Ortho Medicine Lec 1

Front 1

Definition Infection

Back 1

Identifiable source of microbial insult

Front 2

SIRS Definition

Back 2

Systemic inflammatory response syndrome,have Two or more following criteria ▪ temp >/= 38 C Or </= 36 ▪ heart rate >/= 90 beats/min ▪ respiratory >/= 20 breaths /min or paCo2 </=32mmhg or mechanical ventilation ▪ WBC >/= 12.000/ ul or </= 4000/ ul or >/= 10 % bands forms

Front 3

Sepsis Definition

Back 3

Identifiable source of infection + SIRS

Front 4

Severe sepsis Definition

Back 4

Sepsis + organ dysfunction

Front 5

Septic shock Definition

Back 5

Sepsis + cardiovascular collapse " requiring vasopressor support"

Front 6

Advantage of response

Back 6

• Restore tissue function • Eradicate invading microorganisms

Front 7

❖ Aim of recent practice

Back 7

Our aim is to early intervention to support tissue and stop /minimize this response especially in major trauma or infection.

Front 8

Minor injuries

Back 8

: is usually followed by functional restoration w/minimal intervention

Front 9

Major injurie

Back 9

associated with overwhelming inflammatory response 》 failure to give appropriate intervention》 multiple organ failure 》DEATH.

Front 10

Percentage of those who are severely injured

Back 10

30 %

Front 11

Severely injured patients die from their injuries differ from survivors only in

Back 11

the degree and duration of their dysregulated acute inflammatory response process

Front 12

An incidence of Severely injured patients die from their injuries

Back 12

of over 900,000 cases per year

Front 13

Trauma is

Back 13

: is the leading cause of mortality and Morbidity for individual under age 45

Front 14

The understanding of the systemic response to surgical trauma will :

Back 14

Enhance perioperative patient care • Enhance recovery • Decrease hospital stay

Front 15

the aim of modern surgical practice is

Back 15

to ensure stress_free pre_operative care

Front 16

Response components :

Back 16

• Physiological consequences • Metabolic manifestation • Clinical manifestations • Laboratory changes

Front 17

Physiological consequences

Back 17

⬆ cardiac output ⬆ ventilation ⬆ membrane transport ⬆ weight loss ⬆ wound healing

Front 18

Metabolic manifestations

Back 18

• Hypermetabolism

• Accelerated gluconeogenesis

• Enhanced protein breakdown

• Increased fat oxidation

Front 19

❖ Response components

Back 19

• Fever • Leucocytosis/leucopenia • Tachycardia • Hyperglycemia • Tachypnea • Elevated CRP/altered • Presence of wound or acute phase reactants inflammation • Hepatic/renal dysfunction • Anorexia

Front 20

Mediators of injury response

Back 20

• Neuro_endocrine (hormonal) • Immune system (cytokines)

Front 21

❖ Bi phasic

Back 21

1- Acute phase : an activity secreting pituitary and elevated counter regulatory hormones ( cortisol , glucagon , adrenaline ) changes are thought to be beneficial for short – term survival. 2- .Chronic phase : low serum levels of the respective target organ hormones. Changes contribute chronic wasting.

Front 22

Chronic phase :

Back 22

low serum levels of the respective target organ hormones. Changes contribute chronic wasting.

Front 23

1- Acute phase :

Back 23

an activity secreting pituitary and elevated counter regulatory hormones ( cortisol , glucagon , adrenaline ) changes are thought to be beneficial for short – term survival.

Front 24

Phases of response

Back 24

1. EBB 2. Flow 3. Anabolic

Front 25

EBB

Back 25

• Starts at the time of injury and lasts for approximately 24-48 hours • Main hormones in ebb phase are catecholamines, cortisol and aldosterone • It may be attenuated by proper resuscitation but not completely abolished

Front 26

Flow

Back 26

• It lasts for several weeks • This phase involves mobilization of body energy stores for repair and recovery

Front 27

EBB ( untreated shock)

Back 27

• Dec body temp • Dec O2 consumption • Lactic acidosis • Incr stress hormones • Decr insulin • Gluconeogenesis • Inc substrate consumption • Inc substrate consumption • Hepatic acute phase response • Immune activation

Front 28

Flow phase

Back 28

• Inc body temp • Inc O2 consumption • Negative Nitrogen bal • Inc stress hormone • Normal to Inc insulin • Hyperglycemia • Gluconeogenesis • Proteinolysis (Autocannabalism ) • Immunosuppression • Lipolysis

Front 29

Key catabolic elements of flow phase

Back 29

• Hyper metabolism • Alteration in skeletal muscle protein • Alteration in liver protein • Insulin resistance

Front 30

1. Hyper metabolism

Back 30

• Majority of trauma patients – energy expenditure approximately 15-25 %> predicted healthy resting values

Front 31

Factors which increases this metabolism :

Back 31

• central thermo dysregulation • increased sympathetic activity • increased protein turnover • wound circulation abnormalities

Front 32

Skeletal muscle – metabolism

Back 32

• Muscle wasting- result of ⬆ muscle protein degradation + ⬇ muscle protein synthesis ( RS and GIT ) cardiac muscle is spared • Lead – increased fatigue , reduced functional ability and ⬆ risk of morbidity mortality

Front 33

Hepatic acute phase response:

Back 33

Cytokines: 1. IL – 6 ⬅️ مهم 2. ⬆ Synthesis of positive acute phase 3. Protein : foreign and CRP • Negative acute reactants: Albumin decreased

Front 34

Insulin resistance

Back 34

• Hyperglycemia is seen - ⬆ glucose production + ⬇ glucose uptake – peripheral tissues • (Transient induction of insulin resistance seen ) • Degree of insulin resistance is to magnitude of the injuries process • Following routine upper abdominal surgery. Insulin resistance may persist for approximately 2 weeks

Front 35

In critically ill patients with resuscitation 24 hours :

Back 35

Body weight increases due to extracellular water expansion by 6-10 liters : This can be overcome By careful intraoperative management of fluid balance

Front 36

In critically ill patients with resuscitation1-10 days:

Back 36

Total body protein will diminish by 15% and body weight will reach negative balance as the expansion of extra cellular space resolves This can be overcome by blocking neuroendocrines

Front 37

Factors ⬆ response to injury

* Factors were our aim to minimize or eradicate*

Back 37

• Hypothermia • Pain • Starvation • Sepsis • Immobilization • Hypotension

Front 38

Avoidable factors that compound the response of injury

Back 38

• Contributing heamorrhage • Hypothermia • Tissue edema • Tissue under perfusion • Saturation • Immobility

Front 39

Avoidable factors

Back 39

Volume loss

Hypothermia

Administration of activated protein C

Maintaining the normo glycemia:

Starvation

Tissue edema

Immobility

Front 40

Immobility :

Back 40

has been recognized as a potent stimulus for inducing muscle wasting . Early mobilization is an essential measure to avoid muscle wasting

Front 41

Tissue edema :

Back 41

is mediated by the variety of mediators involved in the systemic inflammation . Careful administration of anti- mediators & reduce fluid overload during resuscitation reduces this condition

Front 42

Starvation :

Back 42

during starvation , the body is faced with an obligate need to generate glucose to insulin cerebral energy metabolism ( 100g of per day ) ▪ Provision of at least 2L of IV 5% dextrose for fasting patients provides glucose as above

Front 43

Maintaining the normo glycemia:

Back 43

with insulin infusion during critical illness has been proposed to protect the endothelium and thereby contribute to the prevention of organ failure and death

Front 44

2. Hypothermia

Back 44

maintaining normothermia by an upper body forced air heating cover ⬇Wound infection , cardiac complications , bleeding and transfusion requirements

Front 45

1. Volume loss

Back 45

careful limitation of intraoperative administration of colloids and crystalloid so that there is no weight gain

Front 46

Administration of activated protein C -

Back 46

to critically ill patients has been shown to ⬇organ failure and death . It is thought to act , in part , via preservation of the micro circulation in vital organs

Front 47

App to prevent in necessary aspect of stress response

Back 47

1. Minimal access technique 2. Minimal period 3.epidural analgesia 4. Early mobilization

Front 48

Control of body response to surgery :

Back 48

1. Control of pain : analgesic , local and regional blockade. 2. Less trauma : care in handing tissues , minimally invasive surgery . 3. Control of infection : remove source of toxins , debrdie wounds and drain pus , antibiotics 4. Nutritional support : enteral feeding to maintain gut mucosal barrier integrity and give immunonutrition with added glutamine , arginine and omega 3 FA 5. Remove fear and stress : give anxiolytics 6. Correct hypovolemia : adequate replacement of fluid and electrolyte lost , blood transfusion and Colloid for plasma losses . 7. Correct hypoxemia 8. Correct metabolic alkalosis or acidosis. 9. Drug administration: ( still experimental ) ▪ Steroids, antiedoxin , antibodies , anti- TNF , antibodies , IL – 1 receptor antagonists and PAF receptor antagonists , adrenergic blockers ( decrease metabolic rate )

• Aspirin ( attenuates cytokines actions) • GH and anabolic steroids stimulate protein synthesis . • Inderal ( improve postoperative nitrogen balance • Allopurinol ( inhibit free radical formation )

Front 49

Control of pain :

Back 49

analgesic , local and regional blockade

Front 50

Less trauma :

Back 50

care in handing tissues , minimally invasive surgery .

Front 51

Control of infection :

Back 51

remove source of toxins , debrdie wounds and drain pus , antibiotics

Front 52

Nutritional support :

Back 52

enteral feeding to maintain gut mucosal barrier integrity and give immunonutrition with added glutamine , arginine and omega 3 FA

Front 53

Remove fear and stress :

Back 53

give anxiolytics

Front 54

Correct hypovolemia :

Back 54

adequate replacement of fluid and electrolyte lost , blood transfusion and Colloid for plasma losses .

Front 55

Drug administration: ( still experimental )

Back 55

▪ Steroids, antiedoxin , antibodies , anti- TNF , antibodies , IL – 1 receptor antagonists and PAF receptor antagonists , adrenergic blockers ( decrease metabolic rate )

Front 56

Allopurinol

Back 56

( inhibit free radical formation )

Front 57

Aspirin

Back 57

( attenuates cytokines actions)

Front 58

GH and anabolic steroids

Back 58

stimulate protein synthesis .

Front 59

Inderal

Back 59

( improve postoperative nitrogen balance

Front 60

All of the following hormones regulate the ebb phase except : A. glucagon B. Cortisol C. Aldosterone D. Catacholamines

Back 60

glucagon

Front 61

Which one of the following will not exacerbate the metabolic response to surgical injury 2 ? A. Hypothermia B. Hypertension C. Starvation D. Immobilization

Back 61

Hypertension

Front 62

Which one of the following interleukin promotes the hepatic acute phase response in injury ? A. IL - 4 B. IL - 5 C. IL -6 D. IL -8

Back 62

IL -6