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.
ACUTE
KIDNEY INJURY IN COVID-19
INTENSIVE CARE NEPHROLOGY
Revise please the abbreviation list on: https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372
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 & 3 )
1) 🠝C.O.
2) 🠝Natruresis.
3) 🠝Urine output.
4)
H.F. 🠟Sms.
5)
6)
Removal of🠟“Myocardial depressant” factor.
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:
COMMENTS