Q.541. What is the importance of biocompatible membranes in hemodialysis?
HEAMODIALYSIS
ESRD ptns are particularly vulnerable to severe
COVID-19 (older
age & high frequency of co-morbidity, e.g. DM & HT, in this cohort. The
ASN & ISN
hv issued guidelines and a list of resources to guide nephrologists to provide
life-sustaining DX care. These resources that continue to evolve are frequently
updated, including the following: early
recognition & isolation of individuals with respiratory Sm(s);
ptn separation & cohorting within waiting
areas and within DX unit; use of personal protective equipment in DX unit; with added measures for ptns with
confirmed/suspected COVID-19.
Q.541. What
is the importance of biocompatible membranes in hemodialysis?
A. Once chemical & cellular
components of blood come in contact é artificial DX. membraneØ an inflammatory✺ response, cn be induced. The less
biocompat-ible the membrane, the more likely to activate WBCs &
complement
cascade. Earlier studies: dialyzing ARF ptn.s é older
style non-biocombatible(cellulose-based )Dmembranes Ø é M.R.(25%),
comp. to synthetic membranes. Interestingly, external sources of
inflmm.Ø exacerbate
the underlying dis. processes &
interfere é normal R. recovery.
Q.542. What
are the recommended strategies for prevention of A/V. graft thrombosis?
A. Vascular
access stenosis of A/V graft is initiated
by endothelial cell injury, wch Ø upregulation of adhesion molecules on
the endothelial cell surface. Alth. unproven, measures to prevent neointimal hyperplasia as well as other pharmac-ologic ag. tht address some
of the elements underlying vascular stenosis may help prevent stenosis. High
risk ptn. of initial graft failure & at low risk
for bleedingØ
Start A [dipyridamole + aspirin].
Ptns at high risk of graft failure are those é P.H. of early
thrombosis (=3 m. fr. surgery) of a previous AV
graft. It’s reasonable to forego such therapy given the uncertainty concerning
the benefit & é risk of bleeding. We do NOT recommend warfarin for
prevention of thrombosis & failure of an AV graft. H.DX. ptn é very
early (24-48
h.s of surgery) or recurrent graft thrombosis é abs. of underlying
stenosis, we initiate an evaluation for a coagulation abnormality or
hypercoagulable state. Among selected ptns é such abn. Ø warfarin may be
appropriate..
Q543. What is the role of fish oil in prevention arteriovenous graft failure?
A.: Effect of fish oil (4 g/d.) on arteriovenous (AV) graft failure ws
assessed in a randomized multicenter study tht comp. the effect of fish oil or
placebo capsules taken four times/d. starting seven d.s after graft
creation. At 12 m. of follow-up, compared é placebo, fish
oil ws ass. é lower rate of graft failure, fewer thrombo-ses
& fewer intervenetions. Based upon these data, we sugg.: ttt é fish
oil for ptns who hv an AV graft.
Q.544. How
can the hemodynamic instability (Hypotension,
Hpt) during HDX. be clarified?
A. A.Sm.tc Hpt: 15-50 % Ø é morbidity, thr. two
Aclinical
patterns:
Episodic Hpt: é latter stages of DX. [vomiting, msc cramps & vagal
Sm. (yawning)].
Ch. Persistent Hpt é long-term ptn. é pre-Dx
systolic B.P.<100
mmHg.
ETIOLOGY:
1) Rapid dcr. in pl. osmolality, wch Ø
extracellular water to move into cells .
2) Rapid fluid removal to
attain "D.W.", esp. é large interdialytic wt. gains.
3) Inaccurate
determination of true "D.W.".
4) Autonomic neuropathy.
5) ê cardiac reserve.
6) Use
of acetate rather thn bicarbonate as a Dzt buffer.
7) Intake
of anti-H.T. medications tht cn impair CVS stability.
8) Use
of a lower Na+ concentration é
Dzt.
9) Sudden
release of adenosine dur. organ ischemia .
10)Ingestion
of a meal immediately before or during DX .
11)Arrhythmias/pericardial effusion
é tamponade, vol.-unresponsive Øê B.P.
12)Reactions to Dzr membrane, wch
Ø wheezing
&
dyspnea as well as Hpt.
13)
Incr. synthesis of endogenous vasodilators, such as N.O.
14)
High Mg. concentrations in Dzt.
15)
Failure to incr. pl. vasopressin levels .
Serious
dis.[ %
attention e.g.[
arrhyth., peric.tamponade, valvular diso., M.I., hemo-lysis, hge, septicemia
& air embolism].Whatever the cause, HDX.-ass.
Hpt [ é M.R.
Q.545. How
to manage? @ R
A. A.Sm.tic
Hpt ptn may suffer fr.[light-headedness, msc cramps, n. & v. & dys-pnea]. Ac.
management: UF Ø either
stopped or ê rate. Ptn shd be é Trend-elenburg position & ê QB.
Replace intravasc. vol. é mannitol or saline. We currently
use i.v. bolus of N.S. as 1stline. Further ttt is based upon
etiology, e.g. [occult sepsis, cardiac and/or pericardial
dis. & G.I. bleeding]. Ch. debilitating H.DX Hpt.
due to intolerance to rapid changes in bld vol. may tolerate gradual vol.
changes of P.D. or nocturnal HDX, or é time and/or frequency of HDX.
PREVENTION: Accurate
"D.W.": Adjust it empirically by trial &
error. It’s set at wt below wch unacceptable Sm., e.g. cramping, n. & v., or Hpt occ..“D.W”
is highly variable & fluctuate é intercurrent illnesses (e.g. Drr.
or infc.) & é changes in H.B. (Epo). Other modalities:[bld vol.
monitoring, U/S assessment of I.V.C., natriuretic peptide, extravasc. lung
water indices & bioimpedance]. Best studiesØ bioimpedance:
extra- & intracell.
vol. & total body water assess. Particular promiseØtechnique in wch continuous
intradialytic assess. are confined to the calf since excess extracellular
fluids is greater in L.L.. Steady, constant UF: DX machines
are equipped é accurate UF devicesØ
remove vol. steadily & evenly over sessions Ø tolerance of UF é fewer S.E. Some physicians use
modeling protocols :more (or less) wt is
removed at beginning/end of DX. Efficacy of U.F./sod. Mod-eling help in sp.
cases. Incr. wt. loss us. occ. é setting of a higher Dzt sod. conc..
ñ
Dzt sod. & sod. modeling: Higher
Dzt sod.(≥140 meq/L) hs bn among the most ü efficacious & best
tolerated thpies for episodic Hpt. Dzt êsod.Ømarked
êin
pl. osmo-lality dur. DX, protecting extracellular vol. by êosmotic
fluid loss into cells. Efficacy of higher Dzt
sod. inêHpt &
other untoward DX-related S.E. ws assessed in a blinded, crossover study: A
constant sod.of140meq/LLinear sod. ramping
(155-140 meq/L)Stepwise sod. ramping (155 meq/L /3 h.& 140 meq/L/ one
h.)Both sod. ramping protocols Ø
signif. but small decr.in No. of Hpt episodes comp.e constant Na+DX.K/DOQI 2005: limitations
of sod. modeling:[lacked correlation betw. bld vol.& onset
of Hpt, signif. individual &
interDX variations in sod. levels, thirst, wt gain & postDX
Hpt].
Combined sod. modeling & UF:UF
profiling is ch.ch. by UF being intermittently stopped or decr.
gradually, thereby Ø pl.
refilling. Combin. of UF & sod. profiling cn further enhance pl.
refilling; in turn, this cn Ø greater
stability during HDX.
Sequential UF & isovolemic DX: Maintenance
of pl. osmolality cn also be attained by initial UF alone (without DX) (isolated UF)
foll. by isovolemic DX in wch little or no further
fluid removal occ. due to êTMP.
This sequential procedure often allows large vol.
of fluid to be removed without inducing Hpt. This maneuver, however,
is difficult to perform in out ptn since it needs incr. time of DX.
HCO3Dzt buffer: HCO3 is
now widely available & adaptable to all new DX machines. Diff. in cost betw.
acetate & HCO3DX is minimal, while
B.P. is better maintained é HCO3. Acetate
accumulation in bld Ø V.D.
activity tht Ø dev.
of Hpt & -ve effects upon energy metabolism in the heart tht cn êcardiac function .
ºC control: Low DztºC: improve
hemodynamic stability byé CVS contractility & é v. tone.
Isothermic DX, in wch body ºC remains constant dur. HDX, may
prove useful in stabilizing B.P.. Obs. tht ch. HDF may hv improved
hemodynamic stability comp. to HDX may result directly fr. diff. energy
transfer profiles.
Improvement in CVS performance: Frequency
of DX-ass. hemodynamic instability is greatly incr. é P.H. of [H.F., cardiomegaly, or IHD] Øpoor L.V. performance,
and, importantly, êcardiac
reserve . CVS performance cn be éin the foll. ways:
1) Dzt Ca. However, éDzt Ca
may Ø hypercalcemia
& ê bone
turnover.
2) Using cool ºCHDX, wch cn also é vasc. resistance .
3) Correction of anemia with Epo.
Midodrine: Ptn é A.N.&
thosee sev. HDX Hpt not responsive to the above measures Ø selective a-1
adrenergic agonist midodrine Ø
effective & well tolerated.
Carnitine: ê
incidence of Hpt episodes & msc cramps. Avoid food: Food
ingestion on DX Ø
signif.ê systemic
vasc. resistance tht cn contribute to êin B.P. This effect is not
corrected by concurrent intake of caffeine. Adenosine release: = an
endogenous V.D. tht hs bn related to Hpt episodes on HDX. This is
cn be blunted by caffeine, wch act as adenosine receptor antagonist.
Adenosine
receptor antagonist, FK352, ws found to signif. ê episodes
of intradialytic Hpt . Vasopressin: Vasopressin release is not incr.
in HDX dur. vol. removal. Vasopressin signif. ass. é êincid.
of Sm.tc Hpt episodes & é fluid removal.
Generally, during COVID-19 pandemic, ptns receiving home DX should hv their
regular follow-up visits performed via telemedicine rather than in-clinic visits. Moreover, home
visits by health care professionals shd be minimized or hold. Pnts should hv at least
two weeks of DX supplies with proper medications in case they hv to self-isolation.
If in-person visit is clinically indicated,
proper infection control measures for the outpatient unit should be applied with
limitation of the number of ptns seen per day. Non-urgent procedures should be postponed.
The ASN has provided guidelines for nephrologists caring for hospitalized
patients requiring DX for ESRD and AKI, adherence to the suggested guidelines is advised:
Ptns e COVID-19
should be co-localized on a floor or ICU,
if possible. Co-localization within adjacent
rooms can enable one DX nurse to
simultaneously deliver DX for > one ptn. If ptn is in a negative-pressure isolation
room, then one HDX nurse will need to be dedicated for the care of that ptn in
a 1:1 nurse-to-ptn
ratio. If possible, ptns with suspected/confirmed COVID-19 who’re not critically ill shd be dialyzed in
their own isolation room rather than being transported to the in-ptn DX
unit.
Video & audio streams should be used to troubleshoot alarms from outside the room to minimize the need for DX nurse or the nephrologist to enter an isolation room. CRRT is preferred among critically ill ptns in ICU who hv ESRD/AKI. Even among ptns who’re hemodynamically stable and who cd tolerate intermittent HDX (IHD), CRRT or prolonged intermittent renal replacement therapy (PIRRT), also called sustained low-efficiency DX (SLED), should be performed instead, depending upon machine & staffing availability. As CRRT or PIRRT can be managed without 1:1 HDX support. This would potentially help decrease wastage of personal protective equipment and limit exposure among HDX nurses. With CRRT capacity overwhelming, CRRT machines can be used to deliver prolonged intermittent ttt (eg, 10 hs rather than continuous) with higher flow rates (eg, 40-50 mL/kg/h). This will enable CRRT machine to be more available for care of another ptn after terminal dysinfection. If available, HDX or CRRT machines are scarce, clinicians may need to consider ttt of AKI with PD. Ptns with suspected/confirmed COVID-19 who develop AKI, and an emphasis should be placed on optimizing volume status to exclude and ttt pre-renal (functional) AKI while avoiding hypervolemia, wch may worsen ptn’s respiratory status. Ptns with AKI with no need for DX should be managed on a limited contact bases. Physical evaluation and U/S studies should be coordinated e primary/consulting teams to minimize contact, as much as possible. Ptns receiving ACEi/ARBs) should continue their therapy (unless there’s a contra-indication e.g. hyperkalemia or hypotension). There’s no evidence that stopping ACEi/ARBs limit the severity of COVID-19. Pts e stage 4/5 CKD who’re referred for DX access placement should undergo their procedures as planned (not hv their planned procedure deferred).
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