vehicular / blunt trauma in dogs and cats.

How common and deadly is vehicular trauma in dogs and cats, and what non-medical factor often drives mortality?

• Vehicular trauma is one of the most common causes of severe trauma in small animals and carries worse prognosis than many other trauma types.

• Reported mortality:

  • Dogs: 18–19%

  • Cats: 43–45%

• A major driver of death is euthanasia due to financial constraints, not just medical futility.

What is blunt trauma, how often is polytrauma seen, and which body system is most frequently injured in vehicular trauma?

• Blunt trauma = trauma without skin penetration; vehicular trauma is the most common cause of serious blunt injury.

• Polytrauma = ≥2 body regions injured; present in about 72% of dogs with blunt trauma.

• Thoracic injuries are most common, present in up to 70% of trauma patients.

• Many patients have multiple thoracic injuries concurrently (≈43–62% in some reports).

• Other frequent injuries: hemoabdomen, traumatic brain injury (TBI), fractures and luxations.

What are the key pathophysiologic cascades triggered by blunt trauma, and how do they lead to acute traumatic coagulopathy?

• Blunt trauma delivers mechanical force → tissue damage, hemorrhage, edema.

• Complement activation → neutrophil chemotaxis & activation within hours → cytokine release → protein-rich edema from increased vascular permeability.

• Cytokines attract more inflammatory cells → progressive tissue injury over days.

• Inflammation spreads beyond impact site → systemic inflammation in 24–48 hours.

• Endothelial damage exposes tissue factor → drives coagulation & inflammation.

• Acute traumatic coagulopathy:

  • Related to injury severity, tissue hypoperfusion, and endothelial injury.

  • Proposed mechanisms: protein C activation, platelet activation, glycocalyx damage, fibrinogen depletion, and hyperfibrinolysis (large tPA release + reduced PAI-1 and TAFI activity).

  • Occurs independently of acidosis, hypothermia, or hemodilution (though those worsen coagulopathy).

  • Clinically manifests as hyperfibrinolysis, premature clot breakdown, and bleeding tendency.

• Trauma-induced inflammation, ischemia, and hypovolemia also strip the endothelial glycocalyx, causing capillary leak, edema, platelet aggregation, and impaired vascular responsiveness.

• Net result: risk of multiorgan dysfunction from global hypoperfusion, tissue hypoxia, and microvascular thrombosis.

What are the main thoracic injuries after blunt trauma, and what are their typical incidences and mechanisms?

• Thoracic injuries are most common overall.

• Pulmonary contusions (40–60% of dogs and cats):

  • Due to parenchymal hemorrhage → impaired oxygenation, ↓ compliance, local inflammation.

• Pneumothorax (≈13–63%):

  • From lung rupture and/or rib-fracture laceration.

• Pneumomediastinum:

  • Often accompanies trauma, with or without pneumothorax.

  • Macklin effect: alveolar rupture → air tracks along bronchovascular sheaths into the mediastinum.

  • Also possible with tracheal (or rarely esophageal) tear.

• Hemothorax (≈8–18% in dogs):

  • Usually from pulmonary laceration and/or chest wall hemorrhage; large vessel rupture is possible.

Which thoracic wall and cardiac injuries are associated with vehicular trauma, and why are they important?

• Rib fractures:

  • Indicate significant thoracic trauma; internal thoracic injury is highly likely.

• Flail chest:

  • ≥2 fractures in the same and multiple adjacent ribs → free-floating chest wall segment with paradoxical motion and severe pain.

• Traumatic myocarditis / myocardial injury:

  • Arrhythmias reported in 10–22% of dogs with blunt trauma (many may be extracardiac: hypoxia, splenic disease, ischemia–reperfusion).

  • In one 30-day ambulatory ECG study: 16% had frequent VPCs, 43% had ≥1 VT episode; arrhythmias most significant in first 24 hours post-trauma.

• Less common thoracic injuries:

  • Diaphragmatic hernia

  • Traumatic pulmonary bullae

  • Chylothorax from thoracic duct damage

  • Myocardial rupture, pericardial rupture

  • Tracheal laceration/avulsion

What abdominal injuries are commonly seen after vehicular trauma, and what special mechanisms should you remember?

• Hemoabdomen:

  • Among the most common abdominal injuries; incidence 23–45% in dogs with vehicular trauma.

• Urinary tract rupture:

  • Up to 10% of blunt trauma patients.

  • Usually bladder rupture, but renal, ureteral, and urethral injuries also occur.

• Hernias:

  • Prepubic tendon rupture and ventral abdominal hernia.

  • Abdominal and/or inguinal hernias.

• Pneumoperitoneum:

  • May result from air tracking from pneumomediastinum across the aortic and esophageal hiatuses, not only from GI rupture.

• Intestinal rupture:

  • Rare; can be immediate or delayed (48–72 h later) due to ischemic necrosis.

• Uterine rupture in late-term pregnancy has been reported in cats.

• Gallbladder rupture is very rare in humans and not yet reported in veterinary patients.

How does traumatic brain injury (TBI) and other neurologic trauma present and evolve after vehicular trauma?

• CNS is very trauma-sensitive, and TBI strongly worsens prognosis.

• Primary brain injury (at impact):

  • Concussion, epidural/subdural hematomas, contusions, lacerations, compression from skull fractures.

  • In dogs, subdural hematomas are thought most common; extradural hematomas also occur.

• Secondary brain injury:

  • Excitatory neurotransmitter release → neuronal Ca²⁺ overload → ROS generation → cellular damage, necrosis, cerebral edema, and increased seizure risk.

Which fractures and luxations are common in vehicular trauma, and what are special craniofacial considerations?

• Fractures and luxations are frequent.

• Pelvis: involved in 20–25% of all fractures.

  • Common luxations: coxofemoral and sacroiliac; other joints can also luxate.

• Oral/dental/facial/mandibular fractures:

  • Cats: temporal bone fractures are the most common TMJ region fracture post-vehicular trauma; intra-articular mandibular condyle fractures also frequent.

  • Dogs: maxilla and mandible are commonly fractured.

  • Pterygoid fractures occurred in ≈50% of dogs with blunt craniofacial trauma in one study and are easily missed but painful during eating/swallowing.

• Hard palate fractures may be seen on oral exam.

• Significant hemorrhage can occur at fracture sites, especially long bones (femur, humerus) and pelvis; about 25% of cats undergoing fracture repair required transfusion in one report.

What is the XABCDE primary assessment sequence for trauma patients, and why is it critical?

• All blunt trauma patients require rapid, systematic primary assessment to identify life-threatening problems.

• XABCDE trauma approach:

  • X – Exsanguinating hemorrhage:

    • Immediately control catastrophic external hemorrhage (direct pressure, tourniquet, hemostatic dressings).

  • A – Airway:

    • Check patency and obstruction; secure airway if compromised.

  • B – Breathing:

    • Assess ventilation and oxygenation; provide supplemental O₂.

  • C – Circulation:

    • Evaluate perfusion, HR, rhythm; obtain IV access; manage shock.

  • D – Disability (neurologic):

    • Rapid neurologic assessment (mentation, pupils, motor function).

  • E – Exposure/Environment:

    • Examine the whole patient; address hypothermia and environmental hazards.

What is the goal of the secondary examination in blunt trauma patients, and why must it be repeated?

• Compensatory shock:

  • Quiet–mildly obtunded mentation

  • Tachycardia (dogs), bradycardia in cats

  • Tachypnea

  • Hyperemic mucous membranes, rapid CRT

  • Normal/bounding pulses, normal BP

• Decompensatory shock:

  • Obtunded mentation, weakness

  • Tachycardia or bradycardia

  • Pale/white mucous membranes, prolonged CRT

  • Poor pulse quality, hypotension

• Shock index = HR / systolic BP.

  • In dogs, >1 (HR higher than systolic BP) should raise suspicion for shock and correlates with blood loss severity.

  • Sensitive but nonspecific.

What is the goal of the secondary examination in blunt trauma patients, and why must it be repeated?

• Performed after initial stabilization to identify full injury extent.

• Includes detailed exam of all body systems plus targeted diagnostics.

• Many patients lack overt external injuries despite significant internal damage (radiographs/CT often show injuries in patients with normal skin).

• Trauma is dynamic, so serial exams are necessary, especially during resuscitation.

What are important abdominal, musculoskeletal, and neurologic exam points in blunt trauma patients?

• Abdomen:

  • Fluid wave suggests hemo/uroabdomen but absence does not rule them out.

  • Abdominal pain may reflect visceral trauma (spleen, bladder) or muscle injury.

  • Palpate for hernias, particularly with pelvic trauma.

• Musculoskeletal:

  • Palpate bones/joints, especially in recumbent or lame patients.

  • Rectal exam can help detect pelvic fractures and caudal lumbar pain.

  • Assess gait once hemodynamically stable.

• Neurologic:

  • Perform detailed neuro exam ideally before heavy analgesia/sedation.

  • Check cranial nerves (menace, PLR, oculocephalic reflex).

  • Use modified Glasgow coma scale for TBI objectivity.

  • Anisocoria, bilateral miosis, or bilateral mydriasis with mentation changes suggest progressive intracranial damage.

  • Evaluate motor function and proprioception in non-ambulatory patients.

How do PCV, TS, and CBC help assess hemorrhage in trauma patients, and what are key kinetics and thresholds?

• PCV/TS should be run in all trauma patients.

• PCV/hematocrit changes may lag up to 8 hours after bleeding due to fluid shifts and splenic contraction.

• TS is more sensitive early:

  • TS falls within ~15 minutes of hemorrhage; nadir around 45 minutes.

  • TS ≤5 g/dL had 87% specificity but low sensitivity (36%) for transfusion need—low TS strongly supports hemorrhage and likely transfusion but normal TS doesn’t rule either out.

• CBC:

  • Thrombocytopenia may reflect platelet consumption from hemorrhage and coagulopathy.

  • In cats, neutrophil:lymphocyte ratio correlates with trauma severity but not directly with mortality

Which serum chemistry and venous blood gas changes are common in vehicular trauma, and what targets guide resuscitation?

• Serum chemistry:

  • ALT/AST elevations are common and can be >1,000 U/L after blunt trauma.

  • Hypoproteinemia may indicate blood loss and can be more sensitive than Hct early in hyperacute hemorrhage.

  • Mild hyperglycemia is common (stress → cortisol/catecholamines).

• Venous blood gas:

  • Mild metabolic acidosis is typical early; worsens with shock progression.

  • pH target: > 7.32.

  • Base deficit: reflects tissue hypoxia in hemorrhagic shock.

    • Target –2 to +2 mEq/L.

    • Base deficit ≤–6.6: strongly associated with need for transfusion.

    • Base deficit ≤–7.3: associated with nonsurvival in one study.

  • Lactate:

    • Elevated in hypovolemic shock from tissue hypoxia/anaerobic metabolism.

    • Lactic acidosis is more predictive of hemorrhage severity than some hemodynamic variables.

    • Target <2 mmol/L (<18 mg/dL) after resuscitation.

  • Ionized calcium often decreased and may have prognostic value.

When should coagulation testing be considered in vehicular trauma, and how is acute traumatic coagulopathy characterized?

• Coagulation testing is recommended for:

  • Patients with clinical hemorrhage,

  • Any significantly injured patient where coagulopathy is a concern.

• Routine testing might not be necessary for all, as clinically important changes reported in <10% of dogs and cats with trauma.

• Acute traumatic coagulopathy diagnosis requires:

  • History of trauma

  • Evidence of hypoperfusion and clinical hemorrhage

  • Coag tests showing hypocoagulability with hyperfibrinolysis.

• Laboratory features:

  • Thromboelastography: decreased clot strength, hyperfibrinolysis.

  • Prolonged PT and aPTT.

  • Fibrinogen often <100–150 mg/dL (usually only measurable at reference/university labs).

How should oxygen therapy be used in blunt thoracic trauma patients?

• Provide oxygen to any trauma patient with tachypnea or dyspnea until internal injury is ruled out and normoxemia confirmed.

• Options:

  • Flow-by O₂: 2–3 L/min (often during initial resuscitation).

  • Nasal cannulas if tolerated.

  • Oxygen cage for fractious or highly stressed patients; often combined with IM analgesia ± sedation.

• Sedation must be used cautiously but can reduce distress for both patient and staff when benefits outweigh risks.

What are the main approaches to initial fluid resuscitation in vehicular trauma, and why is large-volume crystalloid use discouraged?

• Secure IV access promptly and collect samples for point-of-care testing.

• For shock:

  • Isotonic crystalloids often first-line.

  • Bolus doses:

    • Cats: 5–10 mL/kg

    • Dogs: 10–20 mL/kg

  • Reassess perfusion after each bolus.

• Problems with large-volume crystalloids:

  • Worsen hemorrhage by raising BP and disrupting clots.

  • Cause hypothermia, acidosis, and dilutional coagulopathy.

  • Promote edema, cellular swelling, and delayed recovery; not retained intravascularly long.

• Practical cap: limit crystalloids to <50% of calculated shock volume (i.e., <45 mL/kg in dogs, <30 mL/kg in cats) when possible.

• Hypertonic saline (7.2–7.5%) ± synthetic colloid:

  • 3–5 mL/kg IV over 10–15 minutes, usually one bolus.

  • Rapid administration can paradoxically cause hypotension if not followed appropriately.

• Synthetic colloids:

  • 5–10 mL/kg IV over 10–15 minutes.

  • Remain intravascular longer but associated with dose-related coagulopathy, platelet dysfunction, and potential acute kidney injury.

• Hypertonic saline + colloid combinations may provide the most efficient hemodynamic support with less “resuscitation injury” compared to crystalloids alone.

What is permissive hypotension, when is it used in trauma, and when is it contraindicated?

• Permissive hypotension:

  • Intentionally tolerating lower BP (systolic 80–90 mmHg, MAP 50–60 mmHg) for up to 60–90 minutes in patients without TBI, to promote clot stability and limit ongoing hemorrhage.

• Rationale:

  • Avoid overzealous fluids that raise pressure enough to disrupt clots and worsen bleeding.

• Use only with close monitoring to avoid progression to decompensation or organ injury.

• Contraindicated in TBI (with or without hemorrhage):

  • These patients need systolic >90–100 mmHg to support cerebral perfusion.

• Short periods do not appear to increase mortality, but untreated or prolonged hypotension will cause organ failure and death.

When should antifibrinolytics be considered in trauma, and what are the dosing strategies?

• Consider in significant trauma with hemorrhage, given hyperfibrinolysis is a key feature of acute traumatic coagulopathy.

• Tranexamic acid (TXA):

  • 10–15 mg/kg IV loading, then 1–5 mg/kg/h IV CRI, or

  • 20 mg/kg IV q8h.

  • Can be emetogenic; premedicate with antiemetic if needed.

• Aminocaproic acid:

  • 100–150 mg/kg IV loading, then 15 mg/kg/h IV CRI, or

  • 100 mg/kg IV q8h.

• Ideally start within 3 hours of trauma and continue 12–24 hours.

How is hemorrhagic shock defined in trauma, what are species blood volumes, and what are primary goals of therapy?

• Hemorrhagic shock typically occurs after >15–20% blood volume loss; massive hemorrhage in humans = >50% volume in 3 hours.

• Blood volumes:

  • Dogs: ≈90 mL/kg

  • Cats: ≈60 mL/kg

• Goals:

  • Stop bleeding, restore effective circulating volume and tissue perfusion.

  • Prevent rebleeding and mitigate coagulopathy, acidosis, hypothermia (“lethal triad”).

Which clinical and lab findings point toward significant hemorrhage and possible transfusion requirements in vehicular trauma patients?

• Evidence of pleural or peritoneal effusion (POCUS or radiographs).

• Thrombocytopenia.

• Total protein ≤5 g/dL.

• Base deficit more negative than –6.6.

• Hyperlactatemia.

• Thromboelastography showing reduced clot strength.

• In dogs needing >25 mL/kg blood products for traumatic hemorrhage, survival in one small study was only ≈33%.

What is the ideal fluid strategy for hemorrhagic shock in trauma, and what are practical transfusion doses?

• Crystalloids: often given initially but continued use discouraged after hemorrhage confirmed.

• Ideal resuscitation = balanced 1:1:1 of:

  • RBC products (whole blood or packed RBCs)

  • Plasma products (fresh/fresh frozen plasma)

  • Platelet products (fresh whole blood, platelet concentrates, lyophilized platelets)

• Doses:

  • Whole blood:

    • Dogs: 20–30 mL/kg

    • Cats: 20 mL/kg

    • Provides RBCs, plasma, platelets, and warmth.

  • If whole blood unavailable:

    • Packed RBCs: dogs 10–15 mL/kg, cats 10 mL/kg

    • Fresh frozen plasma given at similar volume (1:1 RBC:plasma).

  • Platelet support, if available:

    • Leukoreduced canine frozen platelet concentrate: 1 unit/10 kg.

    • Fresh platelet concentrate (dogs): 1 unit/10 kg.

    • Lyophilized platelets: 1.6 mL/kg IV (product currently unavailable in many regions).

    • Feline platelet products not commercially available; canine xenotransfusion has been reported once without acute adverse effects.

When is autotransfusion appropriate in trauma, and what are key technique and safety points?

• Consider in hemothorax or hemoabdomen causing both respiratory compromise and hypovolemic shock.

• Benefits: immediate availability, low cost, full compatibility, normothermic, lower overload risk, no transmission of donor infections.

• Provides RBCs and natural colloids, but not platelets or clotting factors, so donor plasma/platelets should be added if possible to approach the 1:1:1 goal.

• Technique:

  • Use sterile technique; collect blood from thorax/abdomen into syringe, transfer into blood collection set with inline filter, then transfuse.

  • Peritoneal blood is defibrinated after ≈1 hour; often no anticoagulant needed.

  • If active bleeding and clots form, may add CPDA-1 anticoagulant: 1 mL CPDA-1 per 7 mL blood.

• Contraindicated if blood is contaminated with urine, bile, or intestinal contents; if unsure, perform cytologic/biochemical testing (e.g., creatinine, bilirubin, glucose).

What complications are associated with massive transfusion, and when/how should calcium be given?

• Massive transfusion = >100% blood volume in 24 h, or >50% in 3 h.

• Potential complications: hypothermia, hypocalcemia, hypomagnesemia, acidosis, transfusion reactions.

• Monitor ionized calcium; if <0.9 mmol/L or clinical hypocalcemia present, give:

  • 10% calcium gluconate at 1 mL/kg, diluted 1:4, over 20 min.

• If ionized calcium measurement unavailable:

  • Consider prophylactic calcium after the first two citrate-containing units, and every four units thereafter.

How is traumatic hemoabdomen usually managed, and when is surgery needed?

• Most traumatic hemoabdomens can be managed medically with transfusion and supportive care.

• Only about 6% of dogs with traumatic hemoabdomen required surgery in one study.

• Indications for surgery:

  • Persistent hemodynamic instability despite transfusion, suggesting organ avulsion (kidney) or rupture of spleen, liver, or major vessel.

• Adjuncts:

  • Antifibrinolytics usually recommended.

  • Abdominal compression wraps may help but must include entire caudal half of the body including pelvic limbs to be effective and avoid compartment syndrome.

    • Urinary catheter recommended to divert urine.

  • Wraps are contraindicated in thoracic/diaphragmatic, spinal, pelvic, or pelvic limb orthopedic injuries.

How should hemothorax be managed in trauma patients, and when are thoracocentesis, autotransfusion, and surgery considered?

• Provide oxygen for any patient with tachypnea, dyspnea, or hypoxemia.

• Thoracocentesis is indicated when:

  • Large-volume effusion is causing respiratory compromise, or

  • You need fluid for diagnostic purposes (rarely necessary in pure trauma).

• Retained blood can help tamponade bleeding (to stop bleeding by blocking it with pressure or a plug), so thoracocentesis may be avoided if effusion is moderate and patient compensating.

• If large hemorrhagic volume causes both hypovolemia and respiratory distress (>~30 mL/kg), both thoracocentesis and autotransfusion should be considered.

• Surgery considered for:

  • Severe, persistent pleural hemorrhage causing anemia and shock.

  • Ongoing active bleeding >24–48 h (e.g., repeated rib fracture disruption).

• Antifibrinolytics can be helpful if trauma occurred within ≈3 h.

What are key principles of wound and fracture management in vehicular trauma, and when is empiric antibiotic therapy reasonable?

• Cover and protect all wounds with bandages until definitive surgical treatment.

• Bandaging/splinting fractures helps immobilize, reduce pain and hemorrhage, and limit more tissue damage.

• For open fractures or deep soft tissue wounds where repair is delayed, broad-spectrum empiric antibiotics may be appropriate, then de-escalated or discontinued based on culture/clinical course.

How should TBI be managed in vehicular trauma patients, including hyperosmolar therapy and ICP management?

• Hyperosmolar therapy is central:

  • Hypertonic saline 7.2–7.5%: 3–5 mL/kg IV over 10–15 min.

  • Mannitol: 0.5–1 g/kg IV over 15–20 min.

• Supplemental oxygen:

  • Use in patients with respiratory trauma or hypoxemia; avoid unnecessary hyperoxia due to ROS risk.

• Seizure management:

  • Treat clinical seizures; consider empirical anticonvulsants in stuporous/comatose patients due to risk of non-convulsive seizures (evidence sparse).

• N-acetylcysteine may help by restoring glutathione and reducing oxidative damage; promising in human TBI trials.

• Avoid further increases in intracranial pressure (ICP):

  • Maintain systolic BP >90–100 mmHg.

  • Elevate head/body 15–30°.

  • Control vomiting (antiemetics, promotility meds).

  • Avoid jugular compression and jugular venipuncture.

  • Use nasal tubes cautiously (sneezing/coughing can spike ICP).

• Rarely, surgery (craniotomy or removal of depressed skull fragments) is needed for refractory intracranial hypertension

How is uroabdomen managed in trauma patients, and when can conservative treatment be considered?

• Provide urinary diversion:

  • Urethral catheter, or

  • Peritoneal drain when catheter placement is impossible (e.g., urethral avulsion).

• Surgery is usually ideal to repair urinary trauma, but conservative management with continuous diversion for 5–10 days may be an option when surgery is not accessible.

• Urethra and bladder injuries are most common; catheter placement must be radiographically confirmed to ensure it hasn’t passed through a defect.

• Rarely, ureteral avulsion may require peritoneal drainage and surgical planning.

What are the treatment principles for pulmonary contusions following vehicular trauma?

• Provide supplemental oxygen for tachypnea, dyspnea, or hypoxemia (SpO₂ <95%, PaO₂ <80 mmHg); often 40–50% FiO₂ is adequate, but severe cases may need higher.

• Monitor response via RR, effort, and SpO₂; minimize stress associated with pulse oximetry, especially when patient must be removed from O₂ cage.

• If SpO₂ persists <90% despite conventional O₂ (cage, nasal, nasopharyngeal), consider high-flow O₂ or mechanical ventilation.

• Use judicious fluids:

  • Avoid both excessive restriction and generous rates.

  • Generally limit to maintenance rates in anorexic patients; avoid “twice maintenance.”

  • If patient is drinking/eating and not hypoperfused or losing fluids, consider even more restrictive fluids.

• Overly liberal crystalloids or colloids worsen lung injury by promoting further extravasation through damaged pulmonary capillaries.

How should traumatic pneumothorax be managed, and when are thoracocentesis, thoracostomy tubes, and autologous blood patching indicated?

• Provide oxygen to all patients; O₂ accelerates pleural air reabsorption.

• Thoracocentesis recommended for:

  • Pneumothorax with respiratory compromise.

  • Avoid puncturing through fractured ribs or heavily traumatized skin.

• Mild radiographic pneumothorax in asymptomatic patients may be monitored closely, as volume can progress.

• Sedation for thoracocentesis:

  • Fentanyl: 3–8 µg/kg IV (analgesia ± sedation).

  • Ketamine: 0.2–0.5 mg/kg IV ± midazolam 0.1–0.3 mg/kg IV.

  • Dexmedetomidine: 1–10 µg/kg IV (avoid in unstable patients).

  • Local blocks with lidocaine (1–5 mg/kg) or bupivacaine (1–2 mg/kg) help but do not block pleural pain completely.

• Thoracostomy tubes indicated when repeated taps are needed; earlier placement advisable in pneumothorax with significant contusions.

  • Single tube for unilateral pneumothorax; bilateral tubes for bilateral disease unless incomplete mediastinum allows single tube effectiveness.

  • Continuous suction required for persistent air leakage.

  • Negative pressure with worsening clinical signs suggests contusions, not pneumothorax, are driving deterioration.

• Remove tubes once negative aspirations documented for 12–24 h and patient is clinically improved; most seal within 2–5 days.

• Without tapping, spontaneous reabsorption of pleural air occurs at ≈2–5% volume/day, faster with FiO₂ 40–60%.

• Persistent pneumothorax >3–6 days: consider surgical exploration.

• Autologous blood patch pleurodesis:

  • Instill 2–6 mL/kg of fresh patient blood into the pleural space through the tube.

  • Rotate patient to distribute blood; avoid aspirating for 1–2 h.

  • Has documented success in spontaneous pneumothorax due to bullae and in a few trauma cases; may be repeated once before deciding on surgery.

How are traumatic diaphragmatic hernias and pulmonary bullae managed?

• Traumatic diaphragmatic hernia:

  • Requires surgical repair; positive-pressure ventilation needed during surgery.

  • Timing is patient-dependent; earlier surgery may be ideal in stable patients, while delaying surgery in those with severe contusions or other injuries can reduce anesthetic risk.

• Traumatic pulmonary bullae:

  • No specific therapy required apart from monitoring.

  • Owners should be warned about risk of pneumothorax; worsening respiratory signs warrant re-evaluation.

How are ventricular arrhythmias from traumatic myocarditis interpreted and treated?

• Ventricular ectopy common after thoracic trauma.

• Isolated VPCs rarely need treatment.

• Distinguish ventricular tachycardia (VT) from accelerated idioventricular rhythm (AIVR):

  • VT: HR >160 bpm (dogs), >180 bpm (cats); more likely to need therapy.

  • AIVR: HR <160 bpm; usually benign and doesn’t require antiarrhythmics.

• Treat VT when:

  • Poor cardiac output (hypotension, weakness, pale MM, long CRT, collapse/syncope) despite adequate volume resuscitation.

  • Concerning patterns (e.g., R-on-T).

• First-line:

  • Lidocaine (dogs): 2 mg/kg IV slow bolus; may repeat q10–20 min to total 8 mg/kg. If effective but ectopy recurs → 40–80 µg/kg/min CRI.

  • Lidocaine (cats): 0.2–0.7 mg/kg IV slowly; repeat once or twice; if effective → 10–20 µg/kg/min CRI. Use cautiously; some prefer beta-blockers first.

• If lidocaine fails (dogs):

  • Procainamide: 2–4 mg/kg IV over 2–5 min, then 20–50 µg/kg/min CRI.

• If persistent VT despite appropriate volume and pain management:

  • Esmolol: 0.25–0.5 mg/kg IV loading, then 10–200 µg/kg/min CRI.

  • Sotalol:

    • Dogs: 1.5–3.5 mg/kg PO q12h.

    • Cats: 2 mg/kg PO q12h or 10–20 mg/cat PO q12h.

How is pneumomediastinum managed after trauma?

• Usually no specific therapy required.

• Provide analgesia, as pneumomediastinum can cause chest pain.

• Evaluate for associated injuries (tracheal tear, bullae, severe contusions).

What is the overall prognosis for trauma vs vehicular trauma, and which factors worsen outcome?

• Overall trauma prognosis is generally good, but vehicular trauma has one of the highest mortality rates, especially in cats (18–19% dogs, 43–45% cats).

• Financial limitations often drive euthanasia; in one feline trauma study, >50% of euthanasias were financial.

• Negative prognostic indicators:

  • Hypothermia ≤ 37.1°C (98.8°F) at presentation.

  • Severe acidosis and markedly negative base deficit.

  • TBI and lower modified Glasgow coma scores.

  • Requirement for large transfusion volumes.

  • Spinal fracture.

  • Multiorgan dysfunction at admission.

  • Ionized hypocalcemia < 1.25 mmol/L may correlate with mortality in dogs (data conflicting).

  • Animal Trauma Triage (ATT) score ≥ 6–8 associated with increased mortality (though not validated for individual prediction).

  • Some studies suggest female dogs and gonadectomized dogs may have better survival, but mechanism unclear.

Which late complications can occur after blunt vehicular trauma?

• Ascites from caudal vena caval obstruction:

  • Weeks (~3) after trauma, a thoracic caval cicatrix can kink/obstruct flow → hepatomegaly and chronic modified transudate ascites; surgically treatable.

• Hepatic emphysema reported in a dog with hemoabdomen and contusions.

• Multiorgan dysfunction from systemic inflammation and coagulopathy.

What in-hospital monitoring is recommended for vehicular trauma patients, and what is Kirby’s Rule of 20?

• Monitoring:

  • Continuous ECG for at least 24 h in significant thoracic trauma.

  • Regular BP measurements (hypo/hypertension both worrisome, especially with TBI).

  • Pulse oximetry if respiratory changes:

    • Hypoxemia: SpO₂ <95%.

    • Severe hypoxemia: SpO₂ <90%.

    • Persistent hypoxemia despite oxygen → consider high-flow O₂ or mechanical ventilation.

• Kirby’s Rule of 20: checklist of 20 parameters to assess daily (or more often) in critically ill patients, including:

  • Fluid balance, oncotic pressure/albumin, electrolytes and acid–base, mentation, HR/rhythm/contractility, BP, temperature, oxygenation/ventilation, RBC/Hb, coagulation, renal function, GI function, nutrition, glucose, immune status/antibiotics, wound/bandage status, drug dosing/metabolism, pain control, nursing care, and TLC.