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).

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.

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.

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.

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.

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.

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.

Traumatic coagulopathy--part 2: Resuscitative strategies.

OBJECTIVE: To discuss the current resuscitative strategies for trauma-induced hemorrhagic shock and acute traumatic coagulopathy (ATC). ETIOLOGY: Hemorrhagic shock can be acutely fatal if not immediately and appropriately treated. The primary tenets of hemorrhagic shock resuscitation are to arrest hemorrhage and restore the effective circulating volume. Large volumes of isotonic crystalloids have been the resuscitative strategy of choice; however, data from experimental animal models and retrospective human analyses now recognize that large-volume fluid resuscitation in uncontrolled hemorrhage may be deleterious. The optimal resuscitative strategy has yet to be defined. In human trauma, implementing damage control resuscitation with damage control surgery for controlling ongoing hemorrhage, acidosis, and hypothermia; managing ATC; and restoring effective circulating volume is emerging as a more optimal resuscitative strategy. With hyperfibrinolysis playing an integral role in the manifestation of ATC, the use of antifibrinolytics (eg, tranexamic acid and aminocaproic acid) may also serve a beneficial role in the early posttraumatic period. Considering the sparse information regarding these resuscitative techniques in veterinary medicine, veterinarians are left with extrapolating information from human trials and experimental animal models. DIAGNOSIS: Viscoelastic tests integrated with predictive scoring systems may prove to be the most reliable methods for early detection of ATC as well as for guiding transfusion requirements. SUMMARY: Hemorrhage accounts for up to 40% of human trauma-related deaths and remains the leading cause of preventable death in human trauma. The exact proportion of trauma-related deaths due to exsanguinations in veterinary patients remains uncertain. Survivability depends upon achieving rapid definitive hemostasis, early attenuation of posttraumatic coagulopathy, and timely restoration of effective circulating volume. Early institution of damage control resuscitation in severely injured patients with uncontrolled hemorrhage has the ability to curtail posttraumatic coagulopathy and the exacerbation of metabolic acidosis and hypothermia and improve survival until definitive hemostasis is achieved.

Comparison of fluid types for resuscitation in acute hemorrhagic shock and evaluation of gastric luminal and transcutaneous Pco2 in Leghorn chickens.

The objective of this study was to compare the effects of 3 different fluid types for resuscitation after experimentally induced hemorrhagic shock in anesthetized chickens and to evaluate partial pressures of carbon dioxide measured in arterial blood (Paco2), with a transcutaneous monitor (TcPco2), with a gastric intraluminal monitor (GiPco2), and by end tidal measurements (Etco2) under stable conditions and after induced hemorrhagic shock. Hemorrhagic shock was induced in 40 white leghorn chickens by removing 50% of blood volume by phlebotomy under general anesthesia. Birds were divided into 4 groups: untreated (control group) and treated with intravenous hetastarch (haes group), with a hemoglobin-based oxygen carrier (hemospan group), or by autotransfusion (blood group). Respiratory rates, heart rates, and systolic arterial blood pressure (SAP) were compared at 8 time points (baseline [T0]; at the loss of 10% [T10%], 20% [T20%], 30% [T30%], 40% [T40%], and 50% [T50%] of blood volume; at the end of resuscitation [RES]; and at the end of anesthesia [END]). Packed cell volume (PCV) and blood hemoglobin content were compared at 6 time points (T0, T50%, RES, and 1, 3, and 7 days after induced hemorrhagic shock). Measurements of Paco2, TcPco2, GiPco2, and Etco2 were evaluated at 2 time points (T0 and T50%), and venous lactic acid concentrations were evaluated at 3 time points (T0, T50%, and END). No significant differences were found in mortality, respiratory rate, heart rate, PCV, or hemoglobin values among the 4 groups. Birds given fluid resuscitation had significantly higher SAPs after fluid administration than did birds in the control group. In all groups, PCV and hemoglobin concentrations began to rise by day 3 after phlebotomy, and baseline values were reached 7 days after blood removal. At T0, TcPco2 did not differ significantly from Paco2, but GiPco2 and Etco2 differed significantly from Paco2. After hemorrhagic shock, GiPco2 and TcPco2 differed significantly from Paco2. The TcPco2 or GiPco2 values did not differ significantly at any time point in birds that survived or died in any of the groups and across all groups. These results showed no difference in mortality in leghorn chickens treated with fluid resuscitation after hemorrhagic shock and that the PCV and hemoglobin concentrations increased by 3 days after acute hemorrhage with or without treatment. The different CO2 measurements document changes in CO2-values consistent with poor perfusion and may prove useful for serial evaluation of responses to shock and shock treatment.

Choque hipovolêmico em um cão com suspeita de intoxicação por cumarínico: relato de caso / Hypovolemic shock in a dog with suspected coumarin poisoning: case report

Um cão adulto, fêmea, SRD e 5,0 kg foi atendido no Hospital de Clínicas Veterinárias da Universidade Federal do Rio Grande do Sul com sinais de choque. A anamnese não revelou nenhuma informação consistente. No exame clínico, o paciente apresentava estado de estupor, midríase, hipotermia (36,5oC), bradicardia (50 b.p.m), cianose e presença de hemorragia contínua em região digital. O animal foi imediatamente colocado em oxigênio e submetido à fluidoterapia intensiva com fluido cristalóide (90ml/kg/hora).

Peri- and intra-operative management of the goat during acute surgical experimentation.

Goats are used as animal models for surgery and trauma research. The authors discuss appropriate methods for induction of anesthetics, intubation and surgical maintenance of the goat during acute experimentation. Risks imposed by the Q fever pathogen Coxiella burnetii are described, as well as measures that have proven effective in minimizing zoonotic transmission of this pathogen to laboratory personnel. With appropriate knowledge of its applications, peri- and intra-operative management and limitations, the goat is a suitable animal model for a variety of biomedical research applications.

Haemoperitoneum in horses: a retrospective review of 54 cases.

This retrospective study was conducted in the UK and identifies the most frequent causes, diagnoses, treatment and prognoses for short- and long-term survival in 54 cases of horses with haemoperitoneum. Clinical signs of haemorrhagic shock and colic were common, and abdominal ultrasound was very useful for the identification of haemoperitoneum. Causes of haemoperitoneum included uterine injury (22 per cent), involvement of specific blood vessels (20 per cent), splenic injury (19 per cent), neoplasia (13 per cent) and other (4 per cent). No source was identified in 22 per cent of cases. Fifty-seven per cent of cases underwent exploratory laparotomy. Of the surgical cases, a diagnosis was made in 65 per cent, with 42 per cent surviving to discharge. It was felt that exploratory laparotomy had both diagnostic and therapeutic implications. Twenty-eight per cent of cases died, and 33 per cent were euthanased, whereas 39 per cent survived to be discharged from the hospital, with 35 per cent of these surviving in the long term. Idiopathic haemoperitoneum was associated with the best outcome for long-term survival.

Massive transfusion and surgical management of iatrogenic aortic laceration associated with cystocentesis in a dog.

CASE DESCRIPTION: A 4-year-old 29-kg (63.8-lb) spayed female Husky crossbred was referred for emergency treatment because of catastrophic hemorrhagic shock following attempts at cystocentesis for investigation of suspected urinary tract infection. CLINICAL FINDINGS: On arrival at the hospital, clinicopathologic assessments revealed rapidly decreasing PCV and worsening hypoproteinemia, compared with findings immediately prior to referral. The dog had severe hyperlactemia. Ultrasonography revealed the presence of free fluid in the abdomen; the fluid appeared to be blood (determined via abdominocentesis). TREATMENT AND OUTCOME: Urgent surgical exploration was undertaken. Two small lacerations in the ventral aspect of the abdominal aorta just dorsal to the bladder were identified and repaired. Multiple transfusions of packed RBCs (5 units) and fresh frozen plasma (3 units) were administered, and autotransfusion of blood (1.2 L) from the abdomen was performed. The dog recovered well from surgery and anesthesia, but developed signs of severe pain and swelling of both hind limbs, which were attributed to reperfusion injury following aortic occlusion during surgery. Treatment included administration of S-adenosylmethionine (23 mg/kg [10.5 mg/lb], PO, q 24 h) and analgesia; 5 days after surgery, the hind limb problems had resolved and treatments were discontinued. CLINICAL RELEVANCE: In the dog of this report, aortic laceration secondary to cystocentesis was successfully treated with a combination of surgery and massive transfusion; the development of reperfusion injury was an interesting and reversible complication of surgery. The possibility of damage to intra-abdominal structures should be investigated if a dog becomes acutely ill after cystocentesis.

Severe nasal hemorrhage in an anesthetized horse.

An 8-year-old Thoroughbred gelding with colic was anesthetized for surgical correction of right dorsal displacement of the ascending colon. Removal of the nasogastric tube at the end of surgery resulted in hemorrhage from the nares and loss of 24 L of blood. Treatment included administration of acetated Ringer's solution, hypertonic saline solution, and dobutamine. A blood transfusion was started after hemorrhage was controlled, and arterial pressure was restored to the prehemorrhage value, but was stopped after infusion of 2.7 L of blood because of a suspected adverse reaction. This case indicates that infusion of balanced electrolyte solution, hypertonic saline solution, and dobutamine may maintain adequate arterial pressure after severe blood loss, and also supports the suggestion that administration of hypertonic saline solution potentiates blood loss in the absence of hemostasis.

Treatment of dogs in hemorrhagic shock by intraosseous infusion of hypertonic saline and dextran.

Under isoflurane anesthesia, 50% of the calculated blood volume was removed from 11 dogs. After 30 minutes, five dogs were treated with hypertonic saline and dextran (HSD) (5 mL/kg) followed by isotonic saline solution (2 mL/kg) intraosseously. Six dogs (controls) received isotonic saline (7 mL/kg) intraosseously. All treatments were administered through the medullary cavity of the tibia over a 30-minute period. Cardiac output, mean arterial pressure, central venous pressure, packed cell volume, total protein, and blood gases were monitored for 4 hours. Cardiac output, mean arterial pressure, and circulating volume (indicated by packed cell volume and total protein) were significantly improved after administration of HSD. We conclude that intraosseous infusion of HSD is efficacious in treating hemorrhagic shock and believe the technique may prove to be useful in clinical situations when intravenous lines cannot be established rapidly.

Haematological, serum electrolyte and blood gas effects of small volume hypertonic saline in experimentally induced haemorrhagic shock.

The effects of treatment with small volume hypertonic (2400 mOsm/litre) and isotonic (300 mOsm/litre) saline on serum electrolyte and biochemical concentrations, haemograms and blood gases were evaluated in 12 horses using a haemorrhagic shock model. Intravascular catheters were placed surgically for sample collection prior to anaesthesia. Controlled haemorrhage was initiated and continued until mean systemic pressure reached 50 to 60 mmHg. Hypertonic or isotonic saline (2 litres) was administered by intravenous infusion and data collected for 2 h. Following haemorrhage, packed cell volume (PCV), haemoglobin, blood glucose concentrations and erythrocyte numbers increased whereas plasma total protein and albumin concentrations decreased. Infusion of hypertonic saline resulted in a further decrease in total protein and albumin concentrations. Glucose concentrations and other haematological variables were unaffected. Isotonic saline administration did not affect electrolyte, total protein or albumin concentrations. Concentrations of sodium and chloride were unaffected by hypotension but increased significantly following hypertonic saline treatment, exceeding normal values during the immediate post treatment period. Serum osmolality increased concurrently. No significant changes in arterial and venous blood gas values were observed with haemorrhage or isotonic saline treatment. A transient decrease in arterial and venous blood pH and a sustained decrease in venous bicarbonate and base excess concentrations occurred following hypertonic saline administration. No significant increases in any serum biochemical concentrations occurred during hypotension or following infusion of either isotonic or hypertonic saline. These results demonstrate that small volume hypertonic saline can be administered safely to horses without producing extreme changes in electrolyte concentrations, blood gases or haematological parameters.

Management of the severely injured animal.

Initial management of the seriously injured animal involves the immediate recognition of life-threatening abnormalities and prompt resuscitation based on priorities of care. Of equal importance to the ultimate survival of the animal is an aggressive approach to the diagnosis and control of the complications and sequelae of injury. This approach to patient care requires constant attention to details, but offers the most efficient management of these critically ill animals.