/c
Two reasons against a/c
* For
* Possible stroke risk reduction
* Reduced access thrombosis
* Against
* Increased bleed risk
* Lack of evidence for benefit
* Calciphylaxis risk
105
Causes of headache on dialysis
* Dialysis disequilibrium
* Caffeine withdrawal
* Hypotension/volume depletion
* Hypoglycemia
* Hyponatremia
* Hypernatremia
* Uremia
106
6 causes of pruritus in dialysis patients
1. Hyperparathyroidism
2. Malignancy – Leukemia, NHL
3. Uremia/Inadequate dialysis
4. Dialyzer reaction
5. Hematologic Puritis – IDA, PCV
6. Hepatitis/Liver Disease
107
6 non-pharmacologic treatment for pruritus?
1. UVB treatment
2. Parathyroidectomy
3. Increase diaysis time/frequency
4. Low phosphate diet
5. Topical emollient
6. Avoid excessive bathing, fragrance free soap
108
6 pharmacologic tx for pruritus
1. Capsaican cream
2. Tacrolimus cream
3. Pregabalin
4. Gabapentin
5. Hydroxyzine
6. Sertraline
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