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:

1. 🠉O2 balance &
   

2. 🠟 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.}