Name: surgery le2 1
Uploaded: 2022-03-04
Duration: 17 min 4 s
Description: . . lNU COLLEGE OF MEDICINE DEPARTMENT OF SURGERY.

. . lNU COLLEGE OF MEDICINE DEPARTMENT OF SURGERY. 

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lNU COLLEGE OF MEDICINE 
DEPARTMENT OF SURGERY

Jose P. Bulatao Ill. M.D .. DPBS. FPSGS, FPCS. FPAHBSI

. . SHOCK. • The failure to meet the metabolic needs of the cell and the consequences that ensue.. 

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• The failure to meet the metabolic needs of the cell and the 
consequences that ensue.

• The init.ial cellular injury that occurs is reversible;

• however, the injury will become irreversible

. . Core principles in the management of patients in hemorrhagic shock. 

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Core principles in the management of patients in hemorrhagic shock

• (a) control of active hemorrhage must occur promptly

• (b) volume resuscitation with blood products (red blood cells. plasma. and platelets)

• (c) unrecognized or inadequately corrected hypoperfusion increases morbidity and

• ( d) excessive fluid resuscitation may exacerbate bleeding.

• Thus, both inadequate or unrestrained volume resuscitation are harmful.

. . Core principles in the management of patients in septic shock. 

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Core principles in the management of patients in septic shock

• (a) septic shock is an emergency, and rreatment/resusciction should begin as early as possible:

• (b) specific anatomic diagnosis of infection requiring emergent source control be identified or exduded as rapidly as 
possible and that any required source control intervention be implemented as soon as medically and logistically 
practical:

• (c) initiation of broad spectrum antibiotics within I hour of cfiagnosis:

• (d) in the resuscitation from sepsis-induced hypoperfusion. at least 30 mUkg of intravenous cryst:alloid fiuid be given

within the first 3 hours. and additional fiulds be guided by fr~nt reassessment of hemodyn:imic stitus:

• (e) vasopressors (noreplnephrine) should be added to achieve a me:in arterial pressure of 65 mmHg if fluid 
resusciotion Is inadequate.

. . CURRENT DEFINITIONS AND CHALLENGES. • A modern definition and approach to shock acknowledges that. 

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• A modern definition and approach to shock acknowledges that

• shoclk consists of inadequate tissue perfusion

• marked by decreased delivery of required metabolic substrates and inadequate

• This involves failure of oxidative metabolism that can involve defects of oxygen 
(0) delivery. transport. and/or utilization.

. . CURRENT DEFINITIONS AND CHALLENGES. • Current challenges include moving beyond fluid resuscitation based. 

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• Current challenges include moving beyond fluid resuscitation based

upon endpoints of tissue oxygenation and using therapeutic

strategies at the cellular and molecular level.

• Current investigations focus on determining the cellular events that

often occur in parallel to result in organ dysfunction, shocl<

. . PATHOPHYSIOLOGY OF SHOCK. • Regardless of etiology. the initial physiologic responses in shock are driven by. 

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• Regardless of etiology. the initial physiologic responses in shock are driven by

• tissue hypoperfusion and the developing cellular energy deficit.

• This imbalance between cellular supply and demand leads to

• neuroendocrine and inflammatory responses.

• the magnitude of which is usually proportional to the degree and duration of 
shock.

. . • Many of the organ-specific responses are aimed at maintaining perfusion in the cerebral and. 

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• Many of the organ-specific responses are aimed at maintaining perfusion in the cerebral and

• These are regulated at multiple levels including

• (a) stretch receptors and baroreceptors in the heart and vasculature (carotid sinus and

• (d) release of endogenous vasoconst:rictors.

• (e) shifting of fluid into the intra- vascular space. and

• (f) renal reabsorption and conservation of salt and water.

. . HYPO VO LEM IC/HEMORRHAGIC. • The most common cause of shock in the surgical or trauma patient is. 

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• The most common cause of shock in the surgical or trauma patient is

• loss of circulating volume from hemorrh.ige.

• Acute blood loss results in reflexive decreased baroreceptor stimulation from stretch receptors in the large

• decreased inhibition of vasoconstrictor centers in the brain stem.

• increased chemoreceptor stimulation of vasomotor centers. and

• diminished output from atrial stretch receptors.

• These changes increase vasoconstriction and peripheral arterial resistance.

. . HYPOVOLEMIC/'HEMORRHAGIC. • DIAGNOSIS. • The clinical signs: agitation, cool clammy extremities. tachycardia. weak or absent peripheral pulses. and hypocension. 

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• The clinical signs: agitation, cool clammy extremities. tachycardia. weak or absent peripheral pulses. and 
hypocension

• Such apparent clinical shock results from at least 25% to 30% loss of the blood volume.

• Patient is significantly cachycardic or hypotensive. this represents both significant blood loss and physiologic

. . HYPO VO LEM I C/'H EMO RR HAG IC. • DIAGNOSIS. 

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• Such apparent clinical shock r~ulu from at least 25% to 30% loss of the blood volume.

. . ble 5-5 lassification of hemorrhage. CLASS. ARAMETER l II Ill IV. 

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:lood loss (mL) 
<750 
750-1500 
1500-2000 
>2000

lean rn1c (bpm) 
<100 
>100 
>120 
I >14o

ilood pressure 
Nom13J 
Orthosutic 
Hypo1ension 
Severe hypotension

:NS sy1npto1ns 
Nonna! 
Anxious 
Confu.~ 
Obtunded

pm= bc:.3U per minute; CNS = cencnl ncn'OUS S)'Stem.

. . TABLE 3·1 SIGNS ANO SYMPTOMS OF HEMORRHAGE BY CLASS. 

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TABLE 3·1 SIGNS ANO SYMPTOMS OF HEMORRHAGE BY CLASS

PARAMETER 
Cl.ASS I 
0 ass II (MllDJ 
CMOOEUTEJ 
CSEVEA.E)

Gl.1$!()W Com.a Sate score: 
•• 
' 
l 
.

Bue defldt" 
G to -1 mEc;.ll 
-2to ➔ m£tvl 
~ to -10 rnE.q/l 
-10 mE q/L or le»

Ne~ for blood products 
Monlto~ 
~"'lblc 
Yes 
MkSsl¥1e Tr,nsfui,on

. . TREATMENT. • Control of ongoing hemorrhage is an essential component of the resuscitation of the patient in. 

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• Control of ongoing hemorrhage is an essential component of the resuscitation of the patient in

• The appropriate priorities in these patients are as follows:

• (a) control the source of blood loss.

• (b) perform IV volume resuscitation with blood products in the hypotensive patient. and

. . • In trauma. identifying the body cavity harboring active hemorrhage will help focus. 

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• In trauma. identifying the body cavity harboring active hemorrhage will help focus

• however. because time is of the essence,

• diagnostic laparotomy or thoracotomy may be indicated.

• The actively bleeding patient cannot be resuscitated until control of ongoing hemorrhage

• Our current understanding has led to the management strategy known as damage control

. . DAMAGE CONTROL RESUSCITATION. , This strategy begins in the emergency department. continues into the operating room. and into the intensive. 

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, This strategy begins in the emergency department. continues into the operating room. and into the intensive

• PHASE I: EMERGENCY DEPARTMENT ASSESSMENT

• PHASE Ill: INTENSIVE CARE RESUSCITATION

, Initial resuscitation is limited to keep SBP around 80 to 90 mm.Hg.

. . Reasonable conclusions in the setting of uncontrolled hemorrhage include. 

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Reasonable conclusions in the setting of uncontrolled hemorrhage include

• (a) any delay in surgery for control of hemorrhage increases mortality;

• (b) with uncontrolled hemorrhage. attempting to achieve normal blood pressure may

increase mortality. particularly with penetrating injuries and short transport times:

• (c) a goal of SBP of 80 to 90 mmHg may be adequate in the patient with penetrating injury;

• (d) profound hemodilution should be avoided by early transfusion of red blood cells.

. . • Data also support the use of antifibrinolytic agents in bleeding trauma patients, specifically tranexamic acid.. 

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• Data also support the use of antifibrinolytic agents in bleeding trauma 
patients, specifically tranexamic acid.

• The multinational Clinical Randomization of an Antifibrinolytic in

Significant Haemorrhage 2 (CRASH-2) trial suggested that early use of 
Tranexamic Acid

• limits rebleeding and reduces mortality.

. . . . . . . , (..__A_c_id_o_s_is _ _.). Improved perfusion Reversal of hypothermia Reversal of coagulopathy Continued (gentle) resuscitation. 

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Improved perfusion 
Reversal of hypothermia 
Reversal of coagulopathy 
Continued (gentle) resuscitation

.... _,,,-~~ [~--..] Warm blankets 
Hypothermia . Warm fluids 
Forced warm-air devices

· 
Vitamin K 
Calcium 
Limited use of crystalloids

. . TRAUMATIC SHOCK. • soft tissue injury. long bone injury, and blood loss. 

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• soft tissue injury. long bone injury, and blood loss

• hypoperfusion lead to the activation of inflammatory cells and the release of

• such as cytokines and intracellular molecules that modulate the immune

. . TRAUMATIC SHOCK. • Examples of traumatic shock include small volume hemorrhage accompanied. 

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• Examples of traumatic shock include small volume hemorrhage accompanied

• soft tissue injury (femur fracture, crush injury),

• or any combination of hypovolemic. neurogenic. cardiogenic, and

obstructive shock that precipitate rapidly progressive proinflammatory 
activation.

. . TRAUMATIC SHOCK. • Treatment of traumatic shock is focused on correction of the individual elements to diminish the cascade of proinflammatory activation, and includes prompt. 

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• Treatment of traumatic shock is focused on correction of the individual elements to 
diminish the cascade of proinflammatory activation, and includes prompt

• adequate volume resuscitation to correct oxygendebt.

• stabiliz_atjon of bony injuries, and appropriate treatment of soft tissue injuries.

. . SEPTIC SHOCK (Y ASODILATORY SHOCK). • The re.suit of dysfunction of the endothelium and vasculature secondary to. 

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• The re.suit of dysfunction of the endothelium and vasculature secondary to

circulating inflammatory mediators and cells or as a response to prolonged and

• Thus, hypotension re.suits from failure of the vascular smooth muscle to

• characterized by peripheral vasodilation with resultant hypotension and

resistance to treatment with vasopressors.

. . Table 5-6. Causes of septic and vasodilatory shock Systemic response to infection Noninfectious systemic inflammation Pancreatitis Bums Anaphylaxis Acute adrenal insufficiency . Prolonged, severe hypotension · Hemorrl1agic shock Cardiogenic shock Cardiopulmonary bypass Metabolic Hypoxic lactic acidosis Carbon monoxide poisoning. 

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Causes of septic and vasodilatory shock 
Systemic response to infection 
Noninfectious systemic inflammation 
Pancreatitis 
Bums 
Anaphylaxis 
Acute adrenal insufficiency 
. Prolonged, severe hypotension 
· 
Hemorrl1agic shock 
Cardiogenic shock 
Cardiopulmonary bypass 
Metabolic 
Hypoxic lactic acidosis 
Carbon monoxide poisoning

. . Table 5-6. Causes of septic and vasodilatory shock Systemic response to infection Noninfectious systemjc inflammation Pancreatitis Bums Anaphylaxis Acute adrenal insufficiency . Prolonged, severe hypotension · Hemorrhagic shock Cardiogenic shock Cardiopulmonary bypass Metabolic Hypoxic lactic acidosis Carbon monoxide poisoning. 

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Causes of septic and vasodilatory shock 
Systemic response to infection 
Noninfectious systemjc inflammation 
Pancreatitis 
Bums 
Anaphylaxis 
Acute adrenal insufficiency 
. Prolonged, severe hypotension 
· 
Hemorrhagic shock 
Cardiogenic shock 
Cardiopulmonary bypass 
Metabolic 
Hypoxic lactic acidosis 
Carbon monoxide poisoning

. . Septic shocl<. • By-product of the body's response to disruption of the host-microbe equilibrium,. 

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• By-product of the body's response to disruption of the host-microbe equilibrium,

resulting in invasive or severe localized infection.

• The vasodilatory effects are due, in part, to the upregulation of the inducible

isoform of nitric oxide synthase (iNOS or NOS 2) in the vessel wall.

• iNOS produces large quantities of nitric oxide for sustained periods of time.

• This potent vasodilator suppresses vascular tone and

• renders the vasculature resistant to the effects of vasoconstricting agents.

. . • DIAGNOSIS. • Patients with sepsis have evidence of an infection, as well as systemic signs of inflammation (e.g., fever, leukocytosis, and tachycardia).. 

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• Patients with sepsis have evidence of an infection, as well as systemic signs 
of inflammation (e.g., fever, leukocytosis, and tachycardia).

• Hypoperfusion with signs of organ dysfunction is termed severe sepsis.

• Septic shock requires the presence of the aforementioned signs,

associated with more significant evidence of tissue hypoperfusion and 
systemic hypotension.

. . . . Sequentiil or;an F.rilu,e A.ss:eurnent =. 

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P..OjFiO,. mmH; 
N00(".3) 
<.:00 (jlJJ 
<100(40) 
<200(26.7)wilh 
<100 (13.J) • 'Uh 
(\.1'2) 
resj!l:lllor)' ~ppor, 
ttipintDty W;,rM

Bilirubin. mgtc!L 
< 1.2 c=D) 
L2- L9 (20-32) 
2-5.9(33-101) 
&-1 1.9 ( 102-20!) 
>l:? (20,a)

CanflcmucvLar 
MAP ~70 
MAP<70mmHr 
Dopmm,c <.S « 
~ 
S.1-15 or 
Dopm1inc > 15 or

mmH; 
•tc-ib1tzminc 
cpiac,phri,,e sO.l or 
cpioq,hrit,c >0.1 or 
~sO.I 
D<'ll"t'J'UX'phri1X' >O. I

CNS 
GCSsc~c 
IS 
13-1~ 
10-12 
6--9 
<ti

Crc::ui .. -iine. mydl. 
<1.2 (110) 
t.2-1.91 110-170) 
2-3.-' ( 171- Z99) 
3.5-J.9(~) 
>5 ("'40) 
(µmolll.}

MAr. """"...,..'!ft.~ h01 •f,MUl,I ;,,,.,..,• .,,..,.,_ F,O,. tnct-d •i,,n,J ot)= c:xs •""""" ac:n- ,ru,m..GCS :ma.r-
e.,.,.. Sa.lo 
c-.-1,,,1......, ~ 
io Ri\-J.'mtOCllt 
!!!J.~ """ ;,er.,,•""'" INm \'.,..... IL ) S.- R. Tab:.& I, n al Tk SOFA CSq!.rwrlr...-d 0.X,., fwllff ,_...,._,....,... In do<nbc arp,, 
~
.:tiavb,:,ire. OIi bcNJI cl Ille ..,.<rti:,s C-.;, ,,., s.,,.. .. ~ 
r,-, d Cl< F.11..--orcu S<JC>CI) cl IIIICSIW •~ CM'< Mn!lc=. JAJ,,.,,.., C,,,.,

. . . . . ALTERED f.1ENTAL. STATUS. THREE CRITERIA. 

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. . • Recognizing septic shock begins with. • defining the patient at risk.. 

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• The clinical manifestations of septic shock will usually become evident and prompt 
the initiation of treaonent before bacteriologic confirmation of an organism or the 
source of an organism is identified.

• In addition to fever. tachycardia, and tachypnea, signs of hypoperfusion such as 
confusion, malaise. oliguria. or hypotension may be present.

. . • The.se should prompt an aggressive search for infection. including a. 

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• The.se should prompt an aggressive search for infection. including a

• evaluation of intravascular catheters or other foreign bodies.

• adjunctive imaging studies, as needed.

. . TREATMENT. Table 5-7. Surviving Sepsis Campaign bundles of care to be initiated within the first hour after presentation in the patient with sepsis93•94. 

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Surviving Sepsis Campaign bundles of care to be initiated 
within the first hour after presentation in the patient 
with sepsis93•94

Measure scnu11 lactate le\leJ. Remeasure if the initial lactate 
is >2 mn1ol/L 
Obtain blood culture prior to adn1inistrJtion of antibiotics 
Ad1ninister broad spectrum antibiotics 
Rapid administration of 30 ml.Jkg crystalloid for 
hypotcnsion or lactate (!4 mmoVL

Use vasoprcssors iJ the patient is h)rpotensive during or after

fluid resuscitation to maintain a mean arterial pressure 
(!65 n1mHg ...

. . CARDIOGENIC SHOCK. • Defined clinically as circulatory pump failure leading to diminished forward flow and subsequent tissue hypoxia, in the setting of adequate intravascular volume.. 

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• Defined clinically as circulatory pump failure leading to diminished forward flow and 
subsequent tissue hypoxia, in the setting of adequate intravascular volume.

• Most common cause of death in patients hospitalized with acute Ml.

• sustained hypotension (i.e .. SBP <90 mmHg for at least 30 minutes),

• reduced cardiac index (<2.2 Umin per square meter). and

• elevated pulmonary artery wedge pressure (> I 5 mm Hg)

. . . Causes of cardiogenic shock '-
Acute myocardial infarction Pump failure Mechanical complications. 