Q.440. What is the role of “pulmonary cytokines” in AKI?

 INTENSIVE CARE NEPHROLOGY

Revise please the abbreviation list on:

https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372

Q.440. What is the role of “pulmonary cytokines” in AKI?

A. Pulm. cytokines🠊[TNFa, IL. 1,2,8, ,FIAT 128  , Interferon g , granulocyte,  macrophage colony stimulating f.] 🠊All have been associated é R. injury in ischmia/ reperfus-ion model.

Q.441. How to ttt. ARDS?

A. ttt. of ARDS, is mainly Supportive, but as Sepsis is the main culprit المتهم الرئيسي🠞thorough search of Septic foci is mandatory.

-ttt. is mainly by Mchanical.v., as the ARDS/Network recommended 🠞Mch.v. 🠞🠉Survival. 

-Goal: adequate Oxygenation to avoid further lung trauma through tidal vol.= 12-15 ml/min.

Q.442. What is the role of tidal volume magnitude on management of ARDS with R.F.?

A. Overdistension of the alveoli [ 🠉 airway pressure [ Ac. Lung injury (ALI).

-Ventilation é high pressure [[🠉 vsc. permeability, ac. inflmm., alv. hge, radio-graphic infiltrate]. Also, acycled large tidal vol.[ damage of the unaffected segment. So, according to [ARDS/NETW] [ LOTvv = (Low tidal vol. + Low airway  pressure) [ Survival benefit in ARDS. Ptn. cn tolerate high resp. rate (35 breath /min.) When arterial P.H. fell 🠋7.3 é resp. rate of 35 [ infuse [Sod. bicarb.].

- This LOTvv has important implication for Nephrologist caring (ARDS + R.F.). Permissive hypercapnea [ significant acidosis in a ptn. cannot excrete acid load(R.I.). , which necessitate the use of a high bicarb. bath dur. H.DX. or CRRT, as Intensivist will not allow incr. minute vol. to improve acid-base control.

Q.443. What is the role of THAM in the management of ARDS?

A. THAM:   ثَام السَّام [Tris- hydroxymethyl amino-methane]: a buffer that accept one proton per moleculeØ Generation of bicarb, but not Co2. It controls arterial P.H. without incr. Co2 in resp. acidosis. THAM excreted by the kidney, So, NOT used in R.F.

Q.444. What is the role of supra-normal O2 in the management of ARDS/ AKI?

A.  As there is No clear cut benefit to supranormal O2 delivery, wch require volume expansion, as fluid restriction c worsen non-pulmonary organ dysfunction & greatly incr. mortality. So, Maintain Euvolemia  thr.: ➳            {Wdge = 10-14 & CVP= 6-12 }  in ARDS /AKI  thr. use of fluids ð Maintenance of organ perfusion. 

Q.445. What is the role of “corticosteroids” in the management of ARDS?

  A. Glucocorticoids (Methyl prednisolone) hs beneficial anti-inflammation effect only in late stages ➳ Improve (persistent inflammation & fibroblast proliferation).

Q.446. What is the role of posture in the management of ARDS?

  A. Prone position[ to ventilate posterior lung region (whicch’re atelectatic & flooded). Ptn. rotated /12 h. [ improve gas exchange & oxygenation. 

Q.447. What else?

 A. Other tools:

1)         Surfactant: which. normally produced by (type II. pneumocytes) to allow patency of the alveoli at lower airway pressure. Animal studies: benefit fr. [surfactant spray] in animals & dose–dependent trends to lower morbidity & mortality in humans.         

2)         Inhaled N.O. [ Pulm. V.D. [ improves oxygenation, but not M.R.

3)         N-acetylcysteine I.V.  [ Dcreased No. of ac. lung injuries.

4)         IL10, Recombinant human platelet-deriving f.: under study.

5)         Partial Liquid ventilation é “fluorocarbon” liquid which. can dissolve 17 time more O2 compared to water [ encouraging results.

Q.448. Can u please summarize the aforementioned data for management of ARDS?

 A. YES: — Inshallah:

I.        ttt. of ARDS, is mainly Supportive, but as Sepsis is the main culprit 🠞thorough search of Septic foci is mandatory.

II.        Mechanical ventilation, ARDS/Network recommends 🠞Mch.v. 🠞🠝survival. 🠞adequate Oxygenation to avoid further ALI. thr. tidal Vol.= 12-15 ml/min.

III.        LOTvv = (Low tidal vol. + Low airway pressure) [ Survival benefit .  Ptn. can tolerate high R.R. (35 breath/min.) When arterial P.H. fell 🠋 7.3 é resp. rate of 35 [ infuse [Sod. bicarb.]. Maintain Euvolemia  through wdge =  10-14 & CVP= 6-12 in ARDS/AKI é fluids ð Maintenance of organ perfusion. 

IV.        Glucocorticoids (Methyl prednisolone) hs beneficial anti-inflammatory effect only in late stages ð Improve (persistent inflmm. & fibroblast proliferation).

V.        Prone position[ to ventilate posterior lung region (whichch’re atelectatic & flooded). Ptn. rotated /12 h. [ improve gas exchange & oxygenation.

VI.        Surfactant  [ Dose–dependent trends to lower morbidity & mortality.           

VII.        Inhaled N.O.[ Pulm. V.D. [ improves oxygenation, but not M.R.

VIII.        I.V. N-acetylcysteine [ Dcr. No. of ac. lung injuries.

IX.        Partial Liquid ventilation é  “fluorocarbon” liquid.

 

Q.449. Define hypovolemic shock?

A. Hypovolemic shock: [Reduction in effective circulating blood vol.🠞O2 def. in tissues 🠞imbalance betw. O2 demands & O2 supply]🠞Reduction in cell metabolism + Anaerobic metabolism🠞accumulation of CO2 & waste products (lactates)🠞Cell death.

Q.450. What are the possible causes of hypovolemic shock?

   A. Etiology:

1)   External: [trauma, massive hematuria, G.I. bleeding].

2)   Internal: [Aortic hge, dissection, splenic & liver laceration].

3)   Fluid Loss: [Dc. Ketoacidosis-Burns- Adrenal crises].

4)   Lack of volume replacement: [Coma-debilitating elderly].

Q.451. What is the effect of the rate of body fluid loss on its development?

   A. Once 10 % of body fluid lost 🠞Compensatory mechanisms starts.

      - Loss of 40 %   or 25% rapidly🠞[Hypotension & Shock] occur.

Q.452. What are the possible compensatory mechanisms?

   A. “Compensatory mechanisms” to shock: To:

1)   Maximize I.V. volume:

                   i. Renal Adaptation:                

     🠉  ADH.

      🠉Aldosterone.

         ii. Redistribution of i.v. fluids fr. intracelluler & interstitial compartments.

2)   Maximize B.P. 🠞🠉(Symp. activity/catecholamines- Ang.II.- ADH).

3)   Maximize C.O. 🠞(Sympathetic stimulation & incr. contractility).

4)   Maximize O2 delivery:[🠉RBC 2,3 DPG – Metabolic acidosis- Dcr. tissue O2 level].

  The end- result of these mechanisms is to:

           * Dcr. blood flow to a [KIDNEY- Skin- Intestine- Skeletal muscle].

       & to                * Increased blood flow to [Brain & Heart].

Q.453. What is the importance of blood lactate measure in evaluation of hypovolemic shock?

   A. “Blood lactate” [is an indicator of “tissue hypoxia”, it represents a balance between (Lactate production) & (Lactate consumption) by the liver.

Q.454. What is reperfusion injury? How can it will be harmful to vital organs?

A. Although restoration of organ reperfusion is essential for organ function, reperfusion itself cn [ Organ Dge.   .. Once ischemic tissues perfused [ Reactive O2 species formed [ Direct cell membrane dge by:      

      

1)   Lipid peroxidation.

2)   Leukocyte activation & transmigration by stimulating  [ leukocyte adhesion molecules expression.

      The activated leukocytes contribute to cell injury by release of (protease, elastase & cytokines) wch. incr. [ microvascular permeability, edema & microthrombosis.

      Ischemia/reperfusion injury also activate complement [ Cytokine activation, incr. vascular permeability & edema.

      Data suggest: Ca+ influx é cells [ injury by dge of organelles [ inhibit respiration & activation of proteases & P.G.

Q.455.What are the expected drawbacks of reperfusion injury?

   A. Reperfusion injury can cause:     

1)   A. K. I.

2)   M.O.D.F.

3)   Hepatic failure.

4)   Myocardial Ischemia.

5)   Reperfusion arrhythmia.

6)   Breakdown of the Gut mucosal barrier.