haemorrhagic shock

Shock &

Haemorrhagic shock

Shock

• Shock is the clinical syndrome that results from inadequate tissue perfusion which leads to hypoxia and ultimately cellular dysfunction.

• The cellular dysfunction is manifested as aerobic to anaerobic leading to lactic acidosis.

Principle mechanisms

• Not enough blood volume

• Pump failure

• Abnormalities of peripheral circulation (when all small blood vessels dilate)

• Mechanical blockage of outflow from the heart

• Most common type of shock

– Insufficient circulating volume

• Primary cause = loss of blood or body fluids from an internal or external source

• Hemorrhage, severe burns, severe dehydration

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Hypovolemic shock

Scalp laceration 3rd degree/full thickness burn

• Failure of the heart to pump effectively

1. Due to damage to the heart muscle

2. Large myocardial infarction

3. Arrhythmias (too fast or too slow)

4. Cardiomyopathy

5. Congestive heart failure (CHF)

6. Cardiac valve problems

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Cardiogenic Shock

• Similar to hypovolemic shock - insufficient intravascular volume of blood or “relative" hypovolemia

– result of dilation of all blood vessels so the “tank” is much larger

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Distributive shock

Urticaria/anaphylaxis Meningococcic sepsis

• Septic shock– Overwhelming infection leading to profound

systemic vasodilation • Anaphylactic shock

– Severe reaction to an allergen, antigen, drug or foreign protein, releasing histamine causing widespread vasodilation, hypotension and increased capillary permeability

• Neurogenic shock– Rarest form of shock. – Trauma to spinal cord resulting in loss of

autonomic and motor reflexes below injury level. Vessel walls relax uncontrolled, decreasing peripheral vascular resistance, result = vasodilation and hypotension

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Distributive shock examples

• Mechanical block to heart’s outflow

• Pulmonary embolus

• Cardiac tamponade

• Tension pneumothorax

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Obstructive Shock (rare)

Pulmonary embolus Cardiac tamponade

Psychogenic shock

• Immediately follows sudden fright

• Eg bad news, severe pain( blow to the testes)

Haemorrhagic shock

• It is one of the commonest form of hypovolemic shock

• Hypovolemia leads to decreased preload which leads to increased sympathetic activity and vasoconstriction

• Vasoconstriction leads to decreased mean arterial pressure and ischemia which ultimately leads to multiorgan failure-ARDS,HEPATIC FAILURE,STRESS,GI BLEEDING.RENAL FAILURE .

• Ischemia leads to myocardial insufficiency and severe decrease in Systemic Vascular Resistance and finally death

Hemorrhage Classification

External Hemorrhage

• Results from soft tissue injury.

• Most soft tissue trauma is accompanied by mild hemorrhage and is not life threatening.– Can carry significant risks of patient morbidity and disfigurement

• The seriousness of the injury is dependent on:– Anatomical source of the hemorrhage (arterial, venous,

capillary)

– Degree of vascular disruption

– Amount of blood loss that can be tolerated by the patient

Internal Hemorrhage

• Can result from:

– Blunt or penetrating trauma

– Acute or chronic medical illnesses

• Internal bleeding that can cause hemodynamic instability usually occurs in one of four body cavities:

– Chest

– Abdomen

– Pelvis

– Retroperitoneum

Internal Hemorrhage

• Signs and symptoms that may suggest significant internal hemorrhage include:

– Bright red blood from mouth, rectum, or other orifice

– Coffee-ground appearance of vomit

– Melena (black, tarry stools)

– Dizziness or syncope on sitting or standing

– Orthostatic hypotension

• Internal hemorrhage is associated with higher morbidity and mortality than external hemorrhage

Compensated shock

– 0-20% of blood loss

– Blood pressure is maintained via increased vascular tone and increased blood flow to vital organs

The body’s response:

Compensated shock Baroreceptor mediated vasoconstriction!

• Increased epinephrine, vasopressin, angiotensin• Results in:

– Tachycardia– Tachypnoea– Lowered pulse pressure– Slightly lowered urine output

The Organs which well perfused :• Brain• Heart• Kidneys• Liver

The Organs which are less perfused:• Skin• GI tract• Skeletal Muscle

But why

• The body will make whatever adjustments it can to maintain….

Adequate

Cardiac

Output

• Brain and heart perfusions remain near normal while other less critical organ systems are, in proportion to the blood volume deficit, stressed by ischemia.

Uncompensated shock

• 20-40% loss of blood volume

• Decrease in BP

• Tachycardia

The body’s response

Uncompensated shock

• The intravascular volume deficit exceeds the capacity of vasoconstrictive mechanisms to maintain systemic perfusion pressure.

• Increased cardiac output

• Increased respiration

• Sodium retention

Classification

Class I

A. Loss of up to 15% of total blood volume (0 to 750 ml in 70 kg person).

B. Characterized by normal blood pressure, urine output, slight tachycardia, tachypnea, slight anxiety.

Class II

A. Loss of 15 % to 30% of total blood volume (750 to 1,500 ml )

B. Characterized by normal blood pressure, tachycardia, mild tachypnea, decrease urine output and mild anxiety.

Class III

A. Loss of 30% to 40% of total blood volume (1,500 to 2,ooo)

B. Characterized by hypotension, tachycardia, tachypnea, decreased urine output , anxiety and confusion.

Class IV

A. Loss of > 40% of total blood volume (>2,ooo)

B. Characterized by severe hypotension and tachycardia, tachypnea, negligible urine output and lethargy

Class 4Class 3Class 2Class 1

>20001500-2000750-1500<750 ml Blood loss (in ml)

>4030-4015-30<15Blood volume (in%)

>140>120>100<100Heart rate

decreasedDecreased mean arterial pressure<60

Normal (+tilt )Normal or increased

Blood pressure

decreasedDecrease Decreased Normal Pulse pressure

Always delayedUsually delayed

May be delayed

Normal Capillary refill

Always delayedUsually delayed

Mildly delayednormalRespirations

Essentially anuric

5-1520-30>30Urinary output (ml/hr)

Lethargic,obtunded

confusedAnxious Normal or anxious

Mental status

Concomitant Factors

• Pre-existing condition – eg Anaemia, HTN etc

• Rate of blood loss

• Patient Types– Pregnant

• >50% greater blood volume than normal

• Fetal circulation impaired when mother compensating

– Athletes• Greater fluid and cardiac capacity

– Obese• CBV is based on IDEAL weight (less CBV)

• Children

– CBV 8–9% of body weight

– Poor compensatory mechanisms

– TREAT AGGRESSIVELY!

• Elderly

– Decreased CBV

– Medications

• BP

• Anticoagulants

Hemorrhage Assessment

• Blood loss at the scene

• Mechanism of Injury/Nature of Illness• Should only be used in conjunction with vital signs and

other clinical signs of injury to determine the probability of injury

• Need for Additional Resources

• Initial Assessment

– General Impression• Obvious bleeding

– Mental Status

– Interventions• Manage as you go

– O2

– Bleeding control

– Shock

– BLS before ALS!

• Focused History & Physical examination

– Rapid Trauma Assessment• Full head to toe

• Consider air medical if stage 2+ blood loss

– Focused Physical Exam• Guided by c/c

– Vitals, SAMPLE, and OPQRST

– Additional Assessment• Orthostatic hypotension

• Tilt test: 20

– BP or P from supine to sitting

Fractures and Blood Loss

• Pelvic fracture:

• Femur fracture:

• Tibia/fibula fracture:

• Hematomas and contusions:

2,000 mL

1,500 mL

500–750 mL

500 mL

• Ongoing Assessment– Reassess vitals and mental status:

• Q 5 min: UNSTABLE patients• Q 15 min: STABLE patients

– Reassess interventions:• Oxygen• ET• IV• Medication actions

– Trending: improvement vs. deterioration• Pulse oximetry• End-tidal CO2 levels

Management

• C-ABCs of trauma• Control hemorrhage (splint the limb!!)• Obtain IV access and resuscitate with fluids and

blood – 2 liters crystalloid for adults– 20 cc/kg crystalloid x 2 for kids

• Blood vs. Crystalloid??

• Long term critical care management

Management goals AFTER securing the ABCs:

• stop the bleeding!

• restore volume!

• correct any electrolyte/acid-base disturbances!

Apply direct pressure:• with gloved hand,• sterile dressing(s).

Bleeding stopped? YesNo

Elevate extremity:• above victim’s heart,continue direct pressure

Locate pressure point,apply pressure:• maintain direct pressureover wound

Treat for shock:• care for wound,• seek definitive care

Bleeding stopped?

Bleeding stopped?

No

Bleeding fromextremity?

No

Apply tourniquet(last resort)

Yes

No

Definitive therapy

• Apply pressure directly to wound site:

– Gloved hand, dressing

– If dressing soaks thru, add more gauze on top and press harder

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Direct pressure



Elevate extremity:• above victim’s heart,

continue direct pressure

Locate pressure point,apply pressure:• maintain direct pressure

over wound

Treat for shock:• care for wound,

• seek definitive care

Bleeding stopped?

Bleeding stopped?

No


No


Yes

No

Definitive therapy

• If possible, raise wound site above level of victim’s heart

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Elevate wound site






over wound



Bleeding stopped?

Bleeding stopped?

No


No


Yes

No

Definitive therapy

• Find proximal “pressure point” and press on it

(radial, ulnar, brachial, axillary, femoral arteries—not carotid)

• Apply direct pressure to site

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Pressure points






over wound



Bleeding stopped?

Bleeding stopped?

No


No


Yes

No

Definitive therapy

• Apply band above injury site, tighten to stop bleeding:

– Last resort—risky

– Note time of application

– Reassess frequently

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Tourniquet






over wound



Bleeding stopped?

Bleeding stopped?

No


No


Yes

No

Definitive therapy

Volume Resuscitation

• Rapid Responder

– Give 500cc-1 Liter crystalloid rapid improvement of BP/HR/Urine output

– < 20% blood loss

• Transient Responder

– Give 500cc-1 Liter crystalloid improves briefly then deteriorates

– 20-40% blood loss

– Continue crystalloid infusion +/- Blood

• Non Responder

– Give 2 Liters crystalloid/ 2 units Blood no response

– > 40% blood loss

volume resuscitation adequate/inadequate?

• Urine output

• Vital signs

• Skin perfusion

• Pulse Oximetry

• Acidemia??

Correction of any electrolyte/acid-base disturbances

• Normalization of acidosis and oxygen consumption are the best current indicators of adequate resuscitation

• Base deficit and lactate level are good indications of tissue perfusion

• Bicarbonate• HCO3 combined with hydrogen ion to form water and

carbon dioxide

• CO2 diffuses into cells and worsens intracellular acidosis

• It is not indicated for lactic acidosis from HS

• Best treatment of acidosis from HS is restoring perfusion to ischemic tissue.

Complications

• Multi organ dysfunction

• Coagulopathy

Multiple organ failure

• pt who survive HS but die in the hospital later usually die of MOF or sepsis

• MOF results from systemic inflammatory response

• Duration and severity of HS correlate with incidence of MOF

• Patients who get > 6 units of packed RBCs in the first 12 hours of HS resusitation have higher risk of MOF

Coagulopathy

• Hypothermia

– Most common cause of coagulopathy in HS

– Significant coagulopathy begins at 34o c

– Undetectable on lab tests of coagulation ,blood warmed to 37 c before testing

Note that

Treat with warmed fluids and external rewarming

• Platelet dysfunction and deficiency

– Second most common cause

– Hypothermia cause plt dysfunction

– Thrombocytopenia is common is massive HS

– Degree of thrombocytopenia not correlated directly with volume of blood loss

– Platelets transfusion

Health & Medicine

haemorrhagic shock