01Approach to the Critical Patient/attcp50

Immediate stabilization

›Hemorrhagic shock recognition

›SBP <90 mmHg as primary instability threshold

›HR >120 bpm with skin vasoconstriction

›Altered mental status with tachycardia

›ATLS class III/IV hemorrhage pattern

›Class III: 30-40% blood volume loss

›Class IV: >40% blood volume loss, immediately life-threatening

›If hemodynamically unstable, activate massive transfusion protocol immediately

›1:1:1 ratio pRBC:FFP:platelets

›Minimize crystalloid to reduce dilutional coagulopathy

›Airway and access

›Two large-bore IV access minimum

›16-gauge or larger antecubital or femoral

›IO access if IV not achievable in 2 attempts

›Airway protection if GCS <=8 or hemorrhagic shock unresponsive to resuscitation

›RSI preparation

›Anticipated difficult airway in trauma setting

Operative vs nonoperative decision

›Critical branching decision

›Hemodynamically unstable despite resuscitation

›Emergent laparotomy indicated

›Damage control surgery principle

›Peritonitis on exam

›Diffuse rigidity mandates laparotomy

›Rebound and guarding as supporting signs

›Hemodynamically stable

›CT abdomen/pelvis with IV contrast is standard

02History/hx63

Mechanism and event

›Blunt trauma mechanisms

›Motor vehicle collision (most common)

›Speed, seatbelt use, airbag deployment

›Steering wheel deformity

›Ejection from vehicle

›Falls

›Height and surface

›Right-sided or right upper quadrant impact

›Bicycle handlebar injuries

›Especially in pediatric patients

›Direct epigastric compression

›Assault or direct blow to right flank or RUQ

›Penetrating trauma

›Stab wound: location and estimated depth

›Right chest below nipple line or RUQ

›Multiple wounds

›Gunshot wound: entrance, exit, trajectory

›More likely to require operative intervention than blunt

Symptoms

›Abdominal complaints

›Right upper quadrant pain

›Onset and severity

›Radiation to right shoulder (referred diaphragmatic irritation)

›Kehr sign: right shoulder tip pain from hemoperitoneum

›Diaphragmatic irritation by blood

›Ipsilateral (right-sided) in liver injury

›Nausea and vomiting

03Physical Exam/exam43

Vital signs and hemodynamic status

›Hemodynamic assessment

›Blood pressure: SBP <90 mmHg as instability threshold

›ATLS definition of instability

›Trending blood pressure more informative than single value

›Heart rate: >120 bpm as significant tachycardia

›Persistent tachycardia despite resuscitation suggests ongoing hemorrhage

›Bradycardia in hemorrhagic shock is ominous (neurogenic component)

›Respiratory rate: tachypnea reflects shock state

›Temperature: hypothermia worsens coagulopathy (part of lethal triad)

›GCS and mental status: altered consciousness indicates Class III-IV shock

Abdominal exam

›Inspection

›Seatbelt sign across RUQ or lower chest

›Associated with RUQ injury pattern

›Indicates high-energy deceleration mechanism

›Abrasions or ecchymosis over right chest/abdomen

›Grey Turner sign (flank bruising) and Cullen sign (periumbilical bruising)

›Late findings (12-24 hours post injury)

›Suggest significant retroperitoneal hemorrhage

›Abdominal distension

›Rapidly expanding suggests ongoing large-volume hemorrhage

›Palpation

›RUQ tenderness

›Focal tenderness overlying liver

›Right lower rib tenderness (ribs 9-12 fractures strongly associated with liver injury)

›Guarding: voluntary vs involuntary

›Involuntary guarding indicates peritonitis

04Differential Diagnosis/ddx45

Life-threatening hemorrhagic causes

›Solid organ injuries

›Splenic laceration/rupture

›ICD-10 S36.0

›Left-sided mechanism, left shoulder pain (Kehr sign), LUQ tenderness

›Renal laceration

›ICD-10 S37.0

›Flank pain, hematuria, costovertebral angle tenderness

›Pancreatic injury

›ICD-10 S36.2

›Epigastric pain, elevated lipase, central mechanism

›Vascular injuries

›Mesenteric vessel injury

›Hemoperitoneum without solid organ injury on CT

›High-energy mechanism

›Retroperitoneal hemorrhage

›Pelvic fracture, aortic injury

›Stable pelvic x-ray does not exclude pelvic ring fracture

›Aortic injury

›ICD-10 S35.0

›Deceleration mechanism, widened mediastinum

Hollow viscus and other injury

›Hollow viscus injury

›Bowel perforation

›ICD-10 S36.5

›Peritonitis, free air on imaging

›Incidence increases with multiple solid organ injuries

›Diaphragmatic rupture

05Laboratory Tests/lt45

Hemorrhage and resuscitation labs

›Complete blood count

›Hemoglobin/hematocrit: cornerstone of NOM monitoring

›Initial value may be normal despite significant hemorrhage (dilution lag)

›Serial every 4-6 hours during NOM

›Platelet count

›Target >50,000 in actively bleeding patient

›Platelet transfusion threshold in massive hemorrhage

›Unexplained Hgb drop of >=10 g/L prompts repeat CT imaging

›Type and screen/crossmatch

›Immediate crossmatch for all significant liver injuries

›Minimum 4-6 units pRBC on hold

›Activate massive transfusion protocol (MTP) criteria

›ABC score >=2 (penetrating, SBP <=90, HR >=120, positive FAST)

›Coagulation panel

›PT/INR: anticoagulant reversal guidance

›INR >1.5 associated with worse outcomes

›PTT: factor replacement guidance

›Fibrinogen: target >1.5-2 g/L during active hemorrhage

›Cryoprecipitate when fibrinogen <1.5 g/L

›TEG/ROTEM if available: viscoelastic guided resuscitation

›More targeted factor replacement

›Reduces unnecessary blood product use

Organ function and shock markers

›Hepatic transaminases

›AST and ALT elevation strongly associated with liver laceration

›AST >200 U/L with ALT >80-100 U/L prompts CT imaging

›Combined AST >100 + ALT >80 + WBC >10,000: ~90% sensitivity, 92% specificity for liver laceration

06Diagnostic Tests/dt104

Scoring Systems

›AAST Organ Injury Scale (universally accepted grading system)

›Grade I: subcapsular hematoma <10% surface area; capsular tear <1 cm depth

›NOM success rate >95%

›Observation with serial exam often sufficient

›Grade II: subcapsular hematoma 10-50%; intraparenchymal hematoma <10 cm; laceration 1-3 cm depth, <10 cm length

›NOM standard of care

›Angiography rarely required

›Grade III: subcapsular hematoma >50% or expanding; intraparenchymal hematoma >10 cm or expanding; laceration >3 cm depth

›NOM appropriate in stable patients

›Higher angioembolization rate

›Grade IV: parenchymal disruption 25-75% of hepatic lobe or 1-3 Couinaud segments

›NOM possible but higher failure rate

›Angioembolization frequently required

›Grade V: parenchymal disruption >75% of hepatic lobe or >3 Couinaud segments; juxtahepatic venous injury

›Very high mortality

›Operative management usually required

›Grade VI: hepatic avulsion

›Near-universally fatal

›WSES Classification (World Society of Emergency Surgery)

›Integrates AAST grade with hemodynamic status

›WSES Minor (Grade I): AAST I-II, hemodynamically stable

›WSES Moderate (Grade II): AAST III, hemodynamically stable

›WSES Severe (Grade III): AAST IV-V, hemodynamically stable

›WSES Severe (Grade IV): any AAST grade, hemodynamically unstable

›WSES IV mandates operative or emergent angioembolization

›Assessment of Blood Consumption (ABC) Score

›Predicts need for massive transfusion

›Penetrating mechanism: 1 point

›SBP <=90 mmHg: 1 point

›HR >=120 bpm: 1 point

›Positive FAST: 1 point

›Score >=2 activates MTP in most protocols

MRI

›MRI role in liver laceration

›Limited role in acute setting

›Prolonged scan time incompatible with unstable patients

›Availability constraints in emergency setting

›Problem-solving indications in stable patients

›Characterization of complex hepatic lesions

›Differentiation of injury from pre-existing hepatic lesion (hemangioma, cyst)

›Biliary tree anatomy before ERCP or surgery

›MRCP (MR cholangiopancreatography)

›Non-invasive biliary tree assessment

›Evaluation for biloma or bile duct injury

›Useful in delayed presentation with biliary complications

›Contraindications

›Hemodynamic instability (absolute)

›Non-compatible implants (ferromagnetic foreign bodies in penetrating trauma)

CT

›CT abdomen/pelvis with IV contrast

›Gold standard imaging in hemodynamically stable patients

›Sensitivity 96-100%, specificity 96-100% for liver laceration

›Portal venous phase: laceration characterization and grade assessment

›Arterial phase: active extravasation (blush) detection

›Key CT findings

›Laceration: hypodense linear defect in hepatic parenchyma

›Perihepatic hematoma: crescentic hyperdense collection

›Active contrast extravasation (arterial blush): indicates active arterial hemorrhage

›Pseudoaneurysm: focal contrast pooling expanding in delayed phase

›Hemoperitoneum: free fluid in Morrison's pouch, paracolic gutters

›Delayed phase imaging

›Differentiates active bleeding from contained vascular injuries

›Pseudoaneurysm expands in delayed phase; extravasation disperses

›Injury grade assessment on CT

›Depth and extent of parenchymal disruption

›Involvement of hepatic veins or IVC (Grade V marker)

›Segment involvement using Couinaud system

›ACEP recommendation: CT is standard for hemodynamically stable blunt abdominal trauma (Level B recommendation)

›CT chest

›Associated injuries assessment

›Hemothorax or pneumothorax

›Pulmonary contusion

›Right lower rib fractures (ribs 9-12)

›Diaphragmatic continuity

›Follow-up CT imaging

›Routine surveillance CT not recommended in asymptomatic patients

›Asymptomatic surveillance 0% complication detection rate

›Clinical deterioration-prompted imaging detects 39% of complications

›Repeat CT indications: fever, increasing pain, unexplained Hgb drop, jaundice, SIRS

Ultrasound

›E-FAST (Extended Focused Assessment with Sonography for Trauma)

›First-line imaging in hemodynamically unstable patients

›GoR 1A recommendation for trauma assessment

›Rapid detection of intraperitoneal free fluid

›Performed in resuscitation bay without patient transport

›E-FAST views

›RUQ Morrison's pouch (hepatorenal space): most sensitive for hemoperitoneum

›LUQ splenorenal space

›Pelvis (pouch of Douglas/rectovesical pouch)

›Pericardial view: hemopericardium detection

›Bilateral lung: pneumothorax (loss of lung sliding)

›Performance characteristics

›Sensitivity for hemoperitoneum: 63-83% in adults

›Sensitivity lower in pediatrics: 42-52%

›Negative FAST does NOT exclude liver laceration

›Sensitivity for hepatic parenchymal injury <50%

›Limitations

›Operator dependent

›Bowel gas, obesity, subcutaneous emphysema impair views

›Cannot grade injury or detect retroperitoneal injury reliably

›Follow-up ultrasound

›Monitoring biloma formation in Grade IV-V injuries

›Anechoic or hypoechoic perihepatic collection

›Growth trend assessment

›Hepatic artery Doppler post-embolization

›Assess arterial perfusion

›Detect recanalization

07Disposition/dispo43

Operative and interventional pathway

›Immediate operative indications

›Hemodynamically unstable despite initial resuscitation

›Emergent laparotomy

›Damage control surgery: pack, temporize, ICU, re-look at 24-48 hours

›Peritonitis on exam

›Hollow viscus injury cannot be excluded

›Board-like rigidity

›Exsanguinating hemorrhage unresponsive to MTP

›Angioembolization pathway

›Hemodynamically stable with arterial blush on CT

›Interventional radiology activation

›Post-embolization ICU admission for monitoring

›AAST Grade III-V in stable patients

›Prophylactic embolization may reduce NOM failure

›Post-embolization complications monitoring

›Hepatic necrosis, biloma, abscess

Nonoperative management disposition

›ICU admission indications

›AAST Grade III-V injuries

›Serial hemoglobin every 4-6 hours

›Continuous hemodynamic monitoring

›Any patient requiring >2 units pRBC

›Comorbid traumatic brain injury or spinal cord injury

›High NOM failure risk profile (ISS >34, transfusion >4 units)

›Ward admission criteria

›AAST Grade I-II injuries in hemodynamically stable patients

›Serial exam and hemoglobin monitoring

08Treatment/t100

Resuscitation and hemorrhage control

›Damage control resuscitation

›Balanced resuscitation: 1:1:1 ratio (pRBC:FFP:platelets)

›Class I recommendation for massive hemorrhage

›Minimize crystalloid (lactated Ringer's preferred over normal saline)

›Permissive hypotension in penetrating trauma without TBI

›Target SBP 80-90 mmHg until hemorrhage control

›Not applied if concurrent traumatic brain injury

›Tranexamic acid (TXA)

›1 g IV bolus over 10 minutes, then 1 g IV over 8 hours

›Administer within 3 hours of injury per CRASH-2 protocol

›Mortality benefit lost if administered >3 hours post-injury

›Class I recommendation for traumatic hemorrhage within 3 hours

›Anticoagulant reversal

›Warfarin: 4-factor prothrombin complex concentrate (4F-PCC)

›25-50 units/kg IV (dose by INR)

›Plus vitamin K 10 mg IV for sustained reversal

›Dabigatran: idarucizumab 5 g IV (two 2.5 g doses)

›Factor Xa inhibitors (apixaban, rivaroxaban): andexanet alfa

›High dose: 800 mg IV bolus then 960 mg IV over 2 hours

›Low dose: 400 mg IV bolus then 480 mg IV over 2 hours

›Antiplatelet reversal: platelet transfusion (1 apheresis unit)

Nonoperative management

›NOM protocol for blunt liver injury

›Appropriate in 85-90% of blunt liver injuries

›Hemodynamically stable patients

›AAST Grade I-III primary candidates

›Grade IV-V NOM possible in highly selected stable patients at high-volume trauma centers

›Activity restriction

›Strict bedrest initially

›Mobilize as hemoglobin stable and pain allows

›Serial monitoring

›Hemoglobin every 4-6 hours for 24-48 hours

›Repeat CT if clinical deterioration

›NOM failure rate: ~2% Grade I, 3% Grade II, 5% Grade III, 9% Grade IV

›NPO until operative risk cleared

›Resume diet when stable and surgical planning complete

Angioembolization

›Hepatic angioembolization indications

›Active arterial blush on CT in hemodynamically stable patient

›Transcatheter embolization preferred over operative ligation

›High-grade injury (AAST III-V) in stable patient

›Adjunct to NOM to reduce failure rate

›NOM failure with accessible arterial source

›Embolization technique

›Selective vs non-selective embolization

›Selective (lobar/segmental) preferred to preserve hepatic function

›Non-selective used in coagulopathic patients or complex anatomy

›Embolic agents

›Gelfoam pledgets: temporary occlusion for moderate bleeding

›Coils: permanent occlusion for pseudoaneurysm

›N-butyl cyanoacrylate (glue): high-flow arteriovenous fistulae

›Post-embolization complications

›Hepatic necrosis: 2-5%

›Biloma: 4-7%

›Abscess formation

›Post-embolization syndrome: fever, pain (self-limited)

Operative management

›Damage control laparotomy

›Perihepatic packing as first intervention

›Three-point packing: above, below, and lateral to liver

›Target coagulation correction in ICU before re-look

›Re-look laparotomy at 24-48 hours

›Pack removal when coagulopathy corrected

›Hemostasis confirmation

›Fascial closure or temporary closure decision

›Pringle maneuver: portal triad occlusion

›Reduces hepatic inflow temporarily

›Safe for up to 60 minutes in normothermic liver

›Definitive hepatic repair

›Hepatorrhaphy: direct suture of lacerations

›Appropriate for Grade I-II injuries at laparotomy

›Argon beam coagulator or topical hemostatic agents

›Fibrin glue, oxidized cellulose, thrombin-soaked gelfoam

›Hepatic resection

›Reserved for Grade V devascularized segments

›High morbidity in acute trauma setting

›Juxtahepatic venous injury repair

›IVC or hepatic vein injury at hepatocaval junction

›Atriocaval shunt or total hepatic vascular exclusion

›Mortality >50% even with operative repair

Complication management

›Biloma

›Percutaneous drainage under CT or ultrasound guidance

›Indicated when >5 cm or symptomatic

›Culture-directed antibiotics if infected

›ERCP with sphincterotomy or stenting if bile duct communication

›Reduces biliary pressure

›Promotes fistula closure

›Hemobilia

›Angiography and embolization of causative pseudoaneurysm

›Gold standard treatment

›ERCP for clot evacuation if biliary obstruction

›Hepatic abscess

›Percutaneous drainage and culture-directed antibiotics

›Common organisms: Gram-negatives, polymicrobial

›IV antibiotics: piperacillin-tazobactam 3.375 g IV every 6 hours

›Adjust based on culture results

›Pain management

›Opioids as mainstay for acute pain control

›Morphine 2-4 mg IV every 4 hours PRN

›Hydromorphone 0.5-1 mg IV every 4 hours PRN

›Acetaminophen with caution given hepatic injury

›Maximum 2 g/day in hepatic injury

›Avoid NSAIDs: platelet dysfunction and renal risk

09Special Populations/sp73

Pregnancy

›Pregnancy-specific considerations

›Physiologic changes affecting assessment

›Increased blood volume (40-50%): shock signs appear later

›Supine hypotension syndrome from IVC compression

›Maternal tachycardia may be normal (baseline HR 10-15 bpm higher)

›Fetal assessment

›Cardiotocography (CTG) monitoring for viable fetus (>24 weeks)

›Minimum 4 hours if stable mechanism

›Immediate obstetrics consult

›Placental abruption screening

›Uterine pain, vaginal bleeding, non-reassuring fetal heart rate

›Imaging in pregnancy

›E-FAST preferred as first-line (no radiation)

›CT when benefits outweigh radiation risk (life-threatening injury)

›Fetal radiation dose per abdominal CT: approximately 10-35 mGy

›Threshold for fetal harm: >50 mGy (generally safe to perform if maternal benefit)

›MRI as alternative without ionizing radiation if time permits

›Resuscitation targets

›More aggressive volume resuscitation to protect uteroplacental perfusion

›Target maternal SBP >110 mmHg for fetal wellbeing

›Left lateral decubitus positioning to relieve IVC compression

›TXA in pregnancy

›Category B/B3: animal studies suggest safety, limited human data

›Use when hemorrhage benefit outweighs theoretical risk

Geriatric

›Older adult considerations

›Physiologic vulnerability

›Reduced physiologic reserve: tachycardia may be blunted by beta-blockers

›Normal SBP may mask relative hypotension (hypertensive baseline)

›Pre-existing anticoagulation very common

›Injury threshold

›Lower energy mechanisms cause significant injury (ground-level falls)

›Hepatomegaly from fatty liver disease increases injury susceptibility

›Coagulopathy from liver disease common

›Higher risk of NOM failure

›Age >55 historically associated with higher failure rates

›Lower threshold for surgical consultation

›More aggressive monitoring protocol

›Medication management

›Beta-blocker effect: masks tachycardic response to hemorrhage

›Warfarin/DOAC reversal frequently needed

›Renal function adjustment for contrast and medications

›Opioid dosing: reduce by 25-50% to avoid over-sedation

›Goals of care

›Advance directives and surgical candidacy discussion early

›Frailty assessment (CFS or FRAIL score)

›Multidisciplinary team involvement

Pediatrics

›Pediatric-specific approach

›Injury patterns

›Bicycle handlebar injuries are a common pediatric mechanism

›Child abuse must be considered in atypical mechanism

›Rib fractures less common (more elastic chest wall)

›Physiologic differences

›Higher baseline heart rate (age-dependent normal ranges)

›Greater physiologic reserve: shock signs appear late

›Hypotension is a late and ominous sign in children

›NOM success rate higher in pediatric patients

›>90% success rate across all injury grades at pediatric trauma centers

›Non-operative management is standard of care even for high-grade injuries

›Resuscitation volumes

›Initial fluid bolus: 20 mL/kg isotonic crystalloid (max 3 boluses)

›pRBC transfusion: 10 mL/kg for acute hemorrhage

›TXA: 15 mg/kg IV bolus (max 1 g) then 2 mg/kg/hour (max 1 g) over 8 hours

›Activity restrictions

›Grade I-II: 3 weeks restricted activity

›Grade III: 6 weeks

›Grade IV-V: 2-3 months

›Return to contact sports guided by follow-up imaging

›Imaging considerations

›FAST less sensitive in children (42-52%)

›CT with age-appropriate low-dose protocols

›MRI preferred when feasible to reduce radiation burden

›Reporting obligations

›Mechanism inconsistent with injury pattern: child protection services notification

10Background/b74

Epidemiology

›Incidence and burden

›Liver is the most commonly injured abdominal solid organ in both blunt and penetrating trauma

›Accounts for approximately 5% of all trauma admissions

›Most common abdominal injury in high-energy blunt mechanisms

›Distribution by mechanism

›Blunt trauma: 80-85% of liver injuries

›Penetrating trauma: 15-20%

›MVC is the single most common blunt mechanism

›Injury grade distribution

›80-90% of injuries are low-grade (AAST I-III)

›Grade I-II: approximately 50-60% of all cases

›Grade IV-V: <10% but account for disproportionate mortality

›Mortality

›Overall trauma-related liver injury mortality: 5-10%

›Isolated low-grade injuries (I-II): <1% mortality

›Grade V injury mortality: 25-50%

›Juxtahepatic venous injury mortality: >50% even with surgery

›NOM adoption

›Shift from operative to nonoperative management since 1990s

›NOM success rate for blunt injury: 85-90% overall

Pathophysiology

›Injury mechanisms

›Blunt injury mechanisms

›Deceleration: tearing of hepatic parenchyma at fixed points (ligaments, hepatic veins)

›Compression: direct crush between anterior abdominal wall and spine

›Hydraulic burst: sudden pressure increase within parenchyma

›Penetrating injury

›Direct parenchymal disruption along wound track

›Blast effect in high-velocity gunshot wounds

›Hepatic vascular anatomy and hemorrhage

›Dual blood supply: portal vein (75%) and hepatic artery (25%)

›Portal venous injury: slower venous hemorrhage

›Hepatic arterial injury: high-pressure arterial hemorrhage, requires angioembolization or ligation

›Hepatic veins drain directly into IVC

›Juxtahepatic venous injury: catastrophic hemorrhage

›Right adrenal vein enters IVC near right hepatic vein

›Biliary system

›Intrahepatic bile ducts run with portal triads

›Injury causes bile leak, biloma, or hemobilia

›Coagulopathy in hepatic trauma

›Lethal triad: hypothermia, acidosis, coagulopathy

›Mutual reinforcement worsens each component

›Hepatic parenchymal injury reduces clotting factor synthesis

›Especially relevant in pre-existing liver disease

›Dilutional coagulopathy from crystalloid resuscitation

›Reason for balanced 1:1:1 transfusion strategy

Therapeutic Considerations

›NOM evidence base

›85-90% of hemodynamically stable blunt liver injuries managed nonoperatively

›Grade is not the primary NOM criterion; hemodynamic status is

›High-volume trauma centers achieve higher NOM success rates

›Adjuncts improving NOM success

›Angioembolization reduces NOM failure rate by approximately 50%

›Prophylactic embolization in Grade III-V controversial but practiced at many centers

›NOM failure rates (approximate)

›Grade I: 2%, Grade II: 3%, Grade III: 5%, Grade IV: 9%, Grade V: 10%

›Angioembolization evidence

›Primary treatment for arterial hemorrhage in stable patients

›Technical success rate 85-95%

›Major complication rate (necrosis, abscess) 3-7%

›Role of embolization in Grade IV-V

›Reduces need for emergent laparotomy in selected patients

›Requires 24-hour IR availability

›Damage control philosophy

›Abbreviate operative time in physiologically depleted patients

›Perihepatic packing to tamponade venous hemorrhage

›Correct coagulopathy in ICU before definitive repair

›Bundle of care: TXA + MTP + permissive hypotension + damage control surgery

›Evidence-based survival benefit in massive hemorrhage

›Biliary complication management

›Bile leak occurs in up to 20% of Grade IV-V injuries

›ERCP with sphincterotomy reduces biliary pressure

›Percutaneous drainage for biloma formation

›Delayed hemobilia from pseudoaneurysm

›Occurs days to weeks post injury

›Angioembolization is definitive treatment

11Patient Discharge Instructions/pdi28

copy discharge instructions

›Liver laceration home care instructions

›Activity restrictions: no contact sports or heavy lifting for 4-8 weeks minimum

›Grade I-II injuries: restricted activity 4-6 weeks

›Grade III or higher: restrictions 6-12 weeks as directed by your surgeon

›No alcohol: avoid alcohol during recovery to minimize hepatic stress

›Diet: regular diet as tolerated; no special restrictions required

›Pain control: take prescribed medications as directed

›Acetaminophen limited to 2 tablets (500 mg each) every 6 hours maximum

›Avoid ibuprofen, naproxen, and other anti-inflammatory medications

›Return to emergency department immediately if you experience

›Severe abdominal pain, especially in the right upper abdomen

›Dizziness or fainting

›Vomiting blood or material that looks like coffee grounds

›Dark tarry stools (melena)

›Yellowing of the skin or eyes (jaundice)

›Fever above 38.5 C

›Rapid heart rate or feeling of heart pounding

›Increasing abdominal swelling or firmness

›Feeling significantly worse than when you left hospital

›Follow-up appointments

›Trauma surgery clinic in 1-2 weeks: mandatory

›Repeat blood work (hemoglobin) in 1 week

›Repeat CT or ultrasound scan at 4-6 weeks if Grade III or higher injury

›Important reminders

›Do not drive if taking opioid pain medications

›Have a responsible adult with you for the first 24-48 hours at home

›Keep all follow-up appointments even if you feel well: internal healing takes weeks

12References/r26

Guidelines and key sources

›Trauma society guidelines

›Eastern Association for the Surgery of Trauma (EAST): Practice Management Guidelines for Nonoperative Management of Blunt Hepatic Trauma

›NOM appropriate in hemodynamically stable patients regardless of grade

›Angioembolization for arterial extravasation in stable patients

›World Society of Emergency Surgery (WSES): Guidelines on Liver Trauma

›WSES classification integrating grade and hemodynamic status

›GoR 1A for E-FAST in hemodynamically unstable patients

›American College of Surgeons: ATLS (Advanced Trauma Life Support) Protocol

›Hemodynamic instability threshold: SBP <90, HR >120

›Damage control resuscitation principles

›Key studies and evidence

›CRASH-2 Trial: TXA within 3 hours reduces hemorrhage mortality

›1 g IV bolus then 1 g IV over 8 hours

›Mortality benefit lost after 3-hour window

›Peitzman et al: NOM success rates across injury grades at US trauma centers

›Croce et al: Nonoperative management of blunt hepatic trauma

›Established safety of NOM in high-grade injuries at experienced centers

›Kozar et al: Hepatic complications after NOM in Grade IV-V liver injuries

›Coding standards

›ICD-10 S36.1: Injury of liver and gallbladder

›S36.11: Injury of liver, contusion

›S36.12: Laceration of liver, unspecified degree

›S36.13: Minor laceration of liver (AAST I)

›S36.14: Moderate laceration of liver (AAST II-III)

›S36.15: Major laceration of liver (AAST IV-V)

›SNOMED CT: Laceration of liver (disorder) 19843004

Evidence & Review

Evidence & Review