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INTENSIVE CARE NEPHROLOGY

Q.490.What is the goal-directed therapy in hemodynamic support?

 

ACUTE KIDNEY INJURY IN COVID-19

Suspected/confirmed COVID-19 may show an AKI as part of their overall illness. One meta-analysis of hospitalized 13,000 patients, AKI incidence = 17 %, despite the range of AKI incidence was broad (0.5-80 %). About 5 % of ptns required RRT. Incidence may vary by geographic location & % of critically ill ptns in each study.

Clinical characteristics & histopathology: Renal disease among ptns e COVID-19 can manifest as AKI, hematuria/proteinuria syndrome, with a higher risk of mortality (MR). It is unclear if AKI is mainly due to hemodynamic instability and cytokine release or if it is viral-induced direct cytotoxicity. In one observational study of 5449 COVID-19 ptns in New York, AKI was diagnosed in 37 %. Mild AKI (1.5- 2-fold rise in SCr) was observed in 47 %, moderate AKI in 22 %, & severe AKI (> tripled SCr) in 31 %. Hematuria/proteinuria syndrome was seen in 46 and 42 %. DX was required in 15 % of all ptns with AKI, and 97 % of ptns requiring DX were mechanically ventilated. AKI was noted on or within 24 hs of admission in one-third of ptns. AKI correlated with severity of illness; AKI was nearly universal among mechanically ventilated ptns (90 %) but was less common in ptns who’re not critically ill (22 %). Independent predictors of AKI include:

1)    DM,

2)    Older age,

3)    Black race,

4)    hypertension,

5)    CVS disease,

6)    Mechanical ventilation,

7)    Higher interleukin-6 level, and,

8)    Use of vasopressor medications. 

INTENSIVE CARE NEPHROLOGY


Q.490.What is the goal-directed therapy in hemodynamic support? 

A. Goal-directed therapy a use of the foll. end-points to improve M.R.:   ✌ ✌

  C.V.P.

  Hematocrit.

ƒ  Mean arter. B.P.

  C.V. O2  saturation.

- Tools:

1)   Dopamine & Nor. 1st choice in sepsis:Dopamine: limited use, as sepsis incr. its chrono. effect  tachycardia & arrhythmia. - Nor.: as effective as dopa. in  B.P, but less cardiac effect, it doesn’t  C.O. as dopa.

2)   Epinphrine: used in refractory hypotension, but  s. lactate.

3)   Vasopressin: of posterior pituitary V.C. & antidiuresis. It’s incr. (20-200) times in shock, it can spare Nor., B.P. & cardiac index.

-Alth. [Nor.]Profound glom. afferent V.C., [Vasopressin G. efferent V.C. GFR, but Vasopressin coronary V.C AMI. & has No +ve inotropic effect.

4)   Doputamine: can be used to O2, but can potentiate hpt., due to B2 V.D., it is recommended for low cardiac index (< 2.5 L/min/m2) after vol. resuscitation, but if B.P. 80 , it should be used with Nor., to mediate peripheral V.C.

Q.491. What are the recent recommendations in ttt of Sepsis?  

A. Early therapy é central venous O2 Saturation, ScvO2 = 70 % improve M.R., which accomplished by fluids to target C.V.P: 8-12, foll. é RBCs T.X. to target Hct of 30 % , foll. é Dobutamine infusion to a maximum 20 ug/kg/min, until  ScvO2 reaches 70 %.

- The surviving “Sepsis Campaign guide lines” now recomm. the foll. targets:

v CVP:   8-12                  

v MAP: 62  mmhg.      

v Hct.:   30 %

v Dobutamine:20  ug/kg/min.

v ScvO2:  70 %.

v Urine output:  0.5 ml/kg/h.

Q.492. Is there any specific recommendation in ttt of coagulation cascade in sepsis?        

A. No specific ttt, but if hge occur, use: [FFP- Cryoppt.- platelet infusion].

Q.493.What are “additional lines” of therapy of sepsis?        

A.  Additional lines of therapy:

1)   Activated protein C: decrease in sepsis, So, APC🠞restriction of risk of death.

2)   Immunomodulators: [hydrocortisone] 50 mg i.v./6 h.+ 50 ug fludrocortisone/d, via nasogastric tube /7d.  M.R.

-Low dose steroids 🠞(200-300) mg/d/7 d., divided, is recomm. in shock.

-Stimulation test🠞[ACTH] 250 ug. to determine response (>9 ug/d/dl. rise in cortisol, 30-60 min. after ACTH, steroids can be discontinued in these ptn. .

3)   Anti-TNF A.B.:  M.R., in ptn é [IL6] level of >1000  Pg/ml.

Q.494.What is the role of extracorporeal therapy in ttt of sepsis?         

 

A. Removal of cytokines (I.L.1, 6, 8 &TNFa] thr. hemofiltration   improves   outcome, but two points of interest:  

*      High production rate & slow endogenous clearance of cytokines, make the amount of cytokine removal  too small to change the circulatory level.                           

*      Adsorption  of cytokines to Dzr membrane Saturation after short time  Limit clearance.

** However, some studies é APACHE II score  improved outcome é:

[H.F.] + [Adsorption]+ [High volume U.F.]+ [frequent membrane change.]    Improve cytokine clearance.  

Q.495. Define cardiogenic shock?         

A. {A state of dcr. C.O. é setting of adequate intravascular vol. ] inadequate tissue perfusion}.

Q.496. Describe the clinical definition?        

A. Clinically cardiogenic shock:poor tissue perfusion e.g. oliguria, cold extremities + hemodynamic criteria (sustained hypotension), systolic B.P< 90 mmhg, reduced cardiac index < 2.2 L/min/m2 + Congestion (PCWP>18).

Q.497. What is the clinical picture of cardiogenic shock?        

A. C.P.: Universal hypotension, mean H.R.= 96 /min., S3, pulm. rales,   JVP + Sn of hypoperfusion(confusion- skin mottling- Oliguria), AKI occ. é 33 % of cases, MODF, M.R. >33-87% -  IL 6- hypoperfusion  Lactic acidosis.

Q.498. How to evaluate?        

A. AMI. é reduced L.V. systolic function: ECG, Echo., Foley’s catheter, cardiac enzymes, mitral regurge, papillary muscle dysfunction BNP(Brain Natriuretic peptide).

Q.499. How to manage?        

A. Airway- adequate O2-(Bi PAP= +ve Airway Pressure) or (CPAP)= continuous +ve airway Pressur- Stop BB. & Nitrates.  Use inotropes & Recombinant BNP.

Q.500. What is the role of inotropes in management of cardiogenic shock?   

A. Inotropes:

1)   Dobutamine: 1st choice, if systolic < 80 mmhg., B  agonist, but it’s weak B2 & a stimulant, it induces hpt. due to B2 effect, but worsen tachycardia.

2)   Dopamine: Useful é systolic <80 mmhg, é <5 mg/kg/min, B1 predominates, é dose increased  effect  more powerful  peripheral isch. & tachycardia.

3)   Norepinephrine:  pure a agonist, used é inadequate response to dopamine.

Q.501.What is the role of recombinant BNP (Brain Natriuretic Peptide)?        

A. Recomb. human BNP.  C.O.,  PCWP, systolic vasculer resistance, improves natriurisis & diuresis in decompensated H.F., it’ s FDA approved for NYHA IV. CHF., but C.I. in CKD, as it  decline GFR, if used é decompensated HF, … another study: No effect.

Q.502. Mention the other lines?        

A. I.A.B.P. (Intraaortic ballon Pumping)  improves diastolic pressure, cor-onary perfusion & é C.O.   .. However:            

1)   A.K.I. was NOT reported é I.A.B.P.

2)   A.K.I. reported é one 1/3rd of cardiogenic shock ptns., usually necessitating CRRT.

3)   Outcome of cardiogenic shock in AMI is directly rel. to the involved coronary.

Q.503.What is the role of extracorporeal therapy in this situation?        

A. U. F. by CRRT   proposed as a ttt. of Refractory H.F. even é normal R. function.

Q.504. Describe the magic beneficial impact of U.F. on the heart  & kidney?      👍🔔👍 

 

A. Cardiao/Renal benefits: (3   & )

1)   🠝C.O.

2)  🠝Natruresis.

3) 🠝Urine output.

4)     H.F. 🠟Sms.

5)     Shut down🠟of “neuroendocrine cycle  improves refractory H.F.

6)   Removal of🠟Myocardial depressant” factor.  

 
N.B.: Removal of fluids may not be totally tolerated by some R.I. ptns.   Permenatnt R.F., So, use U.F. cautiously.

 

Q.505. Explain how can the neuroendocrine system activation serve in worsening of H.F.?  

A. CRF 🠞Activation of the neuroendocrine system in response to decrease in effective circulatory volume, but it serves to worsen H.F.

- RAAS activation 🠞Na+ & water retention due to the following effects:

1)   Aldosterone secretion.

2)   Sympathetic N.S. activation.

3)   Arginin Vasopressin  (V.C.+ free water retention).

4)   Angio. II.🠞peripheral V.C.🠝L.V. wall stress & worsening of H.F.

Q.506.What is the sequence of events expected to occur as a result of diuretic resistance? 

A. Diuretic resistant ptn., é no pharmacological agent to remove fluids & potentially shut down the cycle of neuroendocrine activation & worsening of H.F. 🠝Ultrafiltration either intermittent or continuous is proposed

Q.507. When the maximum benefit of ultrafiltration could be expected?        

A. Renin, aldosterone & noradrenalin🠞highest é moderate/advanced H.F., NYHA III/IV. & U.O. < 1000 ml/min. So, U.F.🠞🠝 C.O. &  🠝 natriuresis with the greatest benefit can be harvested 👉lowest level of U.O.


Kidney histopathology was examined in an autopsy of 42 ptns died e COVID-19. Mean age was 72 ys; 88 % were > 60 ys. Co-morbidities, e.g. HT (73 %), DM (42 %), coronary artery or cerebrovascular dis (32%), obesity (31%), & CKD (29 %) were common. AKI (mostly stage 3) was noted in 31 of 33 ptns. Most ptns (62%) exhibited varying degrees of ATN, one hd collapsing focal segmental glomerulosclerosis (FSGS), & many show sequelae of their medical comorbidities (eg, HT nephron-sclerosis). ATN was the predominant kidney pathological finding in other studies. Some ptns show collapsing FSGS, called COVID-associated nephropathy (COVAN); such ptns may show nephrotic-range proteinuria. Presence of viral particles have been reported in the kidneys of COVID-19 ptns. However, these may instead be endosomal subcellular structures (eg, clathrin-coated vesicles and multivesicular bodies). Confirmatory ultrastructural in-situ hybridization used in other studies has failed to recognise the presence of virus in the kidney.

REFERENCES:

·  Yang X, Yu Y, Xu J, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med 2020; 8:475.

·  Chen T, Wu D, Chen H, et al. Clinical characteristics of 113 deceased patients with coronavirus disease 2019: retrospective study. BMJ 2020; 368:m1091.

·  Cheng Y, Luo R, Wang K, et al. Kidney disease is associated with in-hospital death of patients with COVID-19. Kidney Int 2020; 97:829.

·  Hirsch JS, Ng JH, Ross DW, et al. Acute kidney injury in patients hospitalized with COVID-19. Kidney Int 2020; 98:209.

·  Ng JJ, Luo Y, Phua K, Choong AMTL. Acute kidney injury in hospitalized patients with coronavirus disease 2019 (COVID-19): A meta-analysis. J Infect 2020; 81:647.

·  Robbins-Juarez SY, Qian L, King KL, et al. Outcomes for Patients With COVID-19 and Acute Kidney Injury: A Systematic Review and Meta-Analysis. Kidney Int Rep 2020; 5:1149.

·  Larsen CP, Bourne TD, Wilson JD, et al. Collapsing Glomerulopathy in a Patient With COVID-19. Kidney Int Rep 2020; 5:935.

·  Su H, Yang M, Wan C, et al. Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China. Kidney Int 2020; 98:219.

·  Kissling S, Rotman S, Gerber C, et al. Collapsing glomerulopathy in a COVID-19 patient. Kidney Int 2020; 98:228.

·  Pei G, Zhang Z, Peng J, et al. Renal Involvement and Early Prognosis in Patients with COVID-19 Pneumonia. J Am Soc Nephrol 2020; 31:1157.

·  Xia P, Wen Y, Duan Y, et al. Clinicopathological Features and Outcomes of Acute Kidney Injury in Critically Ill COVID-19 with Prolonged Disease Course: A Retrospective Cohort. J Am Soc Nephrol 2020; 31:2205.

·  Santoriello D, Khairallah P, Bomback AS, et al. Postmortem Kidney Pathology Findings in Patients with COVID-19. J Am Soc Nephrol 2020; 31:2158.

·  Kudose S, Batal I, Santoriello D, et al. Kidney Biopsy Findings in Patients with COVID-19. J Am Soc Nephrol 2020; 31:1959.

·  Sharma P, Uppal NN, Wanchoo R, et al. COVID-19-Associated Kidney Injury: A Case Series of Kidney Biopsy Findings. J Am Soc Nephrol 2020; 31:1948.

 

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