Abdominal tramua.pdf

Evaluation and Emergency Management of the Trauma Patient Acute abdomen/Abdominal Trauma Carlos Pizarro Ldo. Vet., MSc, PGCAP University Clinician in Small Animal Emergency and Critical Care CP3.14.19 Supporting the Patient Carlos Pizarro 2023 1 Intended Learning Outcomes (ILOs) Year ILOs CP3...

Evaluation and Emergency Management of the Trauma Patient Acute abdomen/Abdominal Trauma Carlos Pizarro Ldo. Vet., MSc, PGCAP University Clinician in Small Animal Emergency and Critical Care CP3.14.19 Supporting the Patient Carlos Pizarro 2023 1 Intended Learning Outcomes (ILOs) Year ILOs CP3005: Perform and interpret a clinical examination, including a pain assessment, in a veterinary patient that requires emergency treatment. CP30011: Explain the aetiology, pathophysiology & epidemiology of conditions of veterinary interest that require emergency treatment including pain, shock, trauma & poisoning CP30017: Select and explain appropriate diagnostic techniques to investigate common veterinary emergencies, including problems arising under anaesthesia, and interpret the findings of these techniques. CP3024b: Formulate a therapeutic plan to treat/manage common veterinary emergencies including complications arising under anaesthesia, demonstrating an understanding of the underpinning science principles. 2 2 Intended Learning Outcomes (ILOs) Lecture ILOs Abdominal Trauma • • • • • • Describe the major conditions following abdominal trauma, including haemoabdomen and uroabdomen. Recognize the clinical manifestations of abdominal trauma and its consequences, including haemoabdomen, uroabdomen. Outline the potential consequences of abdominal trauma and their diagnosis Understand the principles governing the medical management of abdominal trauma. Understand the principles governing the surgical management of abdominal trauma. Make appropriate decisions in the management of haemoabdomen 3 3 Previously on… Evaluation and Emergency Management of the Trauma Patient 4 4 Evaluation and Emergency Management of the Trauma Patient 1. Trauma 1. 2. 3. 4. Relevance Definition and classification Consequences Evaluation 1. 2. 3. 4. 5. 6. Overview Triage and Primary survey Thoracic trauma Head trauma / Traumatic Brain Injury (TBI) Skeletal trauma Abdominal Trauma 2. Clinical Scenario 5 5 Trauma: Setting the Scene… 6-month old Springer Spaniel, Tess, has just been hit by a car. She appeared to lose consciousness briefly and now is dazed and breathing rapidly. Bring Tess straight into the practice! I’ll be prepared for her arrival. In the next 45 minutes we’re going to use Tess to illustrate the various aspects of the initial evaluation and management of the (poly)trauma patient. There are 3 CDMs to complement this lecture. 6 A client phones into the practice to say that their 6-month old Springer Spaniel, Tess, has just been hit by a car. She appeared to lose consciousness briefly and now is dazed and breathing rapidly. You advise the client to bring Tess straight into the practice and prepare for her arrival. 6 2.1 Trauma: Overview superficial wounds CNS / Head injury Abdominal trauma skeletal injuries Road traffic accident Thoracic trauma 7 7 2.1 Trauma: Overview superficial wounds CNS / Head injury Abdominal trauma skeletal injuries Road traffic accident Thoracic trauma 8 8 2.1 Trauma: Overview • Death tends to be associated with… Thoracic trauma Abdominal trauma CNS trauma 9 9 Trauma: Tess, 6 mo FE Springer Spaniel 10 10 Trauma: Tess, 6 mo FE Springer Spaniel A/B • RR 104 breaths/minute • Rapid shallow breathing • Thoracic trauma? C • HR 180 bpm • Pale pink mucous membranes • CRT 2 sec • Fair femoral pulse quality • Shock? • Abdominal trauma? D • Obtunded • Responsive to voice • Mid-range pupils with direct and consensual PLRs • Head trauma? • Shock? 11 11 Trauma: Tess, 6 mo FE Springer Spaniel Supplemental Oxygen Assessment of pulse quality ECG to Assess Cardiac Rhythm Intravenous Access & Fluid Therapy What Next? 12 12 Abdominal trauma vs. Acute abdomen • Acute abdomen: Per-acute, rapidly deteriorating abdominal condition prompting emergency treatment. • Abdominal trauma is a common cause of acute abdomen. ABDOMINAL TRAUMA ACUTE ABDOMEN 13 13 2.6 Abdominal Trauma A. B. C. D. E. F. G. Assessment Haemoperitoneum Uroperitoneum Bile peritonitis Septic peritonitis Pancreatitis (Traumatic pancreatitis) Diaphragmatic rupture 14 14 2.6 Abdominal Trauma A. Assessment A. Primary survey (Physical exam) B. Imaging A. Point of Care Ultrasound (POCUS) C. Effusions / Fluid analysis A. Abdominocentesis B. Fluid categorisation C. Fluid analysis and Smear 15 15 2.6.A.A Assessment – Physical exam • • • • • History and signalment Perfusion parameters External wounds Signs of haemorrhage (ecchymosis, petechiae) Fluid wave – 40 ml/kg of effusion to have a positive wave! • Cardiac arrythmias and pulse deficits 16 16 2.6.A.B Assessment by imaging • • Abdominal POCUS • Abdominal FAST (aFAST): Focused Assessment by Sonography for Trauma • Detection of free abdominal fluid • Sensitive even in the hands of non-radiologists • Serial FAST allows detection of delayed accumulation of fluid and progression Abdominal radiography/CT • Skeletal structures, diaphragmatic hernia, free-gas, abdominal wall trauma 17 POCUS (A-FAST) Spleno-renal: Left flank view to assess the splenorenal interface and areas between the spleen and body wall Diaphragmatic-hepatic: Sub-xiphoid view to evaluate the hepatodiaphragmatic interface, gallbladder region, pericardial sac, and pleural spaces Cysto-colic: A midline bladder view to assess the apex of the bladder Hepato-renal: A right flank view to assess the hepatorenal interface and areas between intestinal loops, right kidney, and the body wall 18 POCUS (A-FAST) 19 2.6.A.C Assessment: Effusion • Abdominocentesis and/or Diagnostic Peritoneal Lavage 20 2.6.A.C Assessment: Effusion • Effusion classification Categories of effusions in Dogs and Cats Transudate Modified Transudate Exudate Specific gravity <1017 1017-1025 >1025 Total Protein (mg/L) <25 25-50 >30 Nucleated cell count (per µl) <1000 500-10,000 >5,000 Lymphocytes Monocytes Mesothelial RBCs Neutrophils Neutrophils Mononuclear cells RBCs Predominant cell type Mononuclear Mesothelial 21 21 2.6.A.C Assessment: Effusion • Fluid analysis Fluid analysis Haemoabdomen Uroabdomen • PCV of abdominal • Creatinine fluid ≃ peripheral • Potassium blood PCV • PCV 10-25% of peripheral blood Septic peritonitis Intestinal perforation • Neutrophils (degenerate) • Intracellular bacteria • Lactate and Glucose Bile peritonitis • Bilirubin of fluid > than plasma • Intra/extracellular levels bacteria • Neutrophils • Particulate material 22 22 2.6 Abdominal Trauma A. B. C. D. E. F. G. Assessment Haemoperitoneum Uroperitoneum Bile peritonitis Septic peritonitis Pancreatitis (Traumatic pancreatitis) Diaphragmatic rupture 23 23 2.6.B. HAEMOABDOMEN • Presence of haemorrhagic effusion in the peritoneal cavity – Non traumatic (idiopathic) – Traumatic • Bleeding from kidneys, spleen and/or liver • Common in RTA • Presentation – Shocked/Collapsed patients – Arrhythmias/ pulse deficits 24 24 2.6.B. HAEMOABDOMEN • Diagnostics – PCV/TS (blood vs. fluid) – Haem/Bio – Coagulation profile – APOCUS – Abdominocentesis • PCVeffusion 10-25% of peripheral blood • Peripheral PCV may drop after fluid resuscitation 25 25 2.6.B. HAEMOABDOMEN • Initial treatment and stabilisation – Goal • Management of Shock • Control source of bleeding – Fluid resuscitation • Goal directed • Hypotensive or Low volume resuscitation – Blood transfusions / Autotransfusion – O2therapy 26 26 2.6.B. HAEMOABDOMEN • Medical/Conservative Management – Pressure bandage: External counter-pressure using an abdominal wrap – Monitor PCV/TS 27 27 2.6.B. HAEMOABDOMEN • Surgical Management • Coeliotomy/ laparotomy: – an incision into the abdomen • Exploratory laparotomy (‘ex lap’): – systematic exploration of the entire abdomen. – Potential requirement for splenectomy, liver lobectomy, nephrectomy, etc. 28 28 2.6.C. UROABDOMEN • Leakage of urine to peritoneal or retroperitoneal • Loss of integrity of urinary system (Kidneys to intraabdominal urethra) – Uroperitoneum • Intraabdominal urethra • Bladder • Distal urether – Uroretroperitoneum • Kidneys • Proximal urether 29 29 2.6.C. UROABDOMEN Kidneys ↑ GFR Aldosterone Na+/K+-ATPasa Abdomen Urine ↑K ↑Crea ↑Urea H2O IV Space ↑K → Hyperkalaemia ↑Urea → Azotaemia Na/Cl → hyponatremia → hypochloraemia AnionGap Metabolic Acidosis Cadiac cells ↑ Action potential Bradyarrhythmias Stafford, J. R., & Bartges, J. W. (2013). A clinical review of pathophysiology, diagnosis, and treatment of uroabdomen in the dog and cat. Journal of Veterinary Emergency and Critical Care, 23(2), 216–229. Images: Text book of Medical Physiology 14th Ed Guyton and Hall La pérdida de integridad en cualquier punto del sistema urinario provocará una fuga de orina que se acumula en el espacio peritoneal o retroperitoneal. Ésta orina en el abdomen, es hiperosmolar y rica en potasio, creatinina y urea, y provoca un efecto de movimiento de agua desde el espacio extracelular hacia el abdomen por gradientes de concentración, favoreciendo la acumulación de agua en el abdomen y contribuyendo a la deshidratación. Vómitos son frecuentes en estos pacientes, lo que contribuye a la pérdida de líquidos en el tercer espacio o espacio extracelular y a mayor deshidratación. La acumulación de orina en el abdomen y su concentración de potasio, urea y creatinina también provoca un movimiento por gradientes de concentración entre el abdomen y el espacio intravascular a a través del peritoneo. Los riñones son los principales encargados de excretar potasio, por lo que la orina acumulada en abdomen es muy rica en potasio, el cual difunde al espacio intravascular causando hiperkalemia. La alta concentración de urea en el abdomen equilibra rápidamente con el espacio intravascular ya que la urea es una molécula de pequeño tamaño de 60 Daltons y difunde rápidamente a través del peritoneo, aumentando su concentración en sangre. No ocurre así con la creatinina, que es una molécula de mayor tamaño, de 112 Daltons, y requiere más tiempo para difundir a circulación sistémica, permaneciendo en mayor concentración en abdomen. No obstante, el fallo de excretar urea y creatinina debido a una falta de integridad del sistema urinario desarrolla una azotemia progresiva en sangre. Hiponatremia e hipocloremia no son tan frecuentes, pero pueden ocurrir debido a la difusión de electrolitos desde la sangre al abdomen, ya que la orina acumulada es rica en potasio pero pobre en sodio y cloro. Además, los vómitos contribuyen a la pérdida de electrolitos. La hiperkalemia que se desarrolla es detectada por el riñon, que en un intento por mantener la homeostasis, aumenta la filtración glomerular y aumenta la excreción de potasio a nivel de túbulo distal renal por activación de aldosterona y su efecto en la bomba sodio-potasio-ATP-asa. Sin embargo, la reabsorción de potasio a través de la membrana peritoneal es más lenta que la excreción, por lo que el potasio permanece en altas concentraciones en el líquido abdominal. Por otra parte, la hiperkalemia aumenta el potencial de membrana basal de las células cardiacas, lo que reduce el gradiente entre potencial de membrana basal y el potencial gatillo. Esto se traduce en un mayor potencial de excitabilidad de membrana celular. Esto tiene gran importancia en las células cardiacas, done un mayor potencial de membrana y un incremento de la excitabilidad darán lugar a bradiarritmias, que en último lugar pueden desarrollar fibrilación ventricular o asístole. Además, el aumento de urea en sangre por su parte, aumenta el anion gap provocando acidosis metabólica. Esto unido a deshidratación e hipovolemia, puede también causar la formación de ácido láctico contribuyendo al empeoramiento de la acidosis metabólica. 30 2.6.C. UROABDOMEN • Diagnosis – Non-specific Clinical signs • Bladder might or might NOT be palpable • +/- Urination • +/- haematuria before uroabdomen – Biochemistry • Azotaemia • Hyperkalaemia – Imaging • APOCUS • Contrast radiography 31 31 2.6.C. UROABDOMEN • Diagnosis – Fluid analysis • • • • Creafluid Creafluid:Creablood ratio K+fluid:K+blood ratio Smear – Rule out bacteria – Concomitant UTI 32 32 2.6.C. UROABDOMEN • Management – Fluid resuscitation – Urinary catheterisation – Abdominal drainage – Electrolyte imbalance (Hyperkalaemia) • (refer to management of AKI and hyperkalaemia in renal lectures) – Medical vs. Surgical • Definitive surgical correction is usually required BUT medical stabilisation is essential before 33 33 2.6.E. SEPTIC PERITONITIS • Sepsis: life-threatening organ dysfunction due to a dysregulated host response to infection. • Septic shock: a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities substantially increase mortality. • Septic abdomen/peritonitis: peritonitis resulting from and identifiable source of intraperitoneal infection, typically bacterial in origin and most commonly a result of leakage of the GI tract. 34 34 2.6.E. SEPTIC PERITONITIS Septic peritonitis Primary Secondary Tertiary spontaneous Leakage of bacteria Recurrence 35 35 2.6.E. SEPTIC PERITONITIS • Diagnosis – Haematology • Neutrophilia to neutropaenia – Biochemistry – Lactate – A-POCUS 36 36 2.6.E. SEPTIC PERITONITIS • Diagnosis – Abdominal effusion • Cytology – intracellular bacteria – Degenerated neutrophils / toxic changes • Peripheral glucose to abdominal – ≥ 38 mg/dl (2.1 mmol/L) • Abdominal lactate to peripheral – > 2.5 mmol/L Koenig, A., & Verlander, L. L. (2015). Usefulness of whole blood, plasma, peritoneal fluid, and peritoneal fluid supernatant glucose concentrations obtained by a veterinary point-of-care glucometer to identify septic peritonitis in dogs with peritoneal effusion. Journal of the American Veterinary Medical Association, 247(9), 37 1027–1032. 37 2.6.E. SEPTIC PERITONITIS • Management – Broad spectrum antibiotics – Fluid resuscitation – Control hypotension • Vasopressors? – Infection source control ! • • • • Broad spectrum antibiotics Ex-Lap Peritoneal Lavage Abdominal drain 38 38 2.6.D. BILE PERITONITIS • Leakage of bile into the peritoneal cavity • Gall bladder rupture after trauma – 7-10 days post incident • • • • Post-hepatic Biliary tract obstruction Chemical/irritant effect on peritoneum Severe inflammation Coagulopathies (Vit K dependent) 39 39 2.6.D. BILE PERITONITIS • Diagnosis – Ictericia – Hyperbilirubinaemia – Abdominal effusion • TBileffusion > Tbilplasma (>2:1) • Bilirubin crystals – Abdominal cytology • Extracellular pigment • Rule out intracellular bacteria and concomitant sepsis • +/- culture and sensitivity 40 40 2.6.D. BILE PERITONITIS • Management – Emergency • Fluid resuscitation/Shock • Vitamin K/FFP if coagulopathy – Surgical • Ex-Lap – Resolution of the source • Peritoneal lavage • Abdominal drain 41 41 2.6.F. TRAUMATIC PANCREATITIS • • • • Direct/Indirect trauma to the pancreas Subcapsular haematomas Interrupted blood supply (ischemia) to the pancreas Leakage of pancreatic enzymes – Autodigestion – Acute Pancreatitis (AP) • Common in cats +/- steatitis (fat necrosis & inflammation) 42 42 2.6.G. DIAPHRAGMATIC HERNIA • Commonly secondary to blunt trauma • Varying severity of dyspnoea • Organs herniated: – Liver, stomach, small intestine, omentum, spleen • Physical exam – Borborygmi on thoracic auscultation to dull/absent lung sounds – ”tucked in” abdomen 43 43 2.6.G. DIAPHRAGMATIC HERNIA • Diagnosis – POCUS is diagnostic in 93% of cases – Radiographs • Presence of abdominal organs in the chest cavity • Loss of visualisation of the diaphragm • Management – Surgery +/- chest drain 44 44 Trauma Summary  Polytrauma is common following RTA  Poor outcome is associated with intra-thoracic, intra-abdominal and CNS trauma  The extent of intra-thoracic and intra-abdominal trauma is not always immediately apparent  Prioritise patient management so that life-threatening injuries are addressed first  Frequent re-assessment of RTA patients is essential for optimising treatment and for early detection of clinical deterioration 45 Questions? [email protected] 46 46