Q.466. So, what is your decision in a critically ill patient?
INTENSIVE CARE NEPHROLOGY
Revise please the abbreviation list on:
https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372
Q.466. So,
what is your decision in a critically ill patient?
A. Vol. resuscitation in critically
ill ptn. a both (colloid + crystalloid) prepared to hasten
volume restoration.
- Vasopressina only
given after:
Adequate fluid expansion.
No expected rise in B.P., so, use P.A.
cath. to keep PCWP= 12-16
mmhg. & CVP= 6-12. wch means =
Adequate vol. expansion.
- Persistent shock is expected
é:
1) A.M.I.
2) peripheral edema.
Q.467. Which
type of acidosis can be seen in hypovolemic shock?
A. [Lactic acidosis ] adue to tissue hypoperfusion is common in hypovolemic shock. Once volume resuscitation achieved:
🠉O2 balance &
🠟 acidosis (which: Myocardial contractility & response to catecholamines).
- Three
reasons a K myocardial contractility, in lactic acidosis:
1) Hypoxia.
2) Sepsis. &
3) Hypoperfusion.
Q.468. What
are the treatment recommendations in dealing with lactic
acidosis?
A. Many ptns. ttt. é (permissive
hypercapnea/Low tidal vol.) dev. acidosis: ttt. : of acidosis here é (Sod. bicarb.) is NOT
beneficial, as No
improvement is expected é hemodynamics
or catabolic response.
: Furthermore, Bicarbonate
inj.:
(1) Worsen “intracellular” acidosis,
beccause Co2 (produced when bicarb. react é acidosis), cn diffuse rapidly across
cell membrane, where as bicarb. cannot.
(2) Bicarb.
increase HB affinity to O2لازق in healthy
volunteers Dcreased O2 delivery.
So, Mangment of “lactic
acidosis” shd NOT
incl. Sodium bicarbonate.
Q.469. How can hypovolemic shock affect kidney function?
A.
AKI is common in hypovol. shock, kid. cn be
affected in “three” ways:
1) Diminished perfusion 🠞 RBF.= the Iry cause, early
cn be corrected by N.O. & P.G. a V.D., but later,
not working.
2) D.I.C. a microvasculer
thrombosis a Renal ischemia.
3) T.N.F.a & IL1 release & activation of C. cascadea AKI. (Revise Sepsis).
Summary:
{ R. hypoperfusion- DIC & R. ischemia- Cytokine & C. activation.
}.
Q.470.What is the incidence of sepsis in I.C.U.? How
much it can affect the kidney?
A. 10 % of I.C.U. ptn hv Sepsis. It is a common cause of AKI > ½
million/y. & account for 100’000 deaths.
Q.471.What is the sepsis cascade ?
A. {Infection > SIRS > Sepsis > Severe
Sepsis > Septic
Shock > MODS}
Q.472. Define
Sepsis cascade? (Lancet, 2005).
SIRS > two or more: °C > 38.5
or < 35, HR >90, RR >20, PCo2 < 32mmhg, WBCs > 12,000 /c.ml, or < 4,000/cml., immature (brand
neutrophil) >10%.
Sepsis> SIRS + [documeted infc. > blood- Ur.- sputum- wound - air under diaphragm.].
Sev. sepsis> [Sepsis + one organ dysfunction] mottled skin, cpll fragility>3 sec, U.O.<
0.5 ml /kg/h., RRT, Lactate> 2 mmol/L., abnormal ECG, DIC, ALI, ARDS, Echo. abnormality, Platt.<100,000 pl /ml.
Septic Shock >
Sever sepsis + one of: B.P.<60 mmhg or <80 if prev.H.T., after 20-30 ml/kg starch or 40-60 ml N.S. or PCWP=12-20 mmhg, Need for
Dopamine > 5 mg/kg/min, or Nor or Epinephrine <0.25 mg/kg/min. to kep B.P.>60 mmhg (80 in prev. H.T).
Refractory Sepsis:
Need for Dopamine > 15
ug/kg/min, or Nor. or Epinephrine > 0.25 mg/kg/min., to keep B.P.> 60 mmhg (80 in previous HT.).
Q.473.What
are the commonest sources of infection?
A. From 1960-70 > G-ve, but now G.+ve is the culprit.
Most common G+ve> S. aureus: 35%, Enterococci 20 %, coagulase-ve Staph 15 %.
The most common
G-ve> Escherichia coli: 25%, Klebsiella, 20 %, Pseudomonas aeruginosa
20%.
Q.474. Explain
the pathophysiology of sepsis?
A. Manif. of sepsis result fr. excessive inflmm. resp. to bacterial
organism:
G –ve: contain lipopolysaccharides > activation of macrophage & C. cascade.
G+ve: Exotoxin> activation of T-cell & macrophage & release
of cell mem-brane component >
Activation of the inflammatory process.
BOTH: Proinflammatory & anti-inflammatory
cytokines are released in response to bacterial invasion. It is
hypothesized that:
“Sepsis is a state of imbalance between
these two components, with pro-inflammatory
cytokines is overexpressed.”
Q.475. What
is the role of proinlflammatory cytokines in the
pathophysiology of sepsis?
A. Proinlflammatory cytokines > [TNFa– IL1B-IL6-IL8]> released in response to
infectious stimuli: TNFa– IL1B> wide
range effects incl.:> {activation
of macrophage , lymphocytes, reticulocytes, incr. expression of
adhesion molecules & incr. production of inflammatory cytokines.}
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