Sidestream dark field imaging and biomarker evaluation reveal minimal significant changes to the microcirculation and glycocalyx in a canine hemorrhagic shock model.

OBJECTIVE: To investigate the effects of hemorrhagic shock and fresh whole blood resuscitation on the microcirculation and endothelial glycocalyx using sidestream dark field (SDF) imaging and plasma biomarkers. ANIMALS: 8 purpose-bred dogs. METHODS: Pressure-targeted hemorrhagic shock was induced in anesthetized dogs. SDF measurement of perfused boundary region and microcirculatory variables (RBC flow, total vessel density, and relative and absolute capillary blood volume), biomarker measurement (heparan sulfate, hyaluronan, VE-cadherin, and syndecan-1), mean arterial blood pressure, and cardiac output measurement were performed before anesthesia (TP0), after induction (TP1), after hemorrhagic shock (TP2), and after 50% retransfusion (TP3) and 100% retransfusion (TP4). RESULTS: At TP1, TP2, TP3, and TP4, mean arterial blood pressure was 74.25 ± 7.17 mm Hg, 49.50 ± 13.74 mm Hg, 63.50 ± 13.29 mm Hg, and 71.38 ± 8.77 mm Hg, and cardiac output was 2.57 ± 1.01 L/min, 0.8 ± 0.36 L/min, 1.81 ± 0.57 L/min, and 2.93 ± 1.22 L/min, respectively. Heparan sulfate, hyaluronan, syndecan-1, and VE-cadherin ranges were 24.80 to 77.72 ng/mL, 5.77 to 105.06 ng/mL, below detection to 1,545.69 pg/mL, and 0 to 2.52 ng/mL, respectively. Perfused boundary region, RBC flow, total vessel density, and relative and absolute capillary blood volume ranges were 1.75 to 2.68 µm, 89.6 to 584.5 µm/s, 51.7 to 1,914.3 mm/m2, 0.94 to 1.53 103 µm3, and 1.50 to 94.30 103 µm3, respectively. Heparan sulfate decreased significantly over time (P = .016). No significant differences were found for microcirculatory variables, perfused boundary regions, or other biomarkers. CLINICAL RELEVANCE: This was the first study to assess microvascular dysfunction and endothelial shedding in a canine hemorrhagic shock model using SDF microscopy (Glycocheck) and plasma biomarkers. Further studies are needed to determine clinical relevance.

Successful blood transfusion in a Holstein cow experiencing hemorrhagic shock under general anesthesia.

A 2-year-old Holstein cow weighing 530 kg at 2 mo gestation was scheduled for a paracostal laparotomy and abomasotomy following diagnosis of a reticular foreign body causing obstruction and abomasal impaction. Hemorrhagic shock occurred during surgery, with a rapid, approximately 60% decrease in arterial blood pressure, and reflex tachycardia with a 2-fold increase in heart rate. Following identification of hemorrhagic shock, arterial blood pressure was supported by reducing the inhalant anesthetic requirement, positive inotropic support (IV dobutamine infusion), and IV fluid therapy. Hypertonic saline was administered IV for initial resuscitation of arterial blood pressure, followed by a whole blood transfusion to replenish red blood cells, support oxygencarrying capacity, and provide intravascular volume to maintain cardiac output and tissue perfusion. A gradual increase in arterial blood pressure and a decrease in heart rate were observed in response to treatment. This case report demonstrates the physiologic compensatory response to hemorrhagic shock and the treatment to stabilize cardiovascular parameters in an anesthetized cow. Key clinical message: This case illustrates the physiological reponses to acute hemorrhage under general anesthesia and the effects of various treatment interventions.

Transfusion sanguine réussie chez une vache Holstein en état de choc hémorragique sous anesthésie générale. Une vache Holstein de 2 ans pesant 530 kg à 2 mois de gestation devait subir une laparotomie paracostale et une abomasotomie à la suite du diagnostic d'un corps étranger réticulaire provoquant une obstruction et une impaction abomasale. Un choc hémorragique est survenu pendant la chirurgie, avec une diminution rapide d'environ 60 % de la pression artérielle et une tachycardie réflexe avec une augmentation du double de la fréquence cardiaque. À la suite de l'identification d'un choc hémorragique, la pression artérielle a été soutenue en réduisant le besoin d'anesthésique inhalé, un soutien inotrope positif (perfusion de dobutamine IV) et une thérapie avec des fluides IV. Une solution saline hypertonique a été administrée par voie intraveineuse pour la restauration initiale de la pression artérielle, suivie d'une transfusion de sang total pour rétablir la quantité de globules rouges, soutenir la capacité de transport d'oxygène et fournir un volume intravasculaire pour maintenir le débit cardiaque et la perfusion tissulaire. Une augmentation progressive de la pression artérielle et une diminution de la fréquence cardiaque ont été observées en réponse au traitement. Ce rapport de cas démontre la réponse physiologique compensatoire au choc hémorragique et le traitement pour stabiliser les paramètres cardiovasculaires chez une vache anesthésiée.Message clinique clé :Ce cas illustre les réponses physiologiques à une hémorragie aiguë sous anesthésie générale et les effets de diverses interventions thérapeutiques.(Traduit par Dr Serge Messier).

Shock index is positively correlated with acute blood loss and negatively correlated with cardiac output in a canine hemorrhagic shock model.

OBJECTIVE: To determine whether shock index (SI) positively correlates with percentage blood loss and negatively correlates with cardiac output (CO) in a canine hemorrhagic shock model and whether SI and metabolic markers may be used as end point targets for resuscitation. ANIMALS: 8 healthy Beagles. PROCEDURES: Between September and December 2021, dogs underwent general anesthesia for experimental induction of hypotensive shock, with the total volume of blood removed, CO, heart rate, systolic blood pressure, base excess, blood pH, and concentrations of hemoglobin, lactate, ionized calcium recorded, and SI calculated at 4 time points (TPs): after anesthetic induction when the dog had been stable for 10 minutes (TP1), 10 minutes after the mean arterial pressure stabilized to a target of 40 mm Hg following jugular removal of up to 60% blood volume to induce hemorrhagic shock (TP2), 10 minutes after autotransfusion of 50% of the removed blood (TP3), and 10 minutes after autotransfusion of the remaining 50% of the removed blood (TP4). RESULTS: Mean SI increased between TP1 (1.08 ± 0.35) and TP2 (1.90 ± 0.73) and did not return to the prehemorrhage values for TP3 or TP4. SI correlated positively with percentage blood loss (r = 0.583) and negatively with CO (r = -0.543). CLINICAL RELEVANCE: An increase in SI may support diagnosis of hemorrhagic shock; however, SI cannot be used as the sole end point of resuscitation. Significant differences in blood pH, base excess, and lactate concentration suggested they may be useful markers of hemorrhagic shock and need for blood transfusion.

Microwave ablation for the control of bleeding from disintegrated mammary tumours in two dogs.

A 16-year-old intact female Miniature Dachshund (dog 1) and a 13-year-old intact female American Cocker Spaniel (dog 2) presented with a chief complaint of bleeding from a mammary gland tumour ulceration. Dog 1 was transferred to hospital from a local hospital in a haemorrhagic shock state with uncontrolled continuous bleeding. Thoracic radiographs revealed multiple nodular shadows suspected to be pulmonary metastasis. Dog 2 presented with intermittent bleeding from a mass lesion in the right fifth mammary gland. Due to high anaesthetic risk secondary to severe mitral valve insufficiency (ASA status III), the owner declined surgical excision of the tumour. Therefore, microwave ablation (MWA) under local anaesthesia was chosen in order to achieve adequate haemostasis. Both dogs received local anaesthesia around the bleeding mass lesion, and the disintegrated site was microwave-ablated; dog 1 underwent MWA after blood transfusion to improve the haemorrhagic shock. The ablation site was protected using a non-adhesive dressing. Scarring of the ulcerated site led to complete haemostasis in both cases. Dog 1 underwent tumorectomy on the 31st hospital day to prevent rebleeding; histopathology results were consistent with mammary adenocarcinoma with the ablation site covered by a capsule structure. To the authors' knowledge, this is the first case report describing the use of MWA to stop bleeding from mammary tumours in veterinary medicine. MWA is a feasible and potentially effective palliative treatment modality to stop bleeding from disintegrated mammary tumours in dogs under local anaesthesia.

Evaluation of resuscitative endovascular balloon occlusion of the aorta catheter placement and comparison to resuscitative thoracotomy with aortic clamping in cadaver dogs.

OBJECTIVE: To describe placement of an aortic occlusion catheter in aortic zone 1 (Z1) and aortic zone 3 (Z3) in dogs and to compare time to placement in these zones with and without external chest compressions (ECC). Additional evaluations of time to placement in Z1 with time for resuscitative thoracotomy with aortic clamping (RT-AC) were performed. DESIGN: Prospective ex vivo study. SETTING: University teaching hospital. ANIMALS: Ten canine cadavers. INTERVENTIONS: Ten cadaver dogs were obtained from client donation after euthanasia. Cadavers were randomized to have balloon catheter placement into the right or left femoral artery via cutdown, with or without ECC. The xiphoid was used as an external anatomical landmark for Z1, and the spinous process of the 5th lumbar vertebra was used for Z3. Balloon placement was confirmed with radiography. Time to balloon placement in Z1 and Z3 and time to RT-AC were recorded. MEASUREMENTS AND MAIN RESULTS: Median body weight was 23.5 kg (9-40 kg). Median time to Z1 placement was 6.6 minutes (4.6-12.4 minutes) with ECC and 6.9 minutes (3.3-13.1 minutes) without ECC and was not statistically different (P = 0.5). Median time to RT-AC was 1 minute (0.6-1.4 minutes), which was significantly faster than time to balloon placement in Z1 with or without ECC (P = 0.004 and P = 0.002, respectively). CONCLUSIONS: Endovascular balloon occlusion of the aorta can be achieved by cutdown with and without ECC, but RT-AC is faster. Successful balloon position in Z1 could be achieved with knowledge of external anatomical landmarks, but landmarks for Z3 need further study.

Pathophysiology of hemorrhagic shock.

BACKGROUND: Hemorrhagic shock is a common condition that may lead to hemodynamic instability, decreased oxygen delivery, cellular hypoxia, organ damage, and ultimately death. CLINICAL IMPORTANCE: This review addresses the pathophysiology of hemorrhagic shock. Hemorrhagic shock can be rapidly fatal and is the leading cause of death in human trauma patients. Understanding the pathophysiology of hemorrhagic shock is imperative in understanding the current hemostatic and resuscitative strategies and is foundational to the development of new therapeutic options. KEY POINTS: Shock is a state of inadequate cellular energy production and can be triggered by many causes Both traumatic and non-traumatic causes of hemorrhage can lead to the development of hemorrhagic shock Prompt recognition and attenuation of hemorrhage is paramount in preventing the onset or potentiation of hemorrhagic shock Acute hemorrhage produces distinct physiological responses depending on the magnitude and rate of hemorrhage. Hemorrhagic shock may be directly related to the initial injury but may also be exacerbated and complicated by a post-traumatic coagulopathy, termed acute traumatic coagulopathy.

The pathophysiology of uncontrolled hemorrhage in horses.

BACKGROUND: Hemorrhagic shock in horses may be classified in several ways. Hemorrhage may be considered internal versus external, controlled or uncontrolled, or described based on the severity of hypovolemic shock the patient is experiencing. Regardless of the cause, as the severity of hemorrhage worsens, homeostatic responses are stimulated to ameliorate the systemic and local effects of an oxygen debt. In mild to moderate cases of hemorrhage (<15% blood volume loss), physiological adaptations in the patient may not be clinically apparent. As hemorrhage worsens, often in the uncontrolled situation such as a vascular breach internally, the pathophysiological consequences are numerous. The patient mobilizes fluid and reserve blood volume, notably splenic stored and peripherally circulating erythrocytes, to preferentially supply oxygen to sensitive organs such as the brain and heart. When the global and local delivery of oxygen is insufficient to meet the metabolic needs of the tissues, a cascade of cellular, tissue, and organ dysfunction occurs. If left untreated, the patient dies of hemorrhagic anemic shock. CLINICAL IMPORTANCE: An understanding of the pathophysiological consequences of hemorrhagic shock in horses and their clinical manifestations may help the practitioner understand the severity of blood volume loss, the need for referral, the need for transfusion, and potential outcome. In cases of severe acute uncontrolled hemorrhage, it is essential to recognize the clinical manifestations quickly to best treat the patient, which may include humane euthanasia. KEY POINTS: Uncontrolled hemorrhage may be defined as the development of a vascular breach and hemorrhage that cannot be controlled by interventional hemostasis methods such as external pressure, tourniquet, or ligation. Causes of uncontrolled hemorrhage in horses may be due to non-surgical trauma, surgical trauma, invasive diagnostic procedures including percutaneous organ biopsy, coagulopathy, hypertension, cardiovascular anomaly, vascular damage, neoplasia such as hemangiosarcoma, toxicity, or idiopathic in nature. When a critical volume of blood is lost, the respondent changes in heart rate, splenic blood mobilization, and microcirculatory control can no longer compensate for decreasing oxygen delivery to the tissues In spite of organ-specific microvascular responses (eg, myogenic responses, local mediator modulation of microvasculature, etc), all organs experience decreases in blood flow during severe hypovolemia Acute, fatal hemorrhagic shock is characterized by progressive metabolic acidosis, coagulopathy, and hypothermia, often termed the "triad of death," followed by circulatory collapse.

Hemorrhagic shock and hemostatic resuscitation in canine trauma.

Hemorrhage is a significant cause of death among military working dogs and in civilian canine trauma. While research specifically aimed at canine trauma is limited, many principles from human trauma resuscitation apply. Trauma with significant hemorrhage results in shock and inadequate oxygen delivery to tissues. This leads to aberrations in cellular metabolism, including anaerobic metabolism, decreased energy production, acidosis, cell swelling, and eventual cell death. Considering blood and endothelium as a single organ system, blood failure is a syndrome of endotheliopathy, coagulopathy, and platelet dysfunction. In severe cases following injury, blood failure develops and is induced by inadequate oxygen delivery in the presence of hemorrhage, tissue injury, and acute stress from trauma. Severe hemorrhagic shock is best treated with hemostatic resuscitation, wherein blood products are used to restore effective circulating volume and increase oxygen delivery to tissues without exacerbating blood failure. The principles of hemostatic resuscitation have been demonstrated in severely injured people and the authors propose an algorithm for applying this to canine patients. The use of plasma and whole blood to resuscitate severely injured canines while minimizing the use of crystalloids and colloids could prove instrumental in improving both mortality and morbidity. More work is needed to understand the canine patient that would benefit from hemostatic resuscitation, as well as to determine the optimal resuscitation strategy for these patients.

Hydroxyethyl starch 130/0.4 (6%) and succinylated gelatine (4%) interfere with refractometry in dogs with haemorrhagic shock.

OBJECTIVE: To determine if low molecular weight synthetic colloid fluids administered to dogs interfere with refractometric estimates of total plasma protein (TPPr) and urine osmolality (UOsm). STUDY DESIGN: Experimental study. ANIMALS: Eighteen healthy Greyhound dogs. METHODS: Anaesthetized Greyhounds subjected to haemorrhage for 60 minutes were given 80 mL kg-1 of Plasma-Lyte 148 (CRYST), or 20 mL kg-1 of hydroxyethyl starch 130/0.4 (HES) or succinylated gelatine (GELO) (n = 6 per group) intravenously over 20 minutes. Refractometric (TPPr) and biuret total plasma protein (TPPb) were measured before haemorrhage (Baseline), at end of shock (Shock), immediately (T20), then 40 minutes (T60), 100 minutes (T120) and 160 minutes (T180) after fluid administration. Urine specific gravity (USG) and UOsm were measured at all time points except T20. Estimated UOsm (eUOsm) was calculated from USG. Bias and limits of agreement (LOA) for TPPr versus TPPb, and eUOsm versus UOsm were calculated at each time point. RESULTS: For dogs given CRYST and GELO, median TPPr and TPPb decreased in parallel, with a small consistent TPP bias (CRYST range of bias, 0.38-0.67 g dL-1; GELO range of bias, 0.42-0.58 g dL-1). Dogs given HES showed divergence between median TPPr and TPPb after T20, with a peak bias at T20 of 1.62 g dL-1 (LOA 1.29-1.95). Dogs given HES and GELO had markedly increased USG [HES peak median USG at T180 of 1.119 (Q1-Q3 1.103-1.122); GELO peak median USG at T120 of 1.114 (Q1-Q3 1.082-1.119)], with large increases in bias between eUOsm and UOsm [HES peak bias at T60 of 2995 mOsm kg-1 (LOA 2032-3958 mOsm kg-1); GELO peak bias at T120 of 2465 mOsm kg-1 (LOA 940-3990 mOsm kg-1)]. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of HES and GELO to dogs with haemorrhagic shock interferes with refractometric measurements for at least 3 hours after administration.

Evaluation of tissue oxygen saturation in naturally occurring canine shock patients.

OBJECTIVE: To measure tissue oxygen saturation (StO2 ) in a population of dogs with naturally occurring shock and to evaluate the relationship of StO2 with an established veterinary severity scoring system (Acute Patient Physiologic and Laboratory Evaluation) and patient survival. DESIGN: Prospective observational study. SETTING: University teaching hospital. ANIMALS: Twenty-five adult dogs presenting in shock, as determined by the presence of hypotension, the calculated shock index, and hyperlactatemia. INTERVENTIONS: StO2 was measured prior to any therapeutic interventions. Blood samples were also collected for measurement of plasma lactate, complete blood count, and a serum biochemical profile. Abdominal and thoracic focused assessment with sonography was also performed. MEASUREMENTS AND MAIN RESULTS: Dogs enrolled in this study had lower mean (±SD) StO2 values (65.12 ± 17.7%) than previously reported in experimental models of canine hemorrhagic shock. There was a moderate correlation between lower StO2 and increasing Acute Patient Physiologic and Laboratory Evaluation scores. A single StO2 value, assessed prior to therapeutic intervention, was not a sensitive predictor of mortality in this population. CONCLUSIONS: Dogs with naturally occurring shock have lower mean StO2 values than those previously reported in dogs with experimentally induced shock. A lower initial StO2 was associated with worse disease severity but was not a significant predictor of survival in this population.

Evaluation of biomarkers of kidney injury following 4% succinylated gelatin and 6% hydroxyethyl starch 130/0.4 administration in a canine hemorrhagic shock model.

OBJECTIVE: To investigate the association between synthetic colloids and biomarkers of acute kidney injury (AKI) in dogs with hemorrhagic shock. DESIGN: Experimental interventional study. SETTING: University. ANIMALS: Twenty-four healthy ex-racing Greyhounds. INTERVENTIONS: Anesthetized Greyhounds subjected to hemorrhage for 60 min were resuscitated with 20 mL/kg of fresh whole blood (FWB), 6% hydroxyethyl starch (HES) 130/0.4, 4% succinylated gelatin (GELO), or 80 mL/kg of isotonic crystalloid (CRYST) over 20 min (n = 6 per treatment). Concentrations of biomarkers of AKI were measured at baseline, end of hemorrhage, and at 40 (T60), 100 (T120), and 160 (T180) min after fluid bolus. Biomarkers included neutrophil gelatinase-associated lipocalin in urine and serum (uNGAL; sNGAL), and urine cystatin C (uCYSC), kidney injury molecule-1 (uKIM), clusterin (uCLUST), osteopontin, gamma-glutamyl transferase, monocyte chemoattractant protein-1 (uMCP), interleukin-6, interleukin-8, protein (uPROT), hyaluronan, and F2 -isoprostanes. Renal histology was scored for tubular injury and microvesiculation. Biomarker fold-change from baseline was compared between groups using mixed effects models (Bonferroni-Holm corrected P<0.05). Frequencies of histology scores were compared by Fisher's exact test. MEASUREMENTS AND MAIN RESULTS: In dogs treated with GELO, uNGAL fold-change was markedly greater compared with all other groups at T60, T120, and T180 (all P<0.001), and uCYSC was greater at T60 compared with CRYST (P<0.001), and at T120 and T180 compared with all other groups (all P<0.001). Smaller, albeit significant, between-group differences in uKIM, uCLUST, uMCP, and urine protein concentration were observed across the FWB, GELO, and HES groups, compared with CRYST. The GELO group more frequently had marked tubular microvesiculation than the other groups (P = 0.015) although tubular injury scores were comparable. CONCLUSION: In dogs with hemorrhagic shock, GELO was associated with greater magnitude increases in urine biomarkers of AKI and more frequent marked tubular microvesiculation, compared with FWB, CRYST, and HES.

Ultrasound-guided catheterization of the femoral artery in a canine model of acute hemorrhagic shock.

OBJECTIVE: To describe a technique for gaining ultrasound-guided access to the femoral artery in an experimental model of acute hemorrhagic shock in anesthetized dogs. CASE SERIES SUMMARY: Five healthy, purpose-bred adult male intact Beagles were enrolled in a respiratory mechanics study under general anesthesia. Upon completion of the primary study a hypovolemic state was induced by blood removal to achieve a mean arterial pressure ≤ 55 mm Hg. Dogs were positioned in dorsal recumbency with the hind limb extended caudally. An ultrasound probe was applied to the medial aspect of the hind limb and positioned in the transverse orientation so that the femoral artery was visualized in its short axis. The artery was identified by lack of compression and presence of visible pulsation. The probe was rotated 90° into the longitudinal orientation such that the artery was visualized in its long axis. Under ultrasound guidance a 19-gauge introducer needle was advanced into the lumen of the femoral artery. Using a modified Seldinger technique the needle was removed and a catheter was placed in the femoral artery. Correct placement of the catheter was verified by observation of the characteristic arterial blood pressure waveform. Upon completion of the study dogs were humanely euthanized. The femoral artery was successfully catheterized in 4/5 dogs and a hematoma was reported in 1/5 dogs. NEW OR UNIQUE INFORMATION PROVIDED: Ultrasound-guided femoral artery catheterization is feasible on anesthetized dogs with concurrent acute hemorrhagic shock.

Tissue oxygen saturation in dogs with acute hemorrhage.

OBJECTIVE: To evaluate initial tissue hemoglobin oxygen saturation (StO2 ) in dogs presenting to an emergency room (ER) for acute hemorrhage. DESIGN: Prospective, observational study. SETTING: University veterinary teaching hospital. ANIMALS: Thirty-eight dogs with acute hemorrhage were enrolled between July 2009 and October 2010. Seventy-eight normal dogs from a previous observational study were included to represent healthy controls ("no shock"). INTERVENTIONS: Tissue oxygen saturation measurement was obtained at enrollment on dogs presented to the ER for acute hemorrhage. Baseline clinicopathologic (CBC, serum biochemical profile, prothrombin time, and activated partial thromboplastin time) and physiologic (plasma lactate concentration, venous blood gas, blood pressure, and hemoglobin oxygen saturation by pulse oximetry) data were recorded from all patients with hemorrhage. An ER clinician blinded to the StO2 value guided patient management. Patient survival to discharge from the hospital in the study group was recorded. Once data collection was complete, 3 emergency and critical care clinicians blinded to the StO2 data retrospectively classified patients into 1 of 4 shock categories (no shock, mild, moderate, or severe shock). MEASUREMENTS AND MAIN RESULTS: The historical group of healthy dogs had higher StO2 concentrations compared to the dogs classified with shock at all 3 levels (mild, moderate, and severe, P = 0.0006, <0.0001, and 0.0018, respectively); however, there was no statistical difference in StO2 between the levels of shock. A cut-off StO2 value of 87.6% identified a patient as having shock (area under the curve: 0.824, 95% confidence interval 0.749, 0.899). CONCLUSIONS: Dogs with hemorrhagic shock have lower StO2 than a population of healthy dogs.

Location is everything: The hemodynamic effects of REBOA in Zone 1 versus Zone 3 of the aorta.

OBJECTIVES: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is an emerging technology to augment proximal blood pressure during the resuscitation of patients with noncompressible torso hemorrhage. Currently, placement choice, supraceliac (Zone 1) versus infrarenal (Zone 3) aorta, depends on injury patterns, but remains a highly debated topic. We sought to compare the proximal hemodynamic support provided by Zone 1 versus Zone 3 REBOA placement and the degree of hemodynamic instability upon reperfusion following intervention. METHODS: Eighteen anesthetized swine underwent controlled hemorrhage of 25% total blood volume, followed by 45 minutes of Zone 1 REBOA, Zone 3 REBOA, or no intervention (control). They were then resuscitated with shed blood, aortic balloons were deflated, and 5 hours of critical care ensued prior to euthanasia. Physiologic parameters were recorded continuously, and blood was drawn for analysis at specified intervals. Significance was defined as p < 0.05. RESULTS: There were no significant differences between groups at baseline or during the initial 30 minutes of hemorrhage. During the intervention period, average proximal MAP was significantly greater in Zone 1 animals when compared with Zone 3 animals (127.9 ± 1.3 vs. 53.4 ± 1.1 mm Hg) and greater in Zone 3 animals when compared with control animals (42.9 ± 0.9 mm Hg). Lactate concentrations were significantly higher in Zone 1 animals (9.6 ± 0.4 mmol/L) when compared with Zone 3 animals (5.1 ± 0.3 mmol/L) and control animals (4.2 ± 0.8 mmol/L). CONCLUSIONS: In our swine model of hemorrhagic shock, Zone 3 REBOA provided minimal proximal hemodynamic support when compared with Zone 1 REBOA, albeit with less ischemic burden and instability upon reperfusion. In cases of impending hemodynamic collapse, Zone 1 REBOA placement may be more efficacious regardless of injury pattern, whereas Zone 3 should be reserved only for relatively stable patients with ongoing distal hemorrhage.

Hyperfibrinolysis diagnosed with rotational thromboelastometry and treated with tranexamic acid in a dog with acute traumatic coagulopathy.

INTRODUCTION: A 4-year old male Australian Cattle Dog involved in a road traffic accident was presented with severe polytrauma to the Small Animal Clinic, University of Zurich. He was presented in hemorrhagic shock, with an initial lactate of 10.3mmol/l and ongoing bleeding from multiple injury sites. Acute traumatic coagulopathy diagnosed with ROTEM within one hour after accident showed marked hypocoagulation and hyperfibrinolysis. Treatment with a total dose of 40mg/kg of tranexamic acid intravenously resulted in successful elimination of hyperfibrinolysis in the following, serially measured ROTEM tracings.

Hydroxyethyl starch 130/0.4 compared with 0.9% NaCl administered to greyhounds with haemorrhagic shock.

OBJECTIVE: To determine the cardiovascular and acid-base effects of 6% hydroxyethyl starch (HES) 130/0.4 and 0.9% sodium chloride (NaCl) administered to anaesthetized greyhounds with haemorrhagic shock. STUDY DESIGN: Prospective, experimental, complete randomized block design. ANIMALS: Twelve healthy adult greyhounds. METHODS: After 60 minutes of isoflurane anaesthesia, 48 mL kg-1 of blood was removed to induce hypotension. Dogs were randomized to receive either 20 mL kg-1 of HES 130/0.4 or 80 mL kg-1 of 0.9% NaCl over 20 minutes. Haemoglobin, arterial and central venous blood gas and electrolytes, lactate, mean arterial pressure (MAP) and cardiac index were measured at: T0, 60 minutes after induction of anaesthesia, immediately prior to blood removal; T1, immediately after blood removal; T2, immediately after fluid administration; and T3, 40 minutes after fluid administration. Oxygen extraction ratio (O2ER) was calculated at each sample time. RESULTS: O2ER increased at T1 and decreased at T2 and T3, with no difference between the two groups. Dogs administered HES 130/0.4 had higher lactate at T2 [mean (95% confidence interval) 1.3 (0.8-1.9) mmol L-1] than dogs administered 0.9% NaCl [0.8 (0.5-1.1) mmol L-1]; p = 0.045. Dogs administered HES 130/0.4 had a higher MAP at T3 [88 (74-102) mmHg] than dogs administered 0.9% NaCl [69 (60-79) mmHg]; p = 0.019. Dogs administered 0.9% NaCl were more acidaemic at T2 and T3, including higher hydrogen ion, lower bicarbonate, lower base excess and higher chloride concentrations. CONCLUSION: and clinical relevance The effect of 20 mL kg-1 of HES 130/0.4 on shock, as measured by O2ER, was no different than that of 80 mL kg-1 of 0.9% NaCl in dogs under general anaesthesia. Acidaemia in the NaCl group is likely attributable to hyperchloraemic metabolic acidosis from the larger volume administered.

Interleukin-8, interleukin-1ß and tumour necrosis factor-α in sequential units of packed red blood cells collected from retired racing Greyhounds.

BACKGROUND: We hypothesised that concentrations of interleukin-8 (IL-8), interleukin-1ß (IL-1ß) and tumour necrosis factor-α (TNF-α) would increase during storage in the third sequential unit (U3) of canine packed red blood cells (PRBC) collected from terminal donors in haemorrhagic shock. We further hypothesised that leucoreduction would prevent cytokine accumulation in U3 and that cytokine concentrations in U3 would be higher than in the first units (U1) collected from the same dogs. METHODS: U1 and U3 were each collected from 12 anaesthetised healthy Greyhounds. Removal of leucocytes from half of each PRBC unit produced one leucoreduced (LR) and one non-leucoreduced (NLR) unit. Canine IL-8, IL-1ß and TNF-α concentrations were measured in samples collected from the units during storage on days 0, 10, 20, 30 and 37. RESULTS: The IL-8 concentration in U3 NLR units was significantly higher on days 10, 20, 30 and 37 than on day 0 and was significantly higher than in the LR units at all time points. The IL-1ß concentration in U3 did not change over time, or between LR and NLR units. TNF-α was not detected in any unit. There were no significant differences in IL-8 or IL-1ß concentrations between U3 and U1 at any time point; however, some NLR U3 units had markedly elevated IL-8 concentrations at day 37 (2060-20,682 pg/mL) compared with NLR U1 units (3369-5280 pg/mL). CONCLUSION: NLR U3 units collected from dogs in haemorrhagic shock showed a significant increase in IL-8 concentrations during storage. Leucoreduction was effective at preventing the accumulation of IL-8. There was no difference detected between U3 and U1.

Fluid Management in Patients with Trauma: Restrictive Versus Liberal Approach.

Massive hemorrhage remains a major cause of traumatic deaths. The ideal fluid resuscitative strategy is much debated. Research has provided inconsistent results regarding which fluid strategy is ideal; the optimum fluid type, timing, and volume remains elusive. Aggressive large-volume resuscitation has been the mainstay based on controlled hemorrhage animal models. For uncontrolled hemorrhagic shock, liberal fluid resuscitative strategies exacerbate the lethal triad, invoke resuscitative injury, and increase mortality while more restrictive fluid strategies tend to ameliorate trauma-induced coagulopathy and favor a greater chance of survival. This article discusses the current evidence regarding liberal and restrictive fluid strategies for trauma.

Platelet closure time in anesthetized Greyhounds with hemorrhagic shock treated with hydroxyethyl starch 130/0.4 or 0.9% sodium chloride infusions.

OBJECTIVE: To measure platelet closure time (PCT) in dogs during controlled hemorrhagic shock and after fluid resuscitation with hydroxyethyl starch (HES) 130/0.4 or 0.9% sodium chloride. DESIGN: Experimental interventional study. SETTING: University veterinary teaching hospital. ANIMALS: Eleven healthy Greyhounds. INTERVENTIONS: Dogs were anesthetized and had 48 mL/kg of blood removed to induce hemorrhagic shock. Dogs received 20 mL/kg of HES 130/0.4 (n = 6) or 80 mL/kg of 0.9% sodium chloride (NaCl; n = 5) intravenously over 20 minutes. PCT was measured using the Platelet Function Analyzer-100 with collagen and adenosine-diphosphate cartridges at: T0 = 60 minutes after induction of anesthesia prior to hemorrhage, T1 = during hemorrhagic shock, and T2 = 40 minutes after completion of fluid bolus. Packed cell volume and platelet count were concurrently measured. MEASUREMENT AND MAIN RESULTS: Hemorrhagic shock did not significantly change PCT, with no difference between T0 and T1. Both the HES 130/0.4 and 0.9% NaCl group had a significantly increased mean PCT at T2 of 91.4 seconds (95% CI 69.3-113.4) and 95.5 seconds (95% CI 78.2-112.8), respectively, compared to T1. The magnitude of change was significantly greater for the 0.9% NaCl group than the HES 130/0.4 group. There was no difference in the magnitude of change in PCV and platelet count between the 2 groups. The PCV and platelet count were >25% and >100,000/µL, respectively, in all dogs, except for dogs in the HES 130/0.4 group at T2 where platelet counts were <100,000/µL. CONCLUSION: Controlled hemorrhagic shock in Greyhounds under anesthesia did not cause a significant change in PCT. Both HES 130/0.4 and 0.9% NaCl administration after induction of shock increased PCT. These results do not support that HES 130/0.4 causes relevant platelet dysfunction beyond hemodilution.