SHOCK

Contents
 Definitions
 Classifications
 Pathophysiology
 Etiology
 Clinical picture
 Management

Definitions
 Shock is a syndrome characterized by decreased tissue perfusion and impaired
cellular metabolism.
 Shock is a state of disparity between ………..
A. Circulating blood volume.
B. Capacity of vascular bed.
 Shock is not only hypotension.
 Shock is a state of peripheral circulatory failure …….
 characterized by:
A. Hypotension.
B. Impaired tissue perfusion.
C. Impaired cellular metabolism.
D. Accumulation of waste products.
E. Severe dysfunction of organs
F. Life threatening.

Classifications
1. Hypovolemic.
2. Cardiogenic.
3. Obstructive.
4. Maldistributive (sever VD)
 Septic
 Anaphylactic
 Neurogenic
 Endocrinal

Pathophysiology
 Normal blood volume >>>>>>> 5 – 6 L
 Arterial system >>>>>>>>>> 10 %
 Capillaries >>>>>>>>>>>>>> 20%
 Venous system and Heart >>> 70%
Pathophysiology of Shock
A. Cellular:
Tissue hypo-perfusion
⇩
↓O₂ delivery to the tissues
⇩
anaerobic metabolism
⇩
metabolic acidosis.
⇩
↓cellular glucose
⇩
auto-digestive enzymes
⇩
Rupture of plasma & lysosomal membranes.

B. Microcirculatory changes:
Catecholamines.
⇩
Pre-capillary sphincters constrict
⇩
Capillary circulation sluggish.
⇩
Untreated hypovolemia
⇩
Hypoxia.

— Under normal conditions: Only 1/3 of capillary bed is open at a time.

— Under ischemic conditions : Opening more capillaries,,
 Slowing of the capillary circulation.
 Spontaneous blood coagulation or (DlC), if extensive.
 Disturbance of capillary endothelium function.
 Leakage of large protein molecules from the vessels into interstitium →
dragging huge amounts of fluid with them → reduces blood volume.

C. Acid-base Imbalance:
Metabolic acidosis, caused by:
1. Accumulation of lactic acid due to anaerobic metabolism.
2. Renal failure due to prolonged ischemia.
D. Systemic:
a) Sympathy-adrenal response:
- Catecholamine→ redistribution of blood from
• non-vital organs (Skin, GIT) to
• vital organs (Coronary Vs) → ↑ HR & contractility.
- Release of stress hormones e. g. cortisol, glucagon...etc.
- Release of ADH
- Activation renin-angiotensin-aldosterone system → VC / Na & water
retention.
b) Individual organs: (Brain, Heart, Kidney, Liver)

Hypovolemic Shock
Etiology:
 Blood loss.
- Hemorrhage →→ Hemorrhagic shock
 Plasma loss (Burns).
 Body water loss.
- Vomiting.
- Diarrhea.
- Dehydration
- Urinary loss (Diabetes)
- Third space loss (IO and Pancreatitis).

HAEMORRHAGE
Etiology:
1- Traumatic: Accidental, surgical and intervential e.g PTC.
2- Pathological:
a. Astherosclerotic: ruptured aortic aneurysm.
b. Inflammatory: bleeding peptic ulcer
c. Neoplastic: haematuria in renal cancer.
3- Bleeding tendency e.g. Hemophilia & purpura

Classification of Hemorrhage
1. ACCORDING TO SITE:
1. External (Revealed): bleeding is visible (through the skin) as in wounds or from body
orifices as in epistaxsis or haematemsis.
2. Internal (Concealed): Haemoperitonium and Haemothorax.
3. Interstitial: bleeding occurs into tissues forming a haematoma e.g. fracture
haematoma

2. ACCORDING TO TIME OF OCCURRENCE:

1. Primary haemorrhage: Occurs with the trauma.
2. Reactionary Haemorrhage: Occurs within 24 hours after the trauma or operation
due to slipping of ligatures or a clot is dislodged as a result of restoration of B.P
3. Secondary hemorrhage: Occurs within 7-14 days after trauma or operation due to
sepsis which dissolves the clot & erodes the vessel wall.
3. ACCODING TO SOURCE
Arterial Venous Capillary
Blood comes in pulsatile jets Continuous steady flow Ooze from granulation tissue
Blood is Bright red Dark red Bright red
The bleeding more from the It is more from the Oozing
proximal than the distal distal than the proximal

4. ACCODING TO AMOUNT (Degree of hemorrhage)

The adult human has 5000 ml of blood (70 ml/kg)
Class I Class II Class III Class IV
Blood loss % < 15% 15-30% 30-40% > 40%

Amount of loss 750 ml 750-1500ml 1500-2000ml > 2000ml

Mental status Normal to Anxious to Aggressive to Drowazy to

anxious resless drowsy unconcious
Skin Normal Pale and cold Pale and colder Pale and very
cold
Pulse/min < 100 100-120 120-140 > 140
Pulse pressure normal low low low
Urine output >30 20-30 10-20 0-10
(ml/h)

Clinical Picture C/P:

A. C/P of shock: →
(1) Rapid weak pulse: (1st sign)
(2) Hypotension:
(3) Subnormal temperature
(4) Increase rate & depth of respiration (air hunger)
(5)Pale cold clammy skin of extremities & nose due to sympathetic overactivity
(6) Collapsed veins & decrease central venous pressure.
(7)Oliguria & Anuria
(8)Thirst sensation.

B. Of the cause:
 Signs of internal hage.
 Burns.
 Intestinal obstruction

C. Of complications:
 Anuria.
 ARDS.
Stages:
1. Compensated Stage:
- The physiological mechanisms tries to restore blood volume & normal function of the
vital organs (brain, kidneys, heart & lungs).
- Compensatory mechanisms fail with loss of > 15 % of blood volume.

2. Decompensated Stage (40% blood loss):

Progressive poor perfusion & micro circulatory changes
→Deterioration of functions of [Brain, Kidney, Heart and Lung].

3. Refractory Stage:
- The shock can no longer be reversed.
- Failure of vital organs & death.

Investigations:
(lt's an emergency condition, investigations are part of resuscitation)
Blood sample for:
1. BT, PT, APTT &CBC → exclude bleeding tendency
2. HB%, Hct, ABO, Rh → blood transfusion.
3. ABG, PH, electrolytes, KFTs & LFTs.
To detect the cause:
 ECG → Exclude cardiogenic causes.
 Abdominal U/S → internal hemorrhage.
 Head CT scan → unconscious patient or with head injury.

Management:
1. Outside hospital or in ER
2. Hospital or in ER At hospital

A. Outside hospital or in ER (1st AID)

• Airway
• Breathing
• Circulation
• Drugs:
1. Morphia: 10 mg Slowly lV to relieve pain "neurogenic shock".
2. Antibiotics
3. Anti-gas gangrene
4. Antitetanic serum.
• Elevate legs & head down to restore cerebral blood flow.
• Fractures should be immobilized.
• Warming (to lethal triad).

Lethal Trauma Triad

 Hypothermia
 coagulopathy
 Acidosis
B. At hospital (Better in ICU)
1- Stop hemorrhage:
 position
 pressure
 Packing
2- Resuscitation:
 cannulas: for fluids & sampling
 O₂ inhalation.
 Ryle Tube.
 Catheter: UOP monitoring.

3- Fluid administration:
 Crystalloids (saline,ringer, dextrose)
 Colloids (albumin,dextran, starch)
 Blood

4- Monitoring :
Routine:
 Pulse
 Blood Pressure
 Temperature
 UOP (Normal urine output is 1-2 ml/kg/min)
 ABGs: PH :Acidosis(Normal 7.35- 7.45 )
O2 tension remains normal (80-100mmHg)
CO2 tension is decreased due to hyperventilation (normal 35-45 mmHg)

Others (in severe shock):

1- CVP catheter: (Normal is 5-15 cm H20)
2- Arterial line:
 Monitor ABP.
 Repeated ABG assessment.
3- Pulmonary artery wedge pressure (PAWP) measured by Swan - Ganz catheter :
 Can measure pressure in SVC, right atrium, right ventricle, pulmonary trunk
&wedged pulmonary pressure.
5- Pharmacological support:
inotropic drugs:
 Dopamine
 Dobutamine
6- Treatment of the cause: eg,
• injured great blood vessel
• Exploration
• Burns

7-Treatment of the complications:

Eg: DIC > > Fresh frozen plasma.
 Cardiogenic Shock
Def:
inadequate blood flow to vital organs due to inadequate COP despite of normal blood
volume.
Etiology:
 Acute myocardial infarction "The COMMONEST"
 Severe arrhythmias.
 Massive pulmonary embolism.
 Cardiac tamponade.
 Myocarditis

C/P:
(Same as hypovolemic shock + C/P of the cause: Chest pain)
Congested neck veins & High CVP.

Treatment:
- O₂ inhalation
- ttt of the cause.

Neurogenic Shock
a- Neurogenic sympathetic (Spinal shock):
Etiology:
 High spinal anesthesia
 Spinal fractures.

C/P:
 Sudden extreme VD
 Bradycardia- skin warmth - ↓ABP…etc.

Treatment:
 Vasopressors + lV fluid therapy

b- Neurogenic vasovagal attack

Etiology:
 Severe pain (Trauma to a trigger area)
 Severe Excitement (Bad or Good news).

C/P:
 Sudden extreme VD
 Bradycardia- skin warmth - ↓ABP…etc.

Treatment:
 Trendelenburg's position.
 Anaphylactic shock
Etiology:
 Administration of Drugs as penicillin, sera or dextran.
 Certain foods:eg, Shellfish.
 Antigen-antibody "lgE" reaction →release of histamine that leads to :
 Bronchospasm or Laryngeal edema.
 Massive Vasodilatation.

Treatment:
 lV crystalloid infusion.
 lV hydrocortisone (the most important).
 Antihistaminics.
 Endotracheal intubation.

Endocrinal shock

Etiology:
1- Adreno-medullary insufficiency:
 After adrenalectomy for pheochromocytoma without pre-operative preparation
by o & B blockers ) sudden withdrawal of high level of catecholamines from the
blood.
2- Adreno-cortical insufficiency:
 After bilateral adrenalectomy.
 After operation on a patient who has had cortisone therapy.
 Addison's disease,( under stress, infections, operations) → Addisonian crisis.
3- Hypo & Hyperthyroidism

Treatment:
 Saline infusion.
 lV hydrocortisone (the most important).

Septic (Endotoxic) Shock

Etiology:
Causative organisms :
Gram -ve bacilli "The COMMONEST". Staphylococci. Candida.
Source of infection
 Peritonitis:
— Perforated viscus.
— Gangrenous bowel.
— Leaking anastomosis.
 Cholangitis or genitourinary infections.
 Infected central venous catheter.
Predisposing factors (low immunity)
 Extremes of age.
 DM.
 Malnutrition.
 Malignancy.
 Chemotherapy.
 Immunosuppressant or corticosteroids

Clinical picture of septic shock:

 Hyper-dynamic "warm" septic shock (Early phase):
 Fever 38 *C + Chills.
 Tachycardia
 Tachypnea
 Skin: flushed, warm & dry.
 Restless & confusion.
N.B: Diagnosis is Difficult & high index of suspicion is required.

 Hypo-dynamic “cold" septic shock (Late phase):

 Similar to hypovolemic shock with ↓ COP.
N.B: Multi-organ failure starts at this stage.

 Clinical picture of the cause:

 Eg; UTI, Chest infection, peritonitis,,,,etc.

Complications & causes of death in septic shock:

 MOF
 ARDS.
 ARF
 Acute erosive gastritis "stress ulcer".
 Hepatic dysfunction.

Criteria of Diagnosis
• The following 2 criteria must be met:
1. Evidence of infection(+ve blood culture.)
2. Refractory hypotension (despite adequate fluid resuscitation).

• Additional ≥ 2 of the following must be met:

1. Hyperventilation RR > 20 B/min.
2. ABGs: PaCO₂ < 32 mmHg.
3. WBC count < 4000 cells/mm3 or > 12000 cells/mm.

Investigations:
1- Assessment of general condition:
- CBC: Marked leukocytosis (or leucopenia, late) & thrombocytopenia
- ABG: PaO₂ , PCO₂, pH (hypoxia & hypercapnia in ARDS).
- Electrolytes & Blood sugar (for dehydration).
2- For the cause & source:
 isolation of organisms from source of infection
 Location of septic focus:
 X-Ray: Abdomen & Chest.
 U/S & CT scan.

3- For the complications:

-KFTs & LFTs. (MOF) - ECG monitoring - Coagulation profile. (DIC)

Treatment of septic shock:

1) Resuscitation:
A- Circulatory Support:
 fluid replacement +/- Inotropes & Vasopressors
 if low Hct. → packed RBCs or whole blood transfusion.

B- Respiratory Support:
 O₂ by mask.
 lf PO ₂ < 60 mm Hg → mechanical ventilation.

C- Renal Support:
 Adequate circulatory support improves renal blood flow.
 Hemodialysis is required in ARF.

D- DIC: Fresh frozen plasma.

2) Fighting infection:
a- Eradication of sepsis:
b- Antibiotics:
 Parenteral, combined, broad spectrum started early without waiting for culture
&then changed according to culture & sensitivity.

3) Continuous monitoring:
 Vital signs (temperature, pulse, BP and RR) and ECG.
 Urine output,CVP.
 repeated blood culture, CBC, coagulation profile & organ profile.
 Strict control of blood sugar.