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INTENSIVE CARE NEPHROLOGY

Q.456. What are the clinical manifestations of hypovolemic shock?

 

INTENSIVE CARE NEPHROLOGY

intensive care nephrology beyond basic intensive care unit nephrology nephrology and intensive care associates


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Q.456. What are the clinical manifestations of hypovolemic shock?

A. C.P.: Early: No hypotension, orthostatic hpt. is a reliable Sn., but : dry  m.m. & dcr. skin turgor [Less reliable but indicative of hypovolemia. Oliguria, peripheral cyanosis, smell of acetone, brown discoloration of m.m. (Addisonian Sns.) due to adrenal failure, cn also be found. Acidosis due to incr. lactate production  & DIC.[ microthrombosis & MODF, cn be observed.

Q.457. How to diagnose?

  A. Diagnosis: P.H. of trauma or blood loss  us. the Iry cause, but Don’t overlook Sepsis, cardiogenic shock, upper & lower endoscopy, chest x-ray (hemothorax, tension pneumothorax), peritoneal lavage (internal hge.), CBC, ECG., full bioch., P.t. & P.t.t.

Q.458. How to manage?

A. Management: The Iry goal is to restore the blood circulation vol. [ 🠝 tissue perfusion & oxygenation, through a large pore (central) i.v. catheter, even before diagnosis is made. Supanoral O2 delivery[ 🠝survival, but large amount blood TX. [🠝mortality, as does the application of pulm. a. cath.[ 🠝M.R. We us. depend on [ B.P.- s. lactate- metabolic acidosis.].

-  O2 tension (expiratory), found to be incr. in septicemia[ an indicator of Dysoxia = [inability to utilize O2], not hypoxia [ contribute to acidosis & organ failure. 

Q.459. What recent tools can be used in management of hypovolemic shock?

A. I. “Gastric Tonometry: nose [stomach[gastric P.H.: A low Phi (gastric PH),means two things:   

1)   Early indicator of reduced global O2 delivery (as splanchnic bed us. prone to hypoperfusion early) & hypoxia.

2)   Intestinal mucosal hypoxia[incr. mucosal permeability [Loss of mucosal barrier [ translocation of bacterial toxins & MODF.

     II. Sublingual “Caprometry [ for tissue perfusion [ not widely used.

Q.460.What else in management?

1)   Dc. Ketoacidosis [ i.v. insulin.

2)   Addisonian crises [i.v hydrocortisone.

3)   Lower G.I. bleeding [endoscopy/surgery.

4)   Oesphageal varices [[Somatostatin], injection sclerotherapy or Sengstaken-blakmore tube.

5)   Upper G.I. bleeding [ i.v. proton pump inhibitor, electrocautery, laser coagulation é nasogastric tttpy.

Q.461. How to start fluid resuscitation for hypovolemic shock?

A. Initially, both colloid (high molecular wt.) & crystalloid (electrolyte solut-ion) cn be used. Isotonic crystalloid [N.S. 0.9 %, ½ N.S. 0.45 %, Ringer’s solution (4 ml Eq/L. K+ & 28 mEq. Lactate] [ used for volume expansion.

: Don’t use Ringer’s sol. in:

             i.    R.F. Hyperkalemia.

            ii.    Liver cell failure [dged liver cannot convert lactate to bicarbonate.

- Once isotonic crystalloid infused [75 % of the vol. infused enter the interstit-ial fluid & 25% remain intravascular.

  : Large amounts of fluid are harmful:  

                                                                     i.    Risk of A.P.O.

                                                                    ii.    Peripheral edema.

                                                                   iii.    Impaired healing of wounds.

Q.462. Explain the role of colloid & hypertonic crystalloid in ttt. of hypo-volemic shock?

A. Hypertonic crystalloid: 3 %, 5 %, 7.5 % [Sodium chloride]= Pl. expanders   a they act thr. moving water fr. interstitium intravascular  Hypernatremia, water retention & cell dge.

- Colloid a  Also, pl. expander, as they’re macromolecules & retained intravascular greater than isotonic crystals.

Q.463. What are the colloids in common use?

 A. Colloids:

1)   Albumin: 69,000 dalton, hs ½ life=15-20 d., it serves as free radicle Scavenger  & incr. intravascular oncotic pressure a protect the lung & other organs fr. odema.       

2)   Dextran: Colloid ag. prepared fr. glucose polymer, dextran 40, 40.000 dalton, both  👉 histamine release fr. mast cells  a Anaphylactoid reaction.                                         

3)   Hydroxethyl starch: (Hetastarch)(HES 200) & (HES 450)anatural starch of highly branched glucopolymer .

4)   Glycogen:200,-450,000 dalton, Pl. ½ life= 17 d.(vol. expander like albumin).

5)   Penta starch: m.w. =260.000 a more volume expansion .

6)   Starch: Recently, proved to reduce cpll. leak after trauma & ischemia   odema formation. Both (HES )& (Pentastarch🠝🠝 Amylase.

7)   Newly administrated solutions:[ Na Cl. 75 % + Dextran 70]-[ NaCl + Dextran 60] – [N.S 7.5 + NES].            

Q.464. Compare colloid vs crystalloid?

   A. Colloids a theoretically better  &   B.P. faster than crystalloids:

*      One L. Dextran 70  👉 🠝🠝 intravascular volume  by  800 ml.

*      One L. HES                👉    🠝🠝   ,,           ,,       ,,   by 750 ml.

*      One L. Abumin 5%  👉  🠝🠝     ,,           ,,       ,,   by 500 ml.

*      One L. N.S.           👉  🠝🠝    ,,           ,,       ,,   by 180 ml.

-      Yet, in Sepsis  👉 Capill. leak , So, both [Albumin] & [N.S.] are equal.

-      Small amounts in AMI & to make A.P.O. é less incidence.

Q.465. What are the “disadvantages’’ of colloids?

   A. Disadvantages: 

1)   Anaphylactoid reaction.

2)   Albumin  👉 –ve inotrope.

3)   Albumin 👉 impair salt & water excretion.

4)   Colloid 👉 inhibit coagulation system cascade.

5)   HES 👉 Risk of AKI é sepsis (inadequate water supply).

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