GC188 Hit By A Van, In Shock With Internal Bleeding Abdominal Injury
A trauma case in which a patient struck by a van presents with hemorrhagic shock due to intra-abdominal organ injury requiring urgent assessment and intervention.
Hit by a Van, in Shock with Internal Bleeding: Abdominal Injury
This GC 188 lecture by Dr S. Tsang is a case-based walkthrough of trauma management centred on an elderly pedestrian struck by a van. It integrates ATLS (Advanced Trauma and Life Support) and Definitive Surgical Trauma Care principles into a scenario that tests your understanding of the primary survey, resuscitation, shock management, abdominal injury evaluation, damage control surgery, and age-specific considerations in elderly trauma patients.
Big idea: Trauma kills in a trimodal distribution — the "golden hour" is where you can change the outcome. Most trauma deaths in that window are from haemorrhagic shock. Your job is to find and stop the bleeding while simultaneously resuscitating, not sequentially.
Trimodal death distribution (Trunkey 1989): Three peaks of trauma mortality — immediate, early, and late. [1]
| Peak | Timing | Cause | Intervention |
|---|---|---|---|
| 1st peak (Immediate) | Seconds to minutes | Massive brain/brainstem injury, high cervical spine injury, major vessel disruption (aorta, heart) | Prevention (seatbelts, helmets, speed limits) — these patients rarely survive even with perfect care |
| 2nd peak (Early) | Minutes to hours | Intracranial haemorrhage, haemopneumothorax, splenic/hepatic laceration, pelvic fractures, multiple haemorrhage sources | Golden hour management — ATLS primary survey, resuscitation, and early surgical intervention |
| 3rd peak (Late) | Days to weeks | Sepsis, Multi-Organ Failure (MOF) | Depends on quality of initial management — preventing the "lethal triad" (hypothermia, acidosis, coagulopathy) |
Why this matters: The lecture emphasizes that the 2nd peak is modifiable. Your competence in the golden hour determines whether the patient survives or progresses to the 3rd peak.
What the trimodal graph shows: deaths plotted against time with three peaks — immediate (prevention), early hours (golden hour management oval), and late weeks (death due to sepsis / multi-organ failure). Your exam job sits under the middle peak. [1]
M/75, pedestrian hit by a van at 50 km/h, thrown 3 metres. Transferred from regional hospital at 9:30 am. Stable vital signs en route. [1]
Key features to extract from the ambulance report:
- Age 75 → elderly, expect blunted physiological responses
- Mechanism: high-energy blunt trauma (50 km/h), thrown 3 metres → significant deceleration forces → think solid organ injury, brain injury, thoracic injury
- "Stable en route" — does NOT mean safe; elderly patients can be normotensive despite significant blood loss due to pre-existing hypertension medications
Primary survey performed simultaneously with resuscitation. Universal precaution and PPE observed. [1]
The primary survey is NOT "assess first, then treat." It is simultaneous — you assess and intervene at the same time, moving through ABCDE in order of lethality.
Assessment Results
| Component | Finding | Interpretation |
|---|---|---|
| A (Airway) | Breathes spontaneously, yells for pain | Patent airway; able to phonate = air moving through larynx |
| B (Breathing) | Symmetrical chest movement | No tension pneumothorax, no flail chest at this point |
| C (Circulation) | (Vital signs not explicitly given initially but later become critical) | Needs large-bore IV access and fluid challenge |
| D (Disability) | GCS 15/15, pupils symmetrical and responsive to light | No acute intracranial emergency at this moment |
| E (Exposure) | (Further findings on secondary survey) | Undress completely, log-roll, assess entire body |
Why simultaneous?
If you wait to finish the entire primary survey before starting resuscitation, a patient with tension pneumothorax or massive haemorrhage will die. You needle-decompress a tension pneumothorax the moment you identify it in "B," not after you've completed "E."
4. Resuscitation
Airway: signs of compromised airway include hoarseness, stridor, charcoal particles (burns). Options: oropharyngeal airway, endotracheal intubation, cricothyroidotomy. Neutral position of head and neck with bimanual in-line stabilization. [1]
Why neutral position? Every blunt trauma patient is assumed to have a cervical spine injury until proven otherwise. Head-tilt chin-lift is CONTRAINDICATED. Use jaw thrust instead.
Indications for intubation/ventilation (from later slide):
| Airway Indications | Breathing Indications |
|---|---|
| Obstruction (facial injury, burn) | Paralysis (spinal injury, drug-induced) |
| Decreased GCS < 8/15 | Apnoea |
| Decreased GCS < 8/15 | |
| CO₂ retention with respiratory acidosis | |
| Hypoxaemia | |
| Haemodynamic instability |
GCS < 8 → intubate. This protects the airway from aspiration and allows controlled ventilation. [1]
Cricoid pressure (Sellick manoeuvre): Prevents passive aspiration during intubation by compressing the oesophagus against the vertebral body.
Variable performance device (e.g., facial mask) vs Fixed performance device (e.g., Venturi mask, ventilator). [1]
| Device Type | Examples | FiO₂ Control |
|---|---|---|
| Variable performance | Simple face mask, nasal cannula | FiO₂ varies with patient's respiratory rate and tidal volume |
| Fixed performance | Venturi mask, ventilator | Delivers precise, predictable FiO₂ |
Avoid hyperventilation. Ensure PaCO₂ between 35–40 mmHg. Avoid respiratory alkalosis → shifts O₂ dissociation curve to left → increased Hb O₂ affinity → decreased tissue O₂ availability. [1]
Why this matters from first principles:
- The oxygen-haemoglobin dissociation curve describes how readily Hb binds and releases O₂
- Left shift = Hb holds onto O₂ more tightly = less O₂ delivered to tissues
- Causes of left shift: ↓CO₂ (alkalosis), ↓temperature, ↓2,3-DPG, ↑pH
- In a trauma patient who is already hypoperfused, the LAST thing you want is further impairment of tissue O₂ delivery
Ambubag ventilation: Minute volume 6–8 L (8–10 mL/kg body weight), Frequency 12–14/min. [1]
4C. Circulation / Fluid Resuscitation
A minimum of 2 large bore intravenous cannulae. 1–2 litres full rate, warmed. Crystalloid: warmed lactate Ringer's (Hartmann's solution) / Normal saline. No evidence to support superiority of colloid over crystalloids. DON'T OVERLOAD! [1]
Why warmed? Cold fluids worsen hypothermia, which is one of the three components of the lethal triad (hypothermia + acidosis + coagulopathy). Hypothermia impairs clotting factor function and platelet aggregation.
Why large bore? Flow rate is governed by Poiseuille's law: flow ∝ r⁴. A wider cannula dramatically increases flow rate. The lecture provides a specific table:
Cannula gauge vs flow rate table: [1]
| Cannula Gauge | Crystalloid Flow (mL/min) | Colloid Flow (mL/min) |
|---|---|---|
| 8.5 | 1000 | 600 |
| 14 | 125 | 90 |
| 16 | 85 | 65 |
| 18 | 60 | 35 |
| 20 | 40 | 17 |
High Yield
An 8.5G (large introducer sheath) delivers 1000 mL/min crystalloid — this is what you use in massive haemorrhage. A 20G cannula only delivers 40 mL/min, which is useless for resuscitation.
t½ of crystalloid (BSS) ≈ 20 minutes. t½ of colloid (e.g., Gelofusine) ≈ 4–6 hours. Trauma leads to leaky cells in pulmonary capillary bed → greater risk of pulmonary oedema with colloid. [1]
Why crystalloid preferred?
- Trauma causes a systemic inflammatory response → capillary leak
- Colloid molecules that leak into the interstitium draw MORE water into the extravascular space → worsens pulmonary oedema
- Despite the shorter intravascular half-life of crystalloids, they don't carry this risk
- Multiple RCTs (SAFE trial, etc.) show no mortality benefit of colloids in trauma
CO = HR × SV. SV depends on preload (intravascular volume), afterload (peripheral resistance), contractility. Possible cardiac failure in elderly or diseased heart. [1]
Why this is critical in this case: The patient is 75 and on Atenolol 100 mg daily (beta-blocker). Beta-blockers:
- Blunt tachycardia → heart rate won't rise appropriately in response to hypovolaemia
- Reduce contractility → heart can't compensate by increasing stroke volume
- This means the usual vital sign responses to shock are MASKED in this patient
Consider early transfusion: dilutional effect of fluid resuscitation on blood oxygen-carrying capacity. [1]
If you give 2L crystalloid to a bleeding patient, you dilute the remaining red cells → haemoglobin drops → less O₂ carrying capacity. This is why early blood transfusion matters.
Bruising over right forehead + left occiput → coup-contrecoup. No signs of skull base fracture. Bruising over right lower chest, no flail chest. Tenderness over upper abdomen, not distended. Pelvis stable, no tenderness. DRE: no blood, no high-riding prostate, anal tone positive. Whole spine: no stepping nor local tenderness. No deformities/tenderness over 4 limbs. [1]
| Finding | Clinical Significance |
|---|---|
| Right forehead + left occiput bruising | Coup-contrecoup mechanism → risk of cerebral contusion, SDH, traumatic SAH |
| No skull base fracture signs | No raccoon eyes, no Battle's sign, no CSF rhinorrhoea/otorrhoea |
| Right lower chest bruising | Underlying rib fractures possible → right hepatic/renal injury from adjacent force transmission |
| Upper abdominal tenderness, not distended | Solid organ injury (liver/spleen) possible; NOT yet distended = early |
| Pelvis stable | Low likelihood of major pelvic fracture (significant bleeding source excluded) |
| DRE: no blood, no high-riding prostate, anal tone +ve | No rectal injury, no urethral injury (safe to insert Foley), no spinal cord injury affecting sphincter |
| Spine: no stepping/tenderness | Low suspicion for spinal fracture |
6. Adjuncts and Investigations
A: Allergies – nil. M: Medications – Atenolol 100 mg daily, Norvasc 5 mg daily, PRN analgesics. P: Past health – hypertension, gout. L: Last meal – breakfast ~8 am. E: Event – accident ~9 am, head-on collision by van at 50 km/h, smashed at windscreen and bumper, thrown 10 metres, landed on back. [1]
Critical Exam Point
Atenolol (beta-blocker) masks tachycardia. This patient's heart rate may NOT increase despite significant hypovolaemia. A "normal" HR of 60–80 in this context is NOT reassuring — it may represent severe occult shock. The lecture later demonstrates this: when the patient crashes, HR is only 60 bpm despite a BP of 80/40.
Last meal at 8 am → relevant for anaesthetic risk (aspiration during emergency intubation).
Event detail: thrown 10 metres (different from initial report of 3m) → very high energy mechanism → expect occult injuries.
CBC / LRFT / Amylase / ABG / Clotting profile / Type and Screen [1]
| Test | Why |
|---|---|
| CBC | Baseline Hb (may be falsely normal initially due to haemoconcentration), WCC, platelets |
| LRFT (LFT + RFT) | Baseline renal function (Cr 130 already elevated → pre-existing CKD or dehydration), liver injury may elevate transaminases |
| Amylase | Elevated in pancreatic injury; also bowel perforation. In this case: 130 U/L (mildly elevated → suspicious) |
| ABG | pH 7.30 = metabolic acidosis → tissue hypoperfusion → lactate production |
| Clotting profile | INR 1.2 → slightly elevated, baseline coagulopathy or early consumption |
| Type and Screen | Essential before transfusion |
XR chest: normal. Hb 10.5 g/dL, WCC 8.0, Plt 150, INR 1.2, Ur 14.1, Cr 130, Amylase 130, pH 7.30, pO₂ 10.6 kPa, pCO₂ 4.2 kPa [1]
Interpretation:
- Hb 10.5 → already low for a male (normal ~13–17) → either chronic anaemia OR has already bled significantly (remember: in acute haemorrhage, Hb may not drop immediately because you lose whole blood)
- pH 7.30 → metabolic acidosis → likely lactic acidosis from hypoperfusion (shock)
- pCO₂ 4.2 kPa (normal ~4.7–6.0) → slightly low → attempting to compensate (blowing off CO₂)
- pO₂ 10.6 kPa → just adequate (normal > 10.7 on room air) → borderline
- Amylase 130 → mildly elevated (normal ~30–110 depending on lab) → pancreatic injury possible
- Cr 130 → elevated → pre-existing renal impairment or acute kidney injury from hypoperfusion
FAST: Morrison's pouch, splenorenal recess, pelvis, pericardial cavity [1]
| FAST View | What You're Looking For |
|---|---|
| Subxiphoid/Pericardial | Pericardial effusion (cardiac tamponade) |
| Morrison's pouch (RUQ) | Hepatorenal free fluid → liver/right kidney injury |
| Splenorenal recess (LUQ) | Perisplenic free fluid → splenic injury |
| Pelvis (suprapubic) | Free fluid in Pouch of Douglas/rectovesical space |
FAST is for FREE FLUID detection, not for grading organ injury. It answers one question: "Is there intraperitoneal fluid?" If FAST is positive in an unstable patient → laparotomy. If stable → CT for detailed assessment. [2]
Visual recognition (RUQ FAST still): labelled liver, kidney, and peri-renal fascia with arrows on an anechoic stripe in Morrison’s pouch — free fluid is the black stripe between solid organs, not a “blurry kidney.” [1]
Insertion of urinary catheter and gastric catheter [1]
- Urinary catheter: Monitor urine output (goal 0.5 mL/kg/hr) as a surrogate for renal perfusion and overall resuscitation adequacy. Do NOT insert if suspected urethral injury (blood at meatus, high-riding prostate, scrotal haematoma) — use suprapubic catheter instead.
- Gastric catheter (NG or OG tube): Decompress stomach (reduce aspiration risk), check for blood.
Marked pathologies (√) in the lecture: [1]
| Body Region | Possible Injuries | Present in This Case? |
|---|---|---|
| Head | Brain contusion, SDH, traumatic SAH, skull fractures | √ (bruising pattern) |
| Chest | Lung/cardiac contusion, cardiac tamponade, haemo/pneumothorax, rib fractures | √ (chest bruising) |
| Abdomen | Liver/splenic laceration or contusion, mesenteric laceration, bowel contusion/perforation | √ (upper abdominal tenderness) |
| Retroperitoneum | Renal contusion, pancreatic contusion/fracture, aortic perforation | √ (high amylase, mechanism) |
| Pelvis/GU | Bladder contusion/perforation, urethral injury | ✗ (pelvis stable, DRE normal) |
| Extremities | Long bone fracture, haemorrhage, fat embolism | ✗ (no deformity) |
Haemodynamically NORMAL patients: ample time for full evaluation. Haemodynamically STABLE patients: investigations to establish source and whether bleeding has stopped. Haemodynamically UNSTABLE patients: CT NOT possible. [1]
What the “Next destination?” collage shows: operating theatre vs CT gantry vs ICU monitor vs ward — haemodynamic status chooses the door. Unstable bleeders belong in theatre (or angioembolisation pathways), not in a prolonged CT queue. [1]
This is the KEY decision point the lecture tests:
Diagnostic Peritoneal Lavage (DPL)
DPL: accurate, fast. Negative finding in shock patients might signify retroperitoneal bleeding. Positive DPL criteria: presence of bowel content/frank blood, RBC ≥ 100,000/mm³ (unspun), unspun WCC ≥ 500/mm³. [1]
DPL Positive Criteria — High Yield
| Criterion | Value |
|---|---|
| Gross blood/bowel content | Immediate positive |
| RBC count | ≥ 100,000/mm³ (unspun) |
| WCC count | ≥ 500/mm³ (unspun) |
A negative DPL in a patient who remains in shock should make you think of retroperitoneal bleeding (e.g., aortic injury, renal pedicle injury, pelvic fracture bleeding) — because DPL only samples the peritoneal cavity, NOT the retroperitoneum.
BP 80/40 mmHg, HR 60 bpm, nil urine output, RR 30/min with accessory muscle use, SaO₂ 88% on 2L O₂ via nasal cannula, equal bilateral air entry, GCS E2M4V2 (=8/15), pupils equal and responsive. [1]
Interpretation:
- BP 80/40 → severe hypotension → Class III–IV haemorrhagic shock
- HR 60 → INAPPROPRIATELY SLOW → beta-blocker effect (Atenolol). A young patient in this state would have HR > 120
- Nil urine output → kidneys are shutting down from hypoperfusion
- RR 30 → tachypnoea → body trying to compensate for metabolic acidosis (Kussmaul-type) AND hypoxia
- SaO₂ 88% on 2L → hypoxaemic → needs higher FiO₂, likely needs intubation
- GCS 8 (E2M4V2) → dropped from 15 → EITHER from brain injury (expanding haematoma) OR from global hypoperfusion to the brain
- Equal bilateral air entry → rules out tension pneumothorax / massive haemothorax as cause of the crash
Importance of frequent re-evaluation [1]
Clinical Pearl
A patient who was GCS 15 and is now GCS 8 needs immediate action. GCS ≤ 8 is an absolute indication for intubation (to protect airway). But you must also address WHY the patient deteriorated — in this case, hypovolaemic shock with possible expanding intracranial haemorrhage.
10. Shock Management
Shock = inadequate organ perfusion and tissue oxygenation [1]
Hypovolaemic? "Blood on the floor and four more…" [1]
| Type | Mechanism | CO | SVR | Preload |
|---|---|---|---|---|
| Hypovolaemic | Volume loss → ↓preload | ↓ | ↑ | ↓ |
| Cardiogenic | Pump failure | ↓ | ↑ | ↑ |
| Obstructive | Tamponade, tension PTx | ↓ | ↑ | ↓ (extrinsic compression) |
| Distributive | Vasodilation (sepsis, neurogenic, anaphylaxis) | ↑ (early sepsis) | ↓ | ↓ |
In trauma patients: assume hypovolaemic shock until proven otherwise. [1]
"Blood on the floor and four more" — the 5 places where significant blood loss can hide:
- External (floor) → visible, control with direct pressure
- Chest (haemothorax)
- Abdomen (with retroperitoneum)
- Pelvis
- Long bones (femur fracture can lose 1–2L)
Tension pneumothorax: clinical diagnosis, needle decompression. Massive haemothorax: chest drainage. Cardiac tamponade: pericardiocentesis. [1]
| Condition | Key Features | Treatment |
|---|---|---|
| Tension pneumothorax | Absent breath sounds, tracheal deviation, distended neck veins, hypotension | Needle decompression (2nd intercostal space, midclavicular line) → then chest drain |
| Massive haemothorax | Dullness to percussion, absent breath sounds, hypotension | Chest drain (5th intercostal space, anterior axillary line). If > 1500 mL initial output or > 200 mL/hr → thoracotomy |
| Cardiac tamponade | Beck's triad (muffled heart sounds, distended neck veins, hypotension), PEA | Pericardiocentesis (subxiphoid approach) |
Chin lift and jaw thrust (NO HEAD TILT). Cricoid pressure to prevent aspiration. Orotracheal intubation. [1]
Full-rate infusion of crystalloid via ≥ 2 large bore angiocatheters. Warmed by storage or via warming device. [1]
ATLS haemorrhagic shock classes (lecture table; Class III–IV highlighted as needing blood) [1]:
| Parameter | Class I | Class II | Class III | Class IV |
|---|---|---|---|---|
| Blood loss (mL) | Up to 750 | 750–1500 | 1500–2000 | > 2000 |
| Blood loss (% volume) | Up to 15% | 15–30% | 30–40% | > 40% |
| Pulse rate | < 100 | > 100 | > 120 | > 140 |
| Blood pressure | Normal / ↑ | Decreased | Decreased | Decreased |
| Urine output (mL/h) | > 30 | 20–30 | 5–15 | Negligible |
| Mental status | Slightly anxious | Mildly anxious | Anxious, confused | Confused, lethargic |
| Fluid replacement | Crystalloid | Crystalloid | Crystalloid + blood | Crystalloid + blood |
Achieve urine output 0.5 mL/kg/hour. Stop the bleeding! Bleeding may increase with increase in BP! [1]
This is the concept of permissive hypotension — you don't try to normalise BP to 120/80 in an actively bleeding trauma patient. Higher BP means higher perfusion pressure to the bleeding site, which means MORE bleeding. Target a SBP ~90 mmHg, MAP ~70 mmHg until surgical haemostasis. [1] [3]
11. Blood Transfusion
Transient/non-responder → blood transfusion indicated. When infusion of BSS > 30 mL/kg, transfusion is indicated. Ratio of RBCs : FFP : Platelets = 1:1:1. No steroid, no vasopressor to treat hypovolaemic shock in trauma patients. Surgical intervention: STOP THE BLEEDING! [1]
Massive Transfusion Protocol — High Yield
Key exam points:
- RBC : FFP : Platelets = 1:1:1 — this balanced ratio reduces the risk of dilutional coagulopathy
- No vasopressors or steroids — vasopressors constrict peripheral vessels and are useless when the tank is empty; steroids are immunosuppressive and don't help haemorrhagic shock
- BSS > 30 mL/kg triggers blood transfusion — for a 70 kg patient, that's ~2.1 L of crystalloid
- Transient responder = BP improves initially with fluid then drops again → still bleeding → needs blood and likely surgery
- Non-responder = BP doesn't improve with fluid → actively exsanguinating → immediate surgery
| Category | Response to Initial 1–2L Crystalloid | Action |
|---|---|---|
| Responder | Vital signs normalise and remain stable | Continue monitoring, investigate |
| Transient responder | Initial improvement then deterioration | Blood transfusion, prepare for surgery |
| Non-responder | No improvement | Immediate blood + surgical intervention |
Storage defect: 2,3-DPG degradation → decreased O₂ affinity [NOTE: the slide says "decreased" but this is actually a LEFT shift = increased affinity = decreased O₂ delivery to tissues]. HyperK⁺: 40–70 mmol/L. Coagulation abnormality: Factor V/VIII decline quickly after 24 hours of collection. Haemostatic failure. Hypothermia (1 unit at 4°C to 37°C = 1255 kJ). Acidosis (citrate and lactate). Blood-transmitted infections (HBV, HCV, CMV, HIV window period, Malaria). Haemolytic transfusion reactions. Immunomodulation: increased suppressor-to-helper T-cell ratio → infection. [1]
Exam Trap: 2,3-DPG and O₂ Affinity
The slide states "2,3-DPG degradation: decreased O₂ affinity" — this is likely a slide error or shorthand. 2,3-DPG depletion in stored blood causes a LEFT shift of the O₂-Hb dissociation curve = INCREASED O₂ affinity = DECREASED O₂ delivery to tissues. The net effect is the same clinically (less O₂ to tissues), but if asked about the dissociation curve, remember: ↓2,3-DPG = left shift = increased affinity.
| Complication | Mechanism | Clinical Significance |
|---|---|---|
| HyperK⁺ | K⁺ leaks from stored RBCs (40–70 mmol/L in storage) | Cardiac arrhythmias, cardiac arrest |
| Hypothermia | Cold blood (4°C) | Worsens coagulopathy, arrhythmia risk |
| Coagulopathy | Dilution + storage loss of Factor V/VIII + platelet dysfunction | Ongoing bleeding despite surgical haemostasis |
| Acidosis | Citrate anticoagulant, lactate from stored cells | Worsens coagulopathy and cardiac function |
| Transfusion reactions | ABO mismatch, febrile non-haemolytic | Ranges from minor to fatal |
| Immunomodulation | ↑ Suppressor : helper T-cell ratio | Increased infection risk |
| Infections | HBV/HCV/HIV (window period), CMV, malaria | Screened but not zero risk |
Inform anaesthetist and OT staff. Initiate massive transfusion protocol. Replacement of 100% of patient's blood volume < 24 hours OR administration of 50% in 1 hour. ± Arrange post-op ICU care. Maintain reasonable BP before operation: SBP ~90 mmHg, MAP ~70 mmHg. Warm operation theatre. Prepare fluid warmer, suction. Prepare cell saver (for autotransfusion). [1]
Massive transfusion protocol (MTP) criteria (from this lecture):
- Replacement of 100% blood volume in < 24 hours, OR
- 50% blood volume in 1 hour
Cell saver: Collects shed blood from the surgical field, washes the RBCs, and returns them to the patient. Advantages: reduces allogeneic transfusion needs, avoids some transfusion complications.
Permissive hypotension target: SBP ~90, MAP ~70 — enough to perfuse brain and kidneys but not enough to blow off clots at bleeding sites.
13. Operative Management: Trauma Laparotomy
Generous midline laparotomy incision: from xiphisternum to pubic symphysis. 4-quadrant packing: RUQ, LUQ, right and left iliac fossae. Scoop out all blood clots. Allow anaesthetists to administer blood products and clotting factors. Remove packs from least bleeding site. DEFINITIVE SURGERY (if stable) OR Damage Control Surgery (DCS). [1]
- Provides maximum exposure
- Can be extended into sternotomy if needed for cardiac injury
- Avoids vascular structures
- Fast entry into peritoneal cavity
- Packs absorb blood AND apply direct pressure to bleeding surfaces
- You pack ALL four quadrants first → this buys time for anaesthesia to catch up with blood products
- Then remove packs sequentially from the least bleeding site → allows systematic identification of bleeding sources
Damage Control Surgery: Stop bleeding → Control contamination (staple off injured bowel WITHOUT anastomosis) → Temporary abdominal closure (limit heat and fluid loss, protect bowels). [1]
DCS cycle: Resuscitation → Damage Control Surgery → Correction of acid/base, clotting and temperature → Definitive Surgery in 24–48 hours. [1]
What the DCS sequence slide shows: corridor/resus photos → theatre packing/control → ICU correction of the lethal triad → return to theatre at 24–48 h for definitive repair. It is a physiological cycle, not “operate once and finish.” [1]
Why DCS instead of definitive repair?
The lethal triad drives this decision:
- Hypothermia → from open abdomen heat loss, cold fluids, cold blood
- Acidosis → from hypoperfusion (lactic acidosis), citrate from blood products
- Coagulopathy → from dilution, consumption, hypothermia impairing clotting cascade
Each component worsens the others in a vicious cycle. If you keep operating for definitive repair (e.g., bowel anastomosis, complex liver repair) while the triad is established, the patient will die on the table.
| DCS Phase | Actions | Goal |
|---|---|---|
| Phase 0 | Resuscitation in ED | Identify need for DCS |
| Phase 1 | Abbreviated surgery: packing, stapling bowel, temporary closure | Stop bleeding, prevent contamination |
| Phase 2 | ICU resuscitation | Correct hypothermia, acidosis, coagulopathy |
| Phase 3 | Return to OR in 24–48 hours | Definitive repair (anastomosis, formal closure) |
Temporary abdominal closure options:
- Bogota bag (IV fluid bag sewn to skin edges)
- Vacuum-assisted closure (VAC)
- Purpose: prevents evisceration, limits heat/fluid loss, avoids abdominal compartment syndrome from forced closure
Abdominal Compartment Syndrome
If you close the abdomen under tension after massive resuscitation (oedematous bowel), intra-abdominal pressure rises > 20 mmHg → compresses IVC (↓venous return), splints diaphragm (↓ventilation), reduces renal perfusion (↓UO). Diagnosis: bladder pressure via Foley catheter. Management: decompressive laparotomy with delayed closure. [2]
Cardiovascular: diminished pump function, lower CO, inability to mount appropriate catecholamine response, reduced flow to vital organs, co-existing medications blunting physiological responses. Respiratory: decreased lung elasticity and compliance, atrophy of bronchial epithelium → decreased particulate clearance. Renal: decreased renal mass, increased vulnerability to nephrotoxic agents. Musculoskeletal: osteoporosis → fracture tendency, decreased muscle mass. Comorbidities: diabetes, liver disease, malignancy, neurological/spinal disease. [1]
| System | Age-Related Change | Clinical Impact in Trauma |
|---|---|---|
| Cardiovascular | ↓ CO, ↓ catecholamine response, medications (β-blockers, CCBs) | Blunted tachycardia, delayed recognition of shock |
| Respiratory | ↓ Elasticity, ↓ compliance, ↓ mucociliary clearance | Higher risk of atelectasis, pneumonia, ARDS |
| Renal | ↓ Renal mass, ↓ GFR | More vulnerable to nephrotoxins (contrast, NSAIDs), AKI from hypoperfusion |
| Musculoskeletal | Osteoporosis, ↓ muscle mass | Lower energy needed to fracture bones; less physiological reserve |
| Comorbidities | DM, liver disease, malignancy, neurological | Impaired healing, immune function, baseline organ dysfunction |
1. Prompt management in the golden hour is important in prognosis. 2. Resuscitation takes place parallel with primary survey. 3. Careful attention to patients' past health and regular medications. 4. Frequent re-evaluation essential to discover adverse changes. 5. Hypovolaemic shock in trauma patients until proven otherwise. 6. Early blood transfusion for transient or non-responder. 7. Surgical intervention indicated for ongoing loss. 8. Attention to age-specific physiologic response to resuscitation. [1]
Take-home message: Trauma patients require TEAM work — Together Everyone Achieves More. [1]
17. Integration with Related GC Lectures
- Classification of injuries (blunt, penetrating, blast)
- Vascular injury assessment in extremities
- GCS assessment and interpretation
- Indications for CT brain
- Types of intracranial haemorrhage [6]
- Gustilo classification of open fractures
- Compartment syndrome (different from abdominal compartment syndrome)
- SIRS response to trauma
- Catabolic phase, ebb and flow phases
- Hormonal response (cortisol, catecholamines, aldosterone, ADH)
Exam Intelligence
| Trap | Correct Understanding |
|---|---|
| "Normal" HR in elderly trauma = reassuring | NO — beta-blockers mask tachycardia; HR 60 with BP 80/40 = severe shock |
| Colloid is better than crystalloid for trauma resuscitation | NO — no evidence of superiority; colloid may worsen pulmonary oedema via capillary leak |
| Negative FAST excludes abdominal injury | NO — FAST detects FREE fluid only; retroperitoneal bleeding and contained organ injuries may be FAST-negative [2] |
| Give vasopressors for hypovolaemic shock | NO — fill the tank first; vasopressors are for distributive shock or as a last resort [1] [3] |
| 2,3-DPG depletion in stored blood decreases O₂ affinity | Actually INCREASES affinity (left shift); less O₂ delivered to tissues |
| DPL-negative in shock = no abdominal problem | NO — think retroperitoneal bleeding (aorta, kidneys, pancreas, pelvis) |
| Close the abdomen after DCS | NO — temporary closure prevents abdominal compartment syndrome |
| Question Type | Discriminator |
|---|---|
| Unstable + FAST positive → | Laparotomy (NOT CT) |
| Stable + FAST positive → | CT abdomen with contrast |
| Unstable + FAST negative → | DPL or consider extra-abdominal source |
| Distributive shock features (↑CO, ↓SVR) → | Septic/neurogenic/anaphylactic (NOT hypovolaemic) |
| When to intubate in trauma → | GCS ≤ 8, airway obstruction, hypoxaemia, haemodynamic instability |
High Yield Summary
-
Trimodal death distribution
- the golden hour (2nd peak) is where YOU make the difference.
-
Primary survey (ABCDE) is SIMULTANEOUS with resuscitation
- not sequential.
-
Assume hypovolaemic shock in ALL trauma patients until proven otherwise.
-
"Blood on the floor and four more"
- external, chest, abdomen/retroperitoneum, pelvis, long bones.
-
Elderly patients on beta-blockers won't mount tachycardia
- a "normal" HR can be falsely reassuring.
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Fluid resuscitation
- 2 large bore IV, warmed crystalloid 1–2L, then assess response. Crystalloid preferred over colloid.
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Permissive hypotension
- Target SBP ~90, MAP ~70 until surgical haemostasis.
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Blood transfusion
- RBC : FFP : Plt = 1:1:1. No vasopressors. Trigger: BSS > 30 mL/kg or transient/non-responder.
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FAST
- answers: "Is there free intraperitoneal fluid?" Unstable + FAST positive → laparotomy. FAST negative + shock → consider retroperitoneal bleed → DPL.
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DPL positive criteria
- Frank blood/bowel content, RBC ≥ 100,000/mm³, WCC ≥ 500/mm³.
- Damage Control Surgery
- Stop bleeding, control contamination, temporary closure → ICU correction of lethal triad → definitive surgery at 24–48 hours.
- Avoid hyperventilation
- respiratory alkalosis → left shift → less O₂ to tissues.
- Stored blood complications
- HyperK⁺, hypothermia, coagulopathy (↓Factor V/VIII), acidosis, ↓2,3-DPG (left shift), infections, immunomodulation.
- GCS ≤ 8 → intubate.
- Frequent re-evaluation is essential.
Active Recall - Lecture Notes
[1] Lecture slides: GC 188. Hit by a van, in shock with internal bleeding Abdominal injury.pdf [2] Senior notes: Maksim Surgery Notes.pdf (Section 2.1 Trauma) [3] Senior notes: Ryan Ho Critical Care.pdf (Section 1.3.3 Management of Hypovolemic Shock) [4] Lecture slides: GC 175. A bus hit a train Multiple trauma; Disaster management.pdf [5] Past papers: 2022 Fourth Summative MCQ.pdf (Q3) [6] Senior notes: Ryan Ho Neurology.pdf (Section 11.3)
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