Haemorrhagic shock in details

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Haemorrhagic Shock - A Detailed Overview

Definition

Haemorrhagic shock is a state of circulatory failure resulting from a rapid reduction in intravascular blood volume due to acute blood loss. It produces an imbalance between systemic oxygen delivery and oxygen consumption, leading to cellular hypoxia, metabolic derangement, and - if untreated - death. It is the most common form of hypovolaemic shock and a component of virtually all other shock states.

Bailey and Love's Short Practice of Surgery, 28th ed
ROSEN's Emergency Medicine

Aetiology / Causes

Blood loss leading to haemorrhagic shock may be:

External haemorrhage:

Trauma (lacerations, fractures)
Gastrointestinal bleed (haematemesis, melaena, PR bleeding)
Obstetric haemorrhage (postpartum, placenta praevia)

Internal haemorrhage:

Haemothorax, haemoperitoneum, retroperitoneal haematoma
Ruptured ectopic pregnancy, ruptured aortic aneurysm
Pelvic fractures (>2000 mL blood loss), femur fractures (800-1000 mL)
Schwartz's Principles of Surgery, 11th ed

Pathophysiology

Macrocirculatory Response

Haemorrhage reduces venous return, preload, and cardiac output. Initially, an increase in heart rate and cardiac contractility is triggered. Baroreceptors in the aortic arch and carotid sinus detect the fall in arterial pressure and activate sympathetic outflow, causing:

Peripheral vasoconstriction (to preserve perfusion to heart, brain, kidneys)
Tachycardia
Release of catecholamines (epinephrine, norepinephrine)
Activation of the renin-angiotensin-aldosterone axis (renin, angiotensin II, aldosterone)
ADH/vasopressin release (water retention + vasoconstriction)
Cortisol, growth hormone, and glucagon release

The initial response is a narrowing of pulse pressure (vasoconstriction raises diastolic pressure) before systolic pressure falls. Hypotension is therefore a late sign of significant haemorrhage.

ROSEN's Emergency Medicine

Microcirculatory Response

Even before cardiac output falls, blood is diverted away from non-critical tissues. Ischemic cells:

Take up interstitial fluid (further depleting intravascular volume)
Produce lactate and free radicals
Cause cellular oedema, which can restrict adjacent capillary flow - the "no-reflow" phenomenon - preventing reversal of ischaemia even with restored macroperfusion

The cells also release inflammatory mediators: prostacyclin, thromboxane, prostaglandins, leukotrienes, endothelin, complement, interleukins, and TNF. Damage-associated molecular patterns (DAMPs), mitochondrial DNA, and formyl peptides amplify the systemic inflammatory response.

Miller's Anesthesia, 10th ed

The Shock Cascade

The "Shock Cascade" (Miller's Anesthesia, 10th ed): Ischemia triggers cellular and immune responses that injure remote, non-ischemic organs - the basis of MODS.

This inflammatory response becomes a self-sustaining disease process independent of its origin, laying the foundation for multiple organ dysfunction syndrome (MODS).

Base Deficit as an Early Marker

Lactic acid accumulates even before cardiac output falls significantly. Bicarbonate in plasma buffers pH, so pH may remain near normal while base deficit worsens. A base deficit more negative than -2 mEq/L is an early marker distinguishing trivial from clinically significant haemorrhage. A base deficit >8 mmol/L implies ongoing cellular shock.

ROSEN's Emergency Medicine; Schwartz's Principles of Surgery

Progressive vs. Nonprogressive Shock

A key physiological concept (Guyton & Hall):

Arterial pressure curves after different degrees of haemorrhage - progressive (red) vs. nonprogressive (black)

Fig. 24.2 (Guyton & Hall): Groups I-III (black lines, BP never below ~45 mmHg) - compensated/nonprogressive shock with recovery. Groups IV-VI (red lines) - progressive shock leading to death despite initial partial recovery.

Beyond a critical threshold of blood loss, shock becomes self-perpetuating - "the shock itself causes more shock." This is a vicious cycle driven by:

Baroreceptor reflexes (powerful sympathetic stimulation)
CNS ischaemic response (activated when MAP <50 mmHg)
Reverse stress-relaxation of blood vessels
RAAS activation
ADH secretion
Adrenal medullary epinephrine/norepinephrine release
Fluid absorption from intestinal tract and capillaries

Guyton and Hall Textbook of Medical Physiology

Organ-Specific Effects

Organ	Response
CNS	Prime neuroendocrine trigger; cortical activity depressed with hypoperfusion (reversible initially, then permanent); failure to recover neurological function = poor prognosis
Kidney	Selective medullary vasoconstriction; inability to concentrate urine (renal hibernation); tubular necrosis with prolonged hypotension; adrenal insufficiency in ~86% of acute haemorrhagic shock cases (high mortality association)
Heart	Protected until late stages; maintained or increased nutrient blood flow; cardiac dysfunction occurs terminally due to lactate, free radicals, and humoral negative inotropes; elderly cannot mount tachycardic response - rapidly progressive
Lung	Acts as a filter for inflammatory by-products; neutrophil/platelet aggregation in capillaries; increased permeability → ARDS (sentinel organ for MODS)
Gut	Earliest organ of hypoperfusion; intense vasoconstriction; "no-reflow" on macro-restoration; barrier breakdown → bacterial translocation → potentiates ARDS
Liver	Complex microcirculation; reperfusion injury; synthetic failure

Miller's Anesthesia, 10th ed

Classification (ATLS / PHTLS Staging)

The Advanced Trauma Life Support classification divides haemorrhagic shock into 4 classes:

Parameter	Class I	Class II	Class III	Class IV
Blood loss (mL)	Up to 750	750-1500	1500-2000	>2000
Blood loss (% BV)	Up to 15%	15-30%	30-40%	>40%
Pulse rate	<100	>100	>120	>140
Blood pressure	Normal	Normal	Decreased	Decreased
Pulse pressure	Normal/increased	Decreased	Decreased	Decreased
Respiratory rate	14-20	20-30	30-40	>35
Urine output (mL/h)	>30	20-30	5-15	Negligible
Mental status	Slightly anxious	Mildly anxious	Anxious/confused	Confused/lethargic

Important caveat: HR and BP are notoriously unreliable as sole indicators of haemorrhagic shock severity. Tachycardia may be blunted by beta-blockers, cardiac disease, or high fitness level. Pregnant patients must lose a larger relative blood volume before manifesting hypovolaemia. Elderly patients may not mount tachycardia.

Schwartz's Principles of Surgery, 11th ed; ROSEN's Emergency Medicine

Clinical Features and Diagnosis

History: Mechanism of injury, estimated visible blood loss, prior medications (anticoagulants, beta-blockers), last known vital signs

Physical exam signs:

Pallor, cold clammy skin, diaphoresis
Tachycardia (may be absent in elderly, beta-blocked patients)
Hypotension (late sign)
Narrowed pulse pressure
Decreased urine output
Altered mental status (confusion, agitation, obtundation)
Prolonged capillary refill time

Initial response to fluid:

Responders - normalise and stay stable; unlikely ongoing haemorrhage
Transient responders - improve then deteriorate; suggest ongoing bleeding
Non-responders - persistent hypotension despite resuscitation; mandate immediate source identification and intervention

Investigations:

Haemoglobin/haematocrit (may be normal acutely due to haemoconcentration)
Base deficit (most sensitive early marker)
Serum lactate
Arterial blood gas
Coagulation screen (PT/INR, aPTT, fibrinogen)
Viscoelastic testing: TEG (thromboelastography) or ROTEM (rotational thromboelastometry) for dynamic clotting assessment
FAST ultrasound (haemoperitoneum, haemopericardium, haemothorax)
Chest and pelvic X-rays
CT (only in stable or rapidly stabilising patients - hazardous to transport hypotensive patient for CT)

The Lethal Triad

A critical concept in haemorrhagic shock management:

Hypothermia + Acidosis + Coagulopathy

These three conditions are mutually reinforcing and progressively worsen outcomes:

Hypothermia impairs clotting factor function and platelet aggregation
Acidosis (partly iatrogenic from crystalloid resuscitation - normal saline pH 5.0, Lactated Ringer's pH 6.5) worsens coagulopathy
Coagulopathy leads to ongoing haemorrhage, further worsening hypothermia and acidosis

The lethal triad is often precipitated or worsened by inappropriate crystalloid resuscitation.

Fischer's Mastery of Surgery, 8th ed; Sabiston Textbook of Surgery

Acute Coagulopathy of Trauma (ACT)

ACT occurs early in haemorrhagic shock, before significant haemodilution from resuscitation fluids. Its mechanisms involve:

Tissue trauma activating the coagulation and fibrinolytic cascades
Consumption of clotting factors
Protein C activation (anticoagulant effect)
Endotheliopathy of trauma

Clinically, ACT is distinct from dilutional coagulopathy (which results from excessive crystalloid resuscitation). Both, however, contribute to ongoing haemorrhage if not recognised and treated.

Management

Prehospital

Direct pressure / tourniquet for compressible external haemorrhage
Pelvic binder for pelvic fractures
Splinting of long bone fractures
Large-bore IV access and commence blood products if available (prehospital blood transfusion reduces mortality in selected cases)

Emergency Department - Primary Survey (ATLS: ABCDE)

Airway with C-spine control
Breathing - address tension pneumothorax, haemothorax (needle decompression / chest drain)
Circulation - haemorrhage control, IV access, blood products
Disability - GCS
Exposure - full exposure, keep warm

Haemorrhage Control

Direct pressure, wound packing, tourniquet
Pelvic external fixation or binder
Resuscitative thoracotomy (in extremis penetrating trauma: cardiac arrest or imminent)
REBOA (Resuscitative Endovascular Balloon Occlusion of the Aorta) - for non-compressible torso haemorrhage as a bridge to definitive surgery; a 2026 systematic review compared REBOA vs resuscitative thoracotomy for this indication

Permissive Hypotension (Hypotensive Resuscitation)

Target systolic BP 80-90 mmHg (MAP ~60 mmHg) until definitive haemorrhage control is achieved. Rationale: aggressive normotension can "pop off" a sealing clot, worsen haemorrhage, dilute clotting factors, and cause hypothermia.

Important contraindications to permissive hypotension:

Traumatic brain injury (TBI): maintain SBP >110 mmHg per Brain Trauma Foundation; if combined haemorrhagic shock + severe TBI: MAP >80 mmHg
Blunt trauma (most cases)
Elderly patients with comorbidities (cardiac disease, carotid stenosis)
Penetrating trauma in urban settings is the primary evidence base
Mulholland & Greenfield's Surgery, 7th ed; Tintinalli's Emergency Medicine

Damage Control Resuscitation (DCR)

The modern paradigm for massive haemorrhage:

1. Avoid crystalloids

Crystalloids worsen dilutional coagulopathy, acidosis, and hypothermia
Use only as a temporary bridge when blood products are unavailable

2. Blood product resuscitation in 1:1:1 ratio

pRBCs : Fresh Frozen Plasma : Platelets = 1:1:1
Rationale: reconstitutes whole blood; the PROPPR trial showed early survival benefit (28-day mortality difference was not statistically significant)
Type O-negative pRBCs for women of childbearing age; pre-thawed AB plasma can be used immediately

3. Whole blood

Recent evidence suggests whole blood may be superior to component therapy when available

4. Tranexamic acid (TXA)

Anti-fibrinolytic agent
Given as early as possible after injury (ideally within 3 hours; benefit is lost after 3 hours)
Standard dose: 1 g IV over 10 min, then 1 g IV over 8 hours

5. Massive transfusion protocol (MTP)

Predefined protocol for patients needing >10 units pRBCs in 24 hours (up to 5% of civilian trauma)
Improves survival and reduces adverse outcomes when activated early

6. Viscoelastic testing (TEG/ROTEM)

Used alongside or instead of empiric MTP
Guides targeted component therapy (when to give FFP, cryoprecipitate, platelets, or TXA)
EAST guidelines endorse TEG in trauma and ICU patients
Mortality benefit over empiric MTP in penetrating trauma receiving >10 units pRBCs (33% vs. 54% mortality in one study)

7. Vasopressors

Minimal evidence for routine use in haemorrhagic shock
May be used as a temporising measure while blood products are administered
A "vasopressin-deficient" state has been described; vasopressin administration can be helpful in this subset
Sabiston Textbook of Surgery; Mulholland & Greenfield's Surgery, 7th ed; Miller's Anesthesia, 10th ed

Keep Warm - Prevent/Treat Hypothermia

Warm all IV fluids and blood products
Warm environment, active patient warming
Goal: prevent the lethal triad

Damage Control Surgery

Early operative bleeding control without full repair
Temporary vascular shunts, abdominal packing, abbreviated laparotomy
Definitive repair once patient physiology is restored in ICU

Endpoints of Resuscitation

Normalisation of:

Vital signs (HR, BP, urine output >30 mL/h)
Mental status
Base deficit (towards >-2 mEq/L)
Serum lactate (clearance rate is prognostic)
CVP / IVC collapse on ultrasound (distinguishes cardiogenic from hypovolaemic shock)

Complications

Early	Late
Exsanguination / cardiac arrest	ARDS
Acute kidney injury	Multi-organ dysfunction syndrome (MODS)
Coagulopathy / DIC	Abdominal compartment syndrome
Hypothermia	Nosocomial infection
Metabolic acidosis	Transfusion-related complications (TRALI, TACO, transfusion reactions)

Special Populations

Pregnancy: Circulating blood volume increases progressively; significantly larger blood loss required before haemodynamic compromise is apparent
Elderly: Cannot mount adequate tachycardia; often on beta-blockers or anticoagulants; haemorrhagic shock is rapidly progressive and unpredictable
TBI with haemorrhagic shock: Permissive hypotension contraindicated; requires higher BP targets to maintain cerebral perfusion pressure

Recent Evidence (2024-2026)

A 2025 systematic review on adjuvant therapies (PMID: 40158128) examined emerging adjuncts beyond standard DCR
A 2025 network meta-analysis (PMID: 41380067) on fluid resuscitation strategies in emergency settings found blood-based resuscitation strategies superior to crystalloid-based
A 2026 meta-analysis (PMID: 41885281) compared REBOA vs. resuscitative thoracotomy for non-compressible torso haemorrhage, adding to the growing literature on endovascular haemorrhage control

Summary Mnemonic: "HALT the Shock"

H - Haemorrhage control (direct pressure, TXA, surgery/REBOA)
A - Avoid crystalloids (use blood products 1:1:1)
L - Low BP tolerance (permissive hypotension unless TBI)
T - Temperature / Triad prevention (warm fluids, prevent hypothermia/acidosis/coagulopathy)

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