Cellular Hypoxia in Multiple Trauma Patients

Kiki LukmanDivision of Digestive Surgery, Department of Surgery

Hasan Sadikin Hospital/Medical School of Univ. PadjadjaranBandung

Outlines

1. Problems in multiple trauma patients2. Cellular Injury3. Body responses to Injury4. Cellular responses to hypoxia5. Management of Cellular Hypoxia

Problems of trauma in Indonesia

Missed/delayed diagnosis and delayed treatment !!!!

What happens to the patients?

Multiple trauma

What is the body response to trauma?

InitialPhysiological

Condition:Homeostasis

Physiologic Response to restore

Homeostasis:Pain,

HemostasisNeuroendocrine

ReflexInflammation:

Local & SystemicMetabolics

WOUND HEALING

Tissues InjuryHemorrhage:• Hypovolemia• Hypercarbia• Hypoxia• Acidosis• Coagulopathy

Tissue EdemaVolume shift

Insult:TRAUMA

CellInjury

Organ injuries

Organ System Responses

What happens to the cells?

Normal cells(homeostasis)

ADAPTATIONmetabolic, structural CELL INJURY

StressAdaptation

fails

Injuriousstimuli: dose

IRREVERSIBLE CELL INJURY

NECROSIS

REVERSIBLECELL INJURY

APOPTOSIS

Progressive, severe

Biochemical mechanisms of cell injuryin Hypoxia

What happens in surgical source controls?

Cells

Stress Factors

Trauma Fear Major Surgery

HypoxiaHypo-perfusionInjury

PainInjuryHypoxiaischemia

Metabolic Changes

Neuro-endocrine responseInflammatory mediators

Stressors

Pain

Blood transfusion

StarvationImmobilization

Systemicinflammation Dehydration

Hypothermia

Opioids

Tissue injury

Blood loss

Anaesthesia Hypoxemia

Overhydration

Impaired tissue perfusion

Stressors in surgery

The Metabolic Stress Response to Surgery and Trauma

How to assess?OxygenationMonitoring

LUNGS

BLOOD

TISSUES

P / F (PF ratio)

The ratio between PaO2 (mmHg) and FiO2 (decimal). (Need BGA !!!)

Normal ratio: > 300 (300 – 500).

Clinical Significance:Showing the degree of O2 diffusion in the alveolar-capillary unit. < 200 : ARDS (acute respiratory distress syndrome).200 – 300 : ALI (acute lung injury).

A-a gradient (AaDO2)

O2 partial pressure different between the alveoli and artery (PAO2 – PaO2).

Formula (Clinical use) :AaDO2 = PiO2 – PaCO2/R – PaO2

R=respiratory quotient= 0.8

Normal Values

Room Temperatures (FiO2: 21%) :< 10 mmHg (young) 10-20 mmHg (elderly)

at FiO2 100% :31 mmHg (young)56 mmHg (elderly).

Purpose

To know the causes of hypoxemia :AaDO2 normal : hypoventilationAaDO2 abnormal :

Gas diffusion dysfunction VA/Q dysfunctionshunting

Blood Oxygen Content

Ca O2 = 1,34 x Hb x SaO2 + 0,003 x PaO2

To monitor:

SaO2

PaO2

SaO2 (Oxygen Saturation)

Showing the Hb capacity to bind O2.SaO2 : arterialSpO2 : by pulse oximetry0% : No O2

100% : saturated with O2

(SaO2)

PULSE Oximetry SpO2

SaO2 vs SpO2 Correlation

1. SpO2 > SaO2:1. Hypoxemia2. Carboxyhemoglobinemia3. Methemoglobinemia4. Sickle cell crises5. Skin pigmentation6. Bright overhead fluorescent light7. Probe malposition

1. SpO2 < SaO2:1. Intravenous dye (meth.blue, indigo carmine)2. Nail polish3. Chylomycron, intravenous lipid

2. Inaccurate reading.1. Low perfusion2. Shivering3. Motion artefacts

SaO2 vs SpO2 Correlation

Etiology of SaO2 (SpO2) ↓

1. Respiratory problems1. Airway2. Ventilation3. Diffusion problems in alveolar-capillary unit

2. Circulatory System Problems (preload, contractility, HR, afterload)

3. FiO2 <4. Installation and Device problems

PaO2 (Oxygen partial pressure in the blood)

Normal : Average value : PaO2 = 5 x FiO2 (%)

( 80 – 100 mmHg ) Age adjusted : 100 – 0,3 { umur (th) – 25 }

Low : - HYPOXEMIA – Mild: 60- 80 mmHg Moderate : 40- 60 mmHg Severe: < 40 mmHg

HYPOXEMIA

Causes:

FiO2 < Hypoventilation Shunt Ventilation-perfusion mismatch O2 diffusion dysfunction alveoli-capillary.

PAO2 < 80 (104 mmHg)

PACO2=40 mmHg

75% 100%

FiO2 <

How to manage?

TISSUE OXYGENATION

Target: To meet the needs of tissue oxygen

How to know?

StO2

Cell Monitoring

StO2

O2ER = 25%

Central Vein Oxygen Saturation (SvO2)

1 Kpa ~ 8 mmHg

The meaning of Svs O2

SvsO2 < 75 % (PvO2 < 42,8 mmHg) :1. DO2 ↓ :

Anemia, hypovolaemia, cardiogenic shock, hypoxemia, R - L shunting, ventilation –perfusion dysfunction.

2. Oxygen need ↑ :Febrile, convulsion, shivering, pain, activity ↑,

hyperthyroidism.

SvsO2 = 75 - 80% (PvO2 = 42 - 44 mmHg):Normal DO2 & O2 consumpti

SvsO2 > 80% (PvO2 > 44 mmHg) :

DO2 ↑ : Cardiac output ↑,L – R shunting, hiyperbaric O2, FiO2 ↑, sepsis.

Oxygen need ↓ :Hypothermia, general anesthesia, neuromuscular block drugs, hypothyroidism, cell necrosis.

HYPERLACTATEMIA

Lactate production Lactate clearance

Anaerobic Aerobic

•Tissue hypoxia•Increased WBC metabolism

• Endogenous production

• Inflammation mediated:

•Accelerated glycolysis

•Inhibition of pyruvate dehydrogenase

• Impaired liver function

HYPERLACTATEMIA

BASE DEFICIT / EXCESS (BD/E)

The amount of acid/base needed to normalize 1L blood (SBC = standard bicarbonate concentration : 22,9 mEq/L ), t : 37oC & PaCO2 : 40 mmHg.

• Classification : Mild : 2 – 5 mmol / L• Moderate : 6 – 14 mmol /L• Severe : > 15 mmol / L

Lactate & Base Deficit Correlation

Husain et al Am J Surg 2003: 185: 485-491

Correlation: Base Deficit & Mortality

Rixen and Siegel , Critical Care 2005 Vol 9 No 5

Impact on Management:

Trauma

Limb/Life threatening conditions

Resuscitation

Post operative conditions

Anatomic + Physiologic derangement

Cells Injury/

Diagnosis

Surgery

Intensive Care ?

Healing

Operating Room

Pain control

Emergency Room

Perioperative oxygenation + Assessmentof O2 consumption

uptake

Utilization by cells

microcirculation

SUMMARY

1. Cellular hypoxia is the initial event of MODS in trauma patients, if left untreated, may lead to MOF.

2. The duration of cellular hypoxia is correlated with the patient outcome.

3. Prolonged cellular hypoxia leads to irreversible cell injury and cell death.

4. The mainstay of the treatment of cellular hypoxia is cell oxygenation, not only by oxygen administration, but also by ensuring oxygen delivery into microcirculation.