Shock-TraumaResuscitation

Otmar Trentz, Zrich

Polytrauma
Polytrauma
Shock
Shock
Alimentation
Alimentation
Rhabdomyolysis
Rhabdomyolysis
Comp
. Syndr
. u.
Comp.
Syndr.
u. ACS
ACS
Traumatic
Traumatic brain
brain injury
injury

Polytrauma
Syndrome of multiple injuries exceeding a
defined severity (ISS 17), with
consecutive systemic reactions which may
lead to dysfunction or failure of remote,
primarily not injured, organs or vital
systems.

Polytrauma
Surgical
Surgical systemic
systemic disease
disease
pathophysiological understanding
complete resuscitation
correct triage
negotiated titration of care

Pathophysiology
Wound = inflammatory focus
Hypoxic zone
Dead
Tissue

Endocrine organ
Release of mediators
Systemic reaction

Cascade of defence mechanisms

Polytrauma
Systemic
Systemic reactions
reactions

Neuro-endocrine responses
Stimulation neuro-immune axis
Metabolic responses
SIRS
Shock
I/R injury

Trauma
Systemic Inflammatory
Response Syndrome
(SIRS)

physiologic
reversible

Host defense response

Host defense failure
disease

Damage healing
Death

pathophysiologic
irreversible

Systemic Inflammatory
Response Syndrome (SIRS)
Temperature >38C or <36C
Heart beat >90/min.
Respiration >20/min. or PaCO2 <4,3 kPa or ventilated
Leukocytes >12000 cells/mm2 or <4000 cells/mm2 or
>10% juvenile Granulocytes
Society of Critical Care Medicine Consensus Conference 1992

If at least 2 of these criterias during 3 consecutive

days
Ertel W. et al., Unfallchirurg 1993

SIRS - Definition
2 or more of the following 4 criteria:
Temperature:

>38.8C or <36.0C

Heart rate:

>90/min

Respiratory rate: >20/min or

PaCo2<32mmHg
PMNL:

>12.000/l or
<4000/l or
>10% juvenile PMNL

Hypoxia
Shock

Infection

Sepsis

SIRS Trauma
Hypotension

Burn
Injury

Second
Second
Hit
Hit

First
First
Hit
Hit

Late
Late
MOF
MOF

vulnerable

Tissue inury
+ shock

SIRS

Recovery
Recovery

Can not resuscitate

Early
Early
MOF
MOF

Primary objectives:
Survival
Normal cognitive functions
Avoid sepsis
Best available function

Killer
Exsanguinating hemorrhage
Tentorial herniation
Hypoxia
Sepsis

Primary survey
ATLS

Resuscitation
oxygenation, perfusion

Evaluation
vital functions?
Response ?

?
secondary survey

Life saving
surgery

Damage control
Bailout surgery
Scoring

ICU

Early total care

Life saving surgery

1. Access to life support system
2. Decompression of cavities
3. Control of exsanguinating hemorrhage
massive hemothorax
hemoperitoneum
crushed pelvis
central amputation

Damage control
The term Damage control is coined by
the US Navy and refers to keeping
afloat a badly damaged ship by
procedures to limit flooding, stabilize
the vessel, isolate fires and explosions
and avoid their spreading. These
measures permit damage assessment and
gain time to establish plans for
definitive salvage.

Rationale
Saving life by deferring
repair of anatomical
lesions and focussing on
restoring physiology.

Definition
Rapid abbreviated laparotomy to
stop hemorrhage and peritoneal
soiling and staged sequential repair
after ongoing resuscitation and
recovery from hypothermia,
coagulopathy, and acidosis.

Stone HH, Strom PR, Mullins RJ.

Management of the major
coagulopathy with onset during
laparotomy.
Ann Surg 1983;197.532-535
1983

10

Rotondo MF, Schwab CW, McGonigal

MD, Phillips,III GR, Fruchterman TM,
Kauder DR, Latenser BA, Angood PA.
Damage control: An approach for
improved survival in exsanguinating
penetrating abdominal injury.
J Trauma 1993;35:375-383
1993

Moore EE. Staged laparotomy for the

hypothermia, acidosis, and
coagulopathy syndrome.
Am J Surg 1996;172:405-410
1996
Moore EE, Burch JM, Franciose RJ,
OffnerPJ, Biffl WL. Staged
physiologic restoration and damage
control surgery.
World J Surg 1998;22:1184-1191
1998

11

Damage control
BailoutBailout-procedure
procedure::
Aborted termination of surgery in a
patient at imminent risk of death.
Preemptive intervention:
intervention:
Calculated early decision to
accomplish definitive correction of
injuries in staged sequential
procedures.

Indications for Damage control

control surgery
1.Physiological criteria hypothermia,
coagulopathy, acidosis.
2.Complex pattern of severe injuries
expecting major blood loss and a
prolonged reconstructive procedure in
an unstable patient.

12

Ancillary issues indicating benefits

of Damage control:
1.Limited experience of the surgical
team in complex injuries.
2.Limited resources in a mass
casualty.
3.Fatigued and overwhelmed surgical
team.

Cave: Over -utilisation of the concept

Selecting Damage control too
careless may mean an unnecessarily
premature termination of surgery in
patients who would otherwise have
recovered from a single definitive
procedure. It would subject the
patients to risks and expenses of
multiple surgical interventions.

13

Damage
control

Control of
Damage

done by lazy,
lingering-surgeons !

The concept of Staging is today

widely accepted and applies to
emergent and scheduled
procedures in the abdomen, pelvis,
chest, and neck as well as
extremities. The judicious surgeon
who chooses this approach must no
longer fear the whispered loss of
his surgical manhood.

14

Stage 1 - Patient selection for

abbreviated laparotomy
Hypothermia: < 34 C
Acidosis: pH < 7.2, Serum
Lactate > 5 mmol / L
Coagulopathy
Blood Pressure < 70 mm Hg
Transfusion approaching 15 Units
Injury Severity Score > 36

Combined vascular, solid and hollow organ

injury
Inaccessible major venous injury
Anticipated need for a time consuming
procedure
Demand for operative control of other
injuries
Inability to close the abdominal incision
Desire to reassess the intraabdominal
contents

15

Stage 2 Operative control of

haemorrhage and contamination
Haemorrhage control:
Repair or ligation for accessible
blood vessels
Inflow-occlusion by cross- clamping
or balloon-tamponade
Packing: 4 quadrants, perihepatic
packing
Intravascular shunting or stenting

Contamination control:
Ligation, suture or stapling of
bowels
Resection of damaged segments
with clips, clamps, or staples
Anastomoses and stomas have to
be deferred

16

Temporary abdominal closure:

Towel clips
Bogota Bag (temporary silo)
Opsite-Sandwich or Vacu-Seal
Mesh closure or Ethizip

Stage 3 Physiological
restoration in the ICU
Rewarming
Correction of coagulation
Correction of acidosis
Optimisation of oxygen delivery
Monitoring and avoidance of an
Abdominal Compartment Syndrome

17

Stage 4 Return to OR for

definitive surgery
Physiological restoration
Removal of packs and definitive repair
Persisting bleeding
Increasing intraabdominal pressure
Scheduled reoperation after repacking
and entensive gut distension due to
reperfusion

Stage 5 Reconstruction of
abdominal wall
Direct closure only without gut
distension
After fascial retraction subsequent
gradual vacuum-assisted closure
Mesh repair
In an hostile abdomen: gauze packing,
secondary granulation and skin grafting
Secondary plastic reconstruction

18

VACVAC
-Therapy and polytraumatized patients

19

Bailout Damage Control

Chest
Abdomen
Pelvis
Extremities

Control of Hemorrhage
Packing
Source control
Dbridement
External fixator
V.A.C.- Vacuum Sealing

20

Workhorse -Damage control

Pelvic ring fixation
Tamponade

True pelvis
Paracolic gutters
Ethizip + second look

21

Rationale of Packing
Main source of bleeding:
venous plexus !
Stable pelvic ring:
Abutment for tamponade !
Packing pelvis and paracolic gutters
Abdominal wall remains open
Monitoring ACS

22

Trauma

Abdomen 204
penetr.
71
blunt
133
Pelvis
Abdomen
+ Pelvis

Isolated /
Packing
Multiple

ACS

Survival

39/32
21/112

17 %
16 %

3%
5%

90 %
76 %

63

7/56

19 %

6%

80 %

44

0/44

25 %

9%

57 %

Ertel et al.: Crit Care Med 28: 1747, 2000

DC Injured Limbs
Dbridement, Fasciotomies
External fixator
Temporary intraluminal vascular shunts
Epigard, Vacuum-Sealing

23

Safe conditions: Early total care

Stable hemodynamics
No need for vasoactive/
inotropic stimulation
No hypoxemia, no hypercapnia
Lactate < 2 mmol/L
Normal coagulation
Normothermia
Urinary output > 1 mL/kg/hour

Physiological status Surgical intervention Timing

Response to
resuscitation:

Life saving surgery

?

"Damage control"

Early total care

Hyper-inflammation
"Window of
opportunity"

"Second look", only!

Scheduled definitive
surgery

Immunosuppression

No surgery!

Recovery

Secondary reconstructive
surgery

Day 1

Day 2-3
Day 5-10

Week 3

24

Shock

Definition
Reduced tissue perfusion leading to
generalized cellular hypoxia with a
persistent discrepancy between
delivery and consumption of oxygen.

25

Oxygen delivery
Intracellular ATP
Cell dysfunction
Cell death

reversible

irreversible

Trauma specific forms

Hemorrhagic shock
Cardiogenic shock
Spinal shock

Hemorrhagic shock and tissue injury

Traumatic-Hemorrhagic
Traumatic-Hemorrhagic shock
shock

26

Pathophysiological
alterations
Loss of fluid
Pump failure
Decreased vascular
resistance

Hemorrhagic shock
Symptoms
Symptoms
Tachycardia

Late symptoms in
young patients !!

Hypotension
Central venous pressure
Hemoglobin

Not occurring in early

posttraumatic period !!

27

TraumaticHemorrhagic shock
Blood
Blood loss
loss
<10%

complete compensation

10% - 25%

cardiac output

>25%

arterial blood pressure

Trauma-Cardiogenic
shock
Tension pneumothorax
Myocardial contusion
Cardiac tamponade
Vena caval obstruction

28

Cardiogenic shock
Symptoms
Symptoms
Hypotension
Tachycardia
Arrhythmia
Central venous pressure
Paradoxic pulse

Spinal shock
Symptoms
Symptoms
Hypotension
Pulse normal or decreased
Pulse feels strong
Skin dry and warm

29

Emergency treatment
Correction of oxygen availability

Fluid
Fluid replacement
replacement
Ventilation
Ventilation therapy
therapy
Vasoconstrictive
Vasoconstrictive and
and
cardiotropic
cardiotropic agents
agents

O2av = CO x O 2sat. x Hbconc. x 1.34

(mL/min) (mL/min) (%)

(g%)

1000 = 5.250 x 95

x 15

x 1.34

300 = 3.500 x 64

x 10

x 1.34

Oxygen debt !
Nunn JF, FreemanJ. Anaesthesia 1964;19:206

30

Alimentation

31

Disease Process

Change in
Metabolic
Activity (%)
100

50

50% Burn
20% Burn,
Infection,
Multiple Trauma
Long Bone Fracture

Normal

Postoperative

Flow phase
The body tries
to maximize gluconeogenesis
from all available sources !

32

Glucose the
sole source for energy
PMNL
RBC
Renal medulla
Bone marrow
RES
Neurons

Acute Nonstress Fasting Metabolism

Free Fatty
Acids

Fat
Fat
Source
Source

Triglyceride

Ketosis
Ketosis

Liver
Liver

Ketone
Bodies

Nonpreferred
Nonpreferred
Glucose
Glucose
Users
Users
(eg.
(eg. kidney,
kidney,
heart,
heart,
muscle
muscle

Glycogen
Glycogen

Glycerol
Lean
Lean Body
Body
Mass
Mass
Amino
Amino Acid
Acid
Stores
Stores

Amino
Acids

GluconeoGluconeogenesis
genesis

Urinary
Nitrogen

Lactate
Lactate

Glucose
Preferred
Preferred
Glucose
Glucose
Users
Users
(eg.
(eg. Brain,
Brain,
RBC)
RBC)

33

Muscle catabolism
Aminoacids:
substrate for gluconeogenesis
in the liver

Byproduct urea:
increased level of urinary urea
nitrogen

Early enteral nutrition

Gut access distal to the pylorus
Gastric suction tube
Transpyloric feeding tube
(Gastroscopic guidance)

34

Rhabdomyolysis

Rhabdomyolysis
Metabolic disturbances
acute renal failure (ARF)

35

Muscle injury
Trauma-mechanical/thermal
I/R-injury
Crush
Seizure
Drug abuse
Malignant hyperthermia

Symptoms
Cramping pain
Progressive weakness
(calves / lower back)
Discoloration of urine

36

Release
Purines (uric acid)
Sulfur-containing protein+hydrogen
(anion gap acidosis)
Creatine (creatinine+BUN)
Myglobine

Release
Aldolase
LDH
sGOT
Creatine-Kinase (CK)
CK-MB (7%)

37

Myoglobine
Not highly protein bound
Filtered at the glomeruli
50 g/L color visible in water
>100 mg/L color visible in urine
Serum concentrations >>>25 mg/L
>25 mg/L hemolysis

Plugging of renal tubuli

Low urine flow
Acidosis
Sludge or urate crystals and
ferrihemate (pH < 5.6)

Myoglobine converted to
ferrihemate
toxic and precipitation

38

Muscle cell lysis

Influx:
Efflux:

sodium + calcium
fluid
potassium + phosphate

Electrolyte
Electrolyte ++ fluid
fluid shifts
shifts
Severe
Severe hypovolemia
hypovolemia

Rhabdomyolysis
>>>ARF in 30 %
Hypovolemia
Free oxygen radicals
Plugging of renal rubuli

39

Therapy
Fluid resuscitation
Bicarbonate
(urine pH 8.0, serum pH 7.45)

Mannitol 25 g / every 6 hrs.

Furosemid 40 - 200 mg
CVVH (pump)

Compartment
Compartment Syndrome
Syndrome
and
and
Abdominal
Abdominal Compartment
Compartment
Syndrome
Syndrome

40

Compartment Syndrome
Raised pressure
Within a closed space
Causing damage to its
contents
Due to decreased capillary
blood flow

Precondition
Ischemia-Reperfusion-Injury
Posttraumatic edema
Low MAP

41

Clinical Diagnosis

Unrelenting pain
Swollen, tense compartment
Painful muscle stretch
Sensory deficit
Muscle weakness

BUT:
BUT: Palpable
Palpable pulses
pulses !!

CPP = MAP - ICP

Critical Treshhold:
CPP <30 mmHg (4 kPa)
ICP >30-40 mmHg (5.3 kPa)

42

I
S
C
H
M
E
I
A

ATP

Edema
Microvascular
Injury

ATP-break-down
Xanthine
Dehydrogenase

OH-.
Fe2+

Conversion

Hypoxanthine
Xanthine

Xanthine
Oxidase

H2O2
O2-.

O2

Uric Acid

REPERFUSION

Trauma
Ischemia
Histamine

C3a / C5a

X.D.

Reperfusion

Hypoxanthine
Xanthine

O2

Xanthine Oxidase

Uric
Acid

O2.OH-.

Microvascular
Injury

43

Abdominal cavity own compartment !!

Intraabdominal increase of volume

Intraabdominal pressure

Risk factors for ACS

2 or more criteria:
Combined abdominal and pelvic
trauma
severe hemorrhagic shock
Abdominal packing
Primary abdominal closure

44

Pathophysiology of increased
abdominal pressure
Cardiopulmonary:
Thoracic pressure
Venous reflow
Preload
Systemic afterload
Cardiac output
Cardiac index

Diagnosis of ACS
Ventilation pressure >35mbar and
Horowitz-quotient

(PaO2/FIO2 )

>20kPa

Urinary output <30ml / hr

Clinically tense abdomen
Bladder pressure >25 mmHg
improvement after decompression

45

Therapy
Decompression !
Ethizip
Secondary abdominal closure

Summary
Abdominal
Abdominal Compartment
Compartment Syndrome
Syndrome after
after
severe
severe abdominal
abdominal and
and pelvic
pelvic trauma:
trauma:
Incidence: 4.4 %
After tamponade: 8%
Organ failure: spleen 100%,
hemodynamics: 86%
Therapy: emergency decompression
Complications: intestinal ischemia

46

Conclusion
Monitoring of bladder pressure
Monitoring of organ functions
Secondary abdominal closure after
emergency laparotomy with
tamponade

Traumatic brain injury

47

Severe brain injury

Avoid secondary brain damage

Hypotension
Hypotension // hypoxemia
hypoxemia

Evacuation
Evacuation of
of intracerebral
intracerebral hemmorrhage
hemmorrhage

Early
Early fracture
fracture fixation
fixation
Fracture reconstruction: Window of opportunity

Chesnut et al. (1993): Traumatic

Coma Database
Secondary Insults

5-4

2-1

307

64

17

Early

30

40

47

Late

117

20

66

Early and late

39

15

77

No hypotension

SBP <90 mmHg

GOS %

48

Brain injury with multiple trauma

1.

Control of shocking hemorrhage

Oxygenation

2.

CNS assessment
Evacuation of EDH / SDH
ICP / pti O2 monitoring
Brain protection

3.

Fixation of major fractures for unrestricted IC

Damage control
Reduction of afferent input

Stress
Stress
Fear
Fear
Pain
Pain
Endotoxin
Endotoxin
Temperature
Temperature

Cortex
Cortex
Hypothalamus
Hypothalamus

Pituitary
Pituitary

Blood
Blood volume
volume
Fluid
shifts
Fluid shifts
Hypoxemia
Hypoxemia
Hypercapnia
Hypercapnia
Acidosis
Acidosis

Receptors
Receptors

Brain
Brain stem
stem

Autonomic
Autonomic
centers
centers

Tissue
Tissue injury
injury

49

ICP - therapy
CBV
BWC
CSF

steal

Therapy ICP > 15 mm Hg

No hemorrhage to evacuate
Normoventilation
Maintenance of CPP (CPP=MAP-ICP)
Optimization of sedation and relaxation
Drainage of liquor
Mannitol
Hyperventilation
Pentothal (Barbiturate)

50

Klassifikation SHT
Wach
Somnolent
Sopors
Komats

Symptomatik
1)
1) Psychopathologisches
Psychopathologisches Syndrom
Syndrom
Vigilanzstrung
Somnolenz
Sopor
Bewusstlosigkeit (Koma)

akustisch weckbar
Abwehr auf Schmerz
unerweckbar
cave: Abwehr auf Sz
kann erhalten sein

Orientierungsstrung
Gedchtnisstrung
Durchgangssyndrom

51

Symptomatik
2)
2) Neurologische
Neurologische Ausflle
Ausflle
Pupillenstrung (Weite und Lichtreaktion)
Reflexstatus
Motorik
Sensibilitt
Muskeltonus

Symptomatik
3)
3) Vegetatives
Vegetatives Syndrom
Syndrom
Schwindel
Brechreiz
Kreislaufinstabilitt
Strung der Wrmeregulation

52