Management of Hypovolemic Shock

Bailey and Love's Short Practice of Surgery, 28th Edition

Definition

Pathophysiology

Cellular Level

• Cells deprived of O2 switch to anaerobic metabolism, producing lactic acid instead of CO2
• Accumulation of lactic acid produces a systemic metabolic acidosis
• As intracellular glucose is exhausted, anaerobic respiration ceases
• Failure of Na+/K+ pumps occurs; intracellular lysosomes release autodigestive enzymes leading to cell lysis
• Intracellular potassium is released into the bloodstream (hyperkalaemia)

Microvascular Level

• Hypoxia and acidosis activate complement and prime leucocytes
• Generation of oxygen free radicals and cytokine release
• Capillary endothelial injury - the endothelium becomes "leaky", fluid escapes into tissues, worsening cellular hypoxia
• Further activation of immune and coagulation cascades

Systemic - Cardiovascular

• Decreased preload and afterload trigger a baroreceptor response
• Increased sympathetic activity and catecholamine release
• Results in tachycardia and systemic vasoconstriction (preserving cerebral and coronary perfusion)

Systemic - Respiratory

• Metabolic acidosis + increased sympathetic response = increased respiratory rate and minute ventilation
• CO2 is excreted more rapidly, producing a compensatory respiratory alkalosis

Systemic - Renal

• Decreased perfusion pressure leads to reduced glomerular filtration and oliguria
• The renin-angiotensin-aldosterone axis is stimulated, causing further vasoconstriction and sodium/water retention

Classification of Shock

Lethal Triad (Physiological Exhaustion)

1. Profound coagulopathy
2. Acidosis
3. Hypothermia

Haemorrhage: Revealed vs Concealed

• Revealed haemorrhage - obvious external bleeding (arterial wound, haematemesis)
• Concealed haemorrhage - blood contained within a body cavity; must be actively suspected and investigated

Acute Traumatic Coagulopathy (ATC)

• Systemic hyperfibrinolysis
• Low fibrinogen levels
• Platelet dysfunction

• Fluid and RBC transfusions cause dilution of coagulation factors
• Hypothermia (worsened by cold fluids/blood) inhibits coagulation proteases
• Severe acidosis further impairs coagulation function
• These cause more bleeding - completing the downward spiral

Management: Damage Control Resuscitation (DCR)

1. Rapid Haemorrhage Control

• Direct pressure over external haemorrhage sites
• Tourniquets, balloon occlusion (e.g. REBOA) or other techniques for temporary control
• Intracavitary haemorrhage: rapid transfer to operating theatre or interventional radiology
• Damage control surgery (DCS): limit surgery to the minimum necessary - stop bleeding, control sepsis; avoid additional tissue damage and physiological stress
• Definitive repairs are delayed until the patient is haemodynamically stable

• Damage control surgery limits operative intervention
• Life-threatening injuries take priority over reconstruction
• Restores physiology before definitive repair
• Used for penetrating, vascular and liver injuries

2. Permissive Hypotension

• During active haemorrhage, targeting a lower-than-normal blood pressure reduces ongoing blood loss
• Allows coronary perfusion without "popping the clot" at the bleeding site
• Bailey and Love stresses this is applied only while bleeding continues - not after haemostasis

3. Avoiding Dilutional Coagulopathy

• Restrict large volumes of crystalloid/colloid which dilute clotting factors
• Prefer blood products over crystalloids
• Balanced transfusion - 1:1 ratio of Red Blood Cells (RBC) to Fresh Frozen Plasma (FFP)

4. Treating Existing Coagulation Deficits

• Tranexamic acid - given early to prevent hyperfibrinolysis (ideally within 1 hour of injury; benefit diminishes after 3 hours)
• Platelets - transfused to correct platelet dysfunction
• Fibrinogen (cryoprecipitate or fibrinogen concentrate) - to correct low fibrinogen
• Coagulation guided by TEG (thromboelastography) or ROTEM (rotational thromboelastometry)
• Correct hypocalcaemia - calcium is essential for coagulation; massive transfusion depletes it

Post-Haemostasis: Perfusion-Targeted Resuscitation

• Adequate preload and afterload (fluids + vasopressors)
• Thromboprophylaxis

Fluid Resuscitation

• Crystalloids (0.9% NaCl, Hartmann's): inexpensive, widely available, but large volumes cause dilutional coagulopathy, hyperchloraemic acidosis (with 0.9% saline), and pulmonary oedema
• Colloids (albumin, gelatins, starches): remain in the intravascular space longer, but synthetic starches (HES) are associated with renal failure and coagulopathy and are no longer recommended
• Blood products are the resuscitation fluid of choice in haemorrhagic shock - they replace lost blood directly
• 1:1 RBC:FFP balanced transfusion minimises dilutional coagulopathy

Monitoring in Hypovolaemic Shock

Minimum Monitoring (Summary Box 2.4):

• ECG (continuous heart rate)
• Pulse oximetry
• Blood pressure (non-invasive, then arterial line if not correcting)
• Urine output (aim: 0.5-1 mL/kg/hr)

Additional Modalities:

• Central Venous Pressure (CVP) - assessed dynamically (not as a single value):
  • Fluid bolus 250-500 mL over 5-10 min
  • Normal response: CVP rises 2-5 cmH2O, drifts back over 10-20 min
  • No CVP rise = patient needs more fluid
  • Large, sustained CVP rise = volume overload or cardiac insufficiency
• Invasive arterial blood pressure
• Cardiac output monitoring (Doppler, pulse waveform analysis, indicator dilution) - helps distinguish shock types; pulmonary artery catheters are less common now
• Base deficit and serum lactate - best markers of adequacy of tissue perfusion and resuscitation endpoint
• During DCR: also monitor electrolytes (Ca2+, K+), PT, fibrinogen, ROTEM/TEG, pH, temperature

Special Considerations

Non-Haemorrhagic Hypovolaemia

Permissive Hypotension - When NOT to Use

Summary of Key Management Principles (Bailey and Love)

1. Identify and control the source of haemorrhage FIRST - resuscitation is supportive, not definitive
2. Avoid the lethal triad: coagulopathy, acidosis, hypothermia
3. Apply Damage Control Resuscitation during active bleeding:
   • Haemorrhage control (damage control surgery if needed)
   • Permissive hypotension
   • Avoid dilutional coagulopathy
   • Treat coagulation deficits (tranexamic acid, platelets, fibrinogen, FFP)
4. Use balanced 1:1 RBC:FFP transfusion
5. Transition to perfusion-targeted resuscitation after haemostasis
6. Monitor with minimum ECG, pulse oximetry, BP, urine output; add CVP and arterial line for patients not rapidly responding
7. Use lactate and base deficit as end-points of resuscitation

Simple Pneumothorax vs. Tension Pneumothorax

Bailey and Love's Short Practice of Surgery, 28th Edition

Definitions

Bailey and Love (Ch. 60): "Tension pneumothorax is when (independent of aetiology) there is a build-up of positive pressure within the hemithorax, to the extent that the lung is completely collapsed, the diaphragm is flattened, the mediastinum is distorted and, eventually, the venous return to the heart is compromised."

Comparison Table

Aetiology / Causes

Simple Pneumothorax

• Common in young males (mid-teens to late twenties); tall stature; family history
• Due to rupture of small blebs, vesicles or bullae - typically at the apex of the upper lobe or upper border of lower/middle lobes
• No underlying lung disease

• Older patients with underlying lung disease (emphysema, TB, cavitating disease, necrotising tumours)
• The pleural leak occurs as part of the underlying disease process
• Less well tolerated due to reduced pulmonary reserve

• Rib fractures, penetrating chest injury
• Central line insertion, positive-pressure ventilation (barotrauma)

Tension Pneumothorax

1. Penetrating chest trauma
2. Blunt chest trauma with parenchymal lung injury and air leak that did not spontaneously close
3. Iatrogenic (e.g. central venepuncture, positive-pressure ventilation)
4. Mechanical positive-pressure ventilation - high airway pressures force air through a small breach

Clinical Features

Simple Pneumothorax

• Sudden onset pleuritic chest pain and breathlessness
• Degree of dyspnoea related to size of pneumothorax and underlying pulmonary reserve
• Reduced chest expansion on affected side
• Hyper-resonance on percussion
• Reduced/absent breath sounds
• Patient is haemodynamically stable
• No tracheal deviation

Tension Pneumothorax

• Increasing restlessness
• Tachypnoea and dyspnoea (severe)
• Distended neck veins (raised JVP - similar to pericardial tamponade)
• Hyper-resonance over affected hemithorax
• Decreased or absent breath sounds over affected side
• Tracheal deviation away from affected side - this is a late finding and is not required to confirm the diagnosis
• Haemodynamic collapse - hypotension, tachycardia, cyanosis
• Deteriorating consciousness

Danger: Tension Pneumothorax vs. Pericardial Tamponade

1. Airway obstruction
2. Tension pneumothorax
3. Pericardial tamponade
4. Open pneumothorax
5. Massive haemothorax
6. Flail chest

Treatment

Simple Pneumothorax

• Small (<2 cm, not breathless) - conservative management, discharge, OPD review in 2-4 weeks
• Large (>2 cm) or breathless - needle aspiration via 16-18G cannula (aspirate <2.5 L)
  • Success (size now <2 cm, breathing improved) - consider discharge
  • Failure - chest drain (8-14 Fr), admit

• 2 cm or breathless - needle aspiration first; if fails, chest drain + admit

• 1-2 cm - admit, high-flow oxygen (unless O2-sensitive), observe 24 hours
• <1 cm - admit, observe

• Second ipsilateral pneumothorax
• First contralateral pneumothorax
• Bilateral spontaneous pneumothorax
• Pneumothorax failing to settle despite drainage
• Spontaneous haemothorax; professions at risk (pilots, divers)
• Pregnancy

• Anterior to the mid-axillary line
• Above the nipple level
• Below and lateral to pectoralis major
• Ideally at the 5th intercostal space; always above the upper border of the lower rib (to avoid neurovascular bundle)
• Current recommendation: small bore (10-14 Fr) Seldinger-type drain, under ultrasound guidance

Tension Pneumothorax - Emergency Treatment

"Tension pneumothorax is a clinical diagnosis and treatment should NEVER be delayed by waiting for radiological confirmation."

• Historically: large-bore cannula (14G) into the 2nd intercostal space, mid-clavicular line
• Current preferred approach: direct chest drain insertion into the "safe triangle" (4th/5th ICS, anterior axillary line)
• In extremis (no equipment/time): finger thoracostomy at the same location - finger inserted through the chest wall to allow immediate air escape

• Formal intercostal chest tube (large bore) connected to underwater seal
• Relieves the positive pressure, allows lung to re-expand

Recurrence

• After 1st episode: ~30% risk of recurrence
• After 2nd episode: risk rises substantially - surgical management indicated