Q.541. What is the importance of biocompatible membranes in hemodialysis?

 

HEMODIALYSIS

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Q.541. What is the importance of bio-compatible membranes in hemodialysis?

A. Once chemical & cellular components of blood come in contact é artificial DX. membrane ⮞ an inflammatory✺ response, can be induced. The less biocompatible the membrane, the more likely to activate WBCs & complement cascade. Earlier studies: dialyzing ARF ptn.s é older style non-biocombatible (cellulose-based )👎membranes ⮞🠝M.R.(25%), comp. to synthetic membranes. Interestingly, external sources of inflmm.⮞ 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, which ⮞ upregulation of adhesion molecules on the endothelial cell surface. Alth. unproven, measures to prevent neointimal hyperplasia as well as other pharmacologic 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 bleeding⮞Start ✌ [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 & 🠉 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 absorption of underlying stenosis, we initiate an evaluation for a coagulation abnormality or hypercoagulable state. Among selected ptns é such abnormal ⮞ warfarin may be appropriate..

 

Q543. What is the role of fish oil in prevention arterio-venous graft failure?

A.: Effect of fish oil (4 g/d.) on arterio-venous (AV) graft failure was assessed in a randomized multicenter study that 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 was ass. é lower rate of graft failure, fewer thromboses & fewer intervenetions. Based upon these data, we suggested: ttt é fish oil for ptns who have an AV graft. 

Q.544. How can the hemodynamic instability (Hypotension, Hpt) during HDX. be clarified?

A. A.Sm.tc Hpt: 15-50 % ⮞🠉morbidity, through two ✌ clinical 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 dcrease in pl. osmolality, which⮞ extracellular water to move into cells .

2)   Rapid fluid removal to attain "D.W.", espicially é large interdialytic wt. gains.

3)   Inaccurate determination of true "D.W.".

4)   Autonomic neuropathy.

5)  🠟 cardiac reserve.

6)   Use of acetate rather than bicarbonate as a Dzt buffer.

7)   Intake of anti-H.T. medications that can impair CVS stability.

8)   Use of a lower Na+ concentration é Dzt.

9)   Sudden release of adenosine duration organ ischemia .

10)Ingestion of a meal immediately before or during DX .

11)Arrhythmias/pericardial effusion é tamponade, vol.-unresponsive⮞🠟B.P.

12)Reactions to Dzr membrane, which ⮞ wheezing & dyspnea as well as Hpt.

13) Increase synthesis of endogenous vasodilators, such as N.O.

14) High Mg. concentrations in Dzt.

15) Failure to increase pl. vasopressin levels .

Serious diseases:[ e.g. attention e.g.[ arrhyth., pericardial tamponade, valvular disorders, M.I., hemolysis, hge, septicemia & air embolism]. Whatever the cause, HDX.-associated Hpt:🠉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 ⮞ either stopped or 🠟rate. Ptn should be é Trendelenburg position & 🠟 QB. Replace intravasc. volume 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 disease & G.I. bleeding]. Ch. debilitating H.DX Hpt. due to intolerance to rapid changes in blood vol. may tolerate gradual vol. changes of P.D. or nocturnal HDX, or 🠉time and/or frequency of HDX.

PREVENTION: Accurate "D.W.": Adjust it empirically by trial & error. It’s set at wt below which unacceptable Sm., e.g. cramping, n. & v., or Hpt occur.“D.W” is highly variable & fluctuate é intercurrent illnesses (e.g. Drr. or infection) & é changes in H.B. (Epo). Other modalities:[blood vol. monitoring, U/S assessment of I.V.C., natriuretic peptide, extravasc. lung water indices & bioimpedance]. Best studies⮞bioimpedance: extra- & intracell. vol. & total body water assess. Particular promise⮞technique in which 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 devices⮞remove vol. steadily & evenly over sessions ⮞ 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. Modeling help in sp. cases. Incr. wt. loss us. occ. é setting of a higher Dzt sod. conc..

🠉 Dzt sodium & sod. modeling: Higher Dzt sod.(≥140 meq/L) has been among the most  efficacious & best tolerated thpies for episodic  Hpt. Dzt 🠋 sodium⮞ marked 🠋in pl. osmolality dur. DX, protecting extracellular volume by🠋osmotic fluid loss into cells. Efficacy of higher Dzt sod. in 🠋Hpt & other untoward DX-related S.E. ws assessed in a blinded, crossover study: A constant sod.of140meq/LLinear sodium. ramping (155-140 meq/L) Stepwise sodium ramping (155 meq/L /3 h.& 140 meq/L/ one h.)Both sod. ramping protocols ⮞ signif. but small decreased in No. of Hpt episodes comp.e constant Na+DX.K/DOQI 2005: limitations of sod. modeling:[lacked correlation between blood volume & 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 ⮞pl. refilling. Combination of UF & sod. profiling can further enhance pl. refilling; in turn, this can ⮞ 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 occur due to 🠋TMP. 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 increased 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 blood ⮞V.D. activity that ⮞dev. of Hpt & -ve effects upon energy metabolism in the heart tht can 🠋cardiac function .

ºC control: Low DztºC: improve hemodynamic stability by🠉CVS contractility & 🠉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] ⮞ poor L.V. performance, and, importantly, 🠋cardiac reserve . CVS performance can be 🠉in  the following ways:

1)   Dzt Ca. However, 🠉Dzt Ca may ⮞ hypercalcemia &🠋bone turnover.

2)   Using cool ºCHDX, which can also 🠉vasc. resistance .

3)   Correction of anemia with Epo.

Midodrine: Ptn é A.N.& thosee severe HDX Hpt not responsive to the above measures ⮞ selective a-1 adrenergic agonist midodrine ⮞effective & well tolerated.

Carnitine:  🠋 incidence of Hpt episodes & msc cramps.     

Avoid food: Food ingestion on DX ⮞ signif.🠋 systemic vasc. resistance tht cn contribute to 🠋in 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, was found to signif. 🠋 episodes of intradialytic Hpt . Vasopressin: Vasopressin release is not incr. in HDX dur. vol. removal. Vasopressin significant ass. é 🠋 incid. of Sm.tc Hpt episodes & 🠉 fluid removal.