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 1^stline. 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).