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Home , Distributive shock, Hypovolemic shock, Obstructive shock, Shock (circulatory)

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Distributive

Garret E. Pachtinger, VMD, DACVECC VETgirl; Veterinary Specialty and Emergency Center Levittown, Pennsylvania

Clinical Clues YOU HAVE ASKED ... is generally associ- What is distributive shock, and ated with altered vasomotor tone— notably inappropriate (eg, how do I treat it? , systemic inflammatory response syndrome), excessive THE EXPERT SAYS ... (eg, following trauma or ), or abnormalities in normal flow Shock (ie, inadequate cellular energy (eg, obstructive diseases such as gastric production or the body’s inability to dilatation-volvulus [GDV] or pericardial supply cells and tissues with and effusion)—resulting in maldistribution nutrients and remove waste products1-3) of blood flow. can cause quick clinical deterioration and requires rapid identification and Patients with septic distributive shock treatment. Distributive shock is a gen- often have hyperemic mucous mem- eral classification for syndromes that branes caused by uncontrolled vasodila- cause massive maldistribution of blood tion from inflammatory mediators and flow (see References, page 96). Anaphy- cytokine release (see References, page lactic, obstructive, and are 96). Patients with anaphylactic or GDV = gastric dilatation- common forms of distributive shock. obstructive distributive shock show volvulus

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clinical signs such as , pale mucous membranes, delayed SIGNS OF refill time, poor quality, and altered mentation3; cats may be pre- h Tachycardia (in cats, ; in dogs, sented with bradycardia rather than decompensated shock [ie, when tachycardia. Additional clinical signs of compensatory mechanisms cannot anaphylactic shock in cats and dogs may respond to ongoing blood loss]) include , , pruritus, h Altered mentation and signs consistent with hypovolemic h Pale pink mucous membranes shock (see Signs of Hypovolemic Shock). Cats in anaphylactic shock may be pre- h Prolonged capillary refill time sented in respiratory distress because of h Weak femoral laryngeal or pharyngeal edema, bron- h Cold extremities choconstriction, and mucus produc- tion4,5; this can occur in dogs but is less h common. h Hyperlactatemia Adapted from Dr. Pachtinger’s article Hypovolemic Diagnostic Testing & Evaluation Shock, available at cliniciansbrief.com/article/ Diagnostic testing for distributive shock hypovolemic-shock depends on signalment, history, and findings. There are many diagnostics to consider, but immediate point-of-care diagnostics and the importance of the physical examina- second- or third-tier diagnostics that are tion cannot be overemphasized. For valuable but not immediately needed. example, a patient presented on emer- gency after vaccine administration Point-of-care diagnostic testing may should prompt the clinician to consider include a basic minimum database (ie, treatment for anaphylactic shock, packed volume, total , blood whereas a large-breed dog presented glucose, AZO test or blood urea nitro- with a distended and nonpro- gen/ test), followed by more ductive retching suggests GDV. The cli- advanced testing (eg, CBC with blood nician should identify the need for smear to assess WBCs for toxic changes and pathogens associated with leuko- cytes or erythrocytes, serum chemistry profile, urinalysis, parame- ters, serum lactate, mea- surement). Thoracic and abdominal The importance of the physical radiography as well as thoracic and examination cannot be overemphasized. abdominal ultrasonography may also be indicated.

A lactate test is important to assess tis- sue . With adequate perfusion, patients in shock often develop hyper- lactatemia caused by anaerobic metabo- lism. The normal lactate concentration

94 cliniciansbrief.com October 2016 in adult dogs and cats is <2.5 mmol/L.6 Persistently elevated lactate concentra- tions in dogs may help predict mortality in specific diseases, notably GDV.6-9 Distributive Although single lactate readings were shock is generally initially used to predict mortality, trends in serial lactate concentration measure- associated ments may be more beneficial during with altered and have been found to be a better predictor of outcome.10-12 vasomotor tone.

Treatment When a patient is presented with pre- sumptive distributive shock, a typical Glucocorticoids are often administered triage assessment including ABC (air- for allergic or hypersensitivity reac- way, , circulation) should be tions; however, in states of anaphylactic performed. If warranted, IV access and shock, glucocorticoids do not have fluid resuscitation should be performed immediate effect and are not a first-line to correct malperfusion and hypoten- therapy. The anti-inflammatory effects sion. Isotonic crystalloids at a shock may not occur for several hours after bolus rate (dogs, 20-40 mL/kg; cats, administration, and, although they may 10-20 mL/kg over 15-30 minutes) should help reduce the severity of a biphasic be administered. Supplemental oxygen reaction, they are not a first-line therapy should be administered via flow-by for anaphylaxis. If needed for inflamma- methods (50-150 mL/kg/min) or nasal tion or in cases of respiratory distress oxygen cannulas (50-100 mL/kg/min). caused by oropharyngeal edema, dexa- methasone phosphate at 0.05- Anaphylactic Shock 0.1 mg/kg IV once or twice a day is If anaphylaxis is suspected, epineph- recommended.13 A constant rate infusion rine, a potent α- and ß-adrenergic ago- of a vasopressor or positive may nist, is recommended (0.01 mg/kg IV be required in patients unresponsive to or IM, repeated every 5 minutes as fluid and epinephrine therapy. 13,14 needed). Stimulation of α1-adrenergic receptors results in vasoconstriction. See Table (next page) for and doses used for treating anaphylactic

H1-receptor antagonists (eg, diphen- shock. hydramine 2-4 mg/kg IM) can also be considered, notably to reduce pruritus, erythema, urticaria, , and Obstructive shock occurs when there is angioedema. In conjunction with H1- an obstruction to flow, such as with GDV antagonists, H2-antagonists (eg, famoti- or . Resolution is dine 1-2 mg/kg/IV) decrease erythema directed at correcting the cause of and decrease gastric acid production. shock. As with anaphylactic shock These should not be substi- patients, patients presented with pre- tuted for epinephrine but rather used sumptive obstructive shock should GDV = gastric dilatation- volvulus adjunctively with epinephrine.14,15 receive triage assessment. If warranted,

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IV access and fluid resuscitation should increased intrapericardial pressure, be performed to correct malperfusion which equals or exceeds right atrial/ven- and . Isotonic crystalloids tricular pressure and results in decreased at a shock bolus rate (dogs, 20-40 mL/ ventricular filling. This decreases kg; cats, 10-20 mL/kg over 15-30 min- volume, leading to decreased cardiac out- utes) should be administered. Supple- put and finally decreased blood pressure. mental oxygen should be administered Poor perfusion is treated with IV fluid with flow-by oxygen methods (50-150 boluses given to effect, followed by peri- mL/kg/min) or nasal oxygen cannulas cardiocentesis and resolution of pericar- (50-100 mL/kg/min). dial tamponade. The goal of treatment is to improve and reduce In patients with GDV, gastric distension and reperfusion. obstructs venous return in the caudal vena cava, leading to decreased cardiac Conclusion preload and . Poor perfu- Distributive shock, whether anaphylactic sion is treated with IV fluid boluses or obstructive, should be carefully evalu- given to effect, followed by gastric ated and quickly treated, as it often decompression and surgical return of results in severe cardiovascular abnor- the stomach to its normal position. malities, multiple failure, and/or death. Aggressive fluid resuscitation Pericardial effusion, another common alone to promote adequate perfu- GDV = gastric dilatation- cause of obstructive shock, can lead to sion may be unsuccessful, and additional volvulus pericardial tamponade resulting from therapy is often needed. n

TABLE References 1. Hopper K, Silverstein D, Bateman S. Shock DOSES TO TREAT ANAPHYLACTIC SHOCK syndromes. In: DiBartola SP, ed. Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice. 4th ed. St. Louis, MO: Elsevier Saunders; 2012:557-583. 2. de Laforcade AM, Silverstein DC. Shock. In: Silverstein Drug Dose Route Class DC, Hopper K, eds. Small Animal Critical Care Medicine. St. Louis, MO: Elsevier Saunders; 2009:41-45. 3. Manji RA, Wood KE, Kumar A. The history and Epinephrine 0.01 mg/kg IV or IM potent α- and evolution of circulatory shock. Crit Care Clin. 2009;25(1):1-29. b-adrenergic agonist 4. Sigrist NE, Adamik KN, Doherr MG, Spreng DE. Evaluation of respiratory parameters at presentation Diphenhydramine 2-4 mg/kg IV or IM H1-antihistamines as clinical indicators of respiratory localization in dogs and cats with respiratory distress. J Vet Emerg Crit Care (San Antonio). 2011;21(1):13-23. Famotidine 1-2 mg/kg IV or IM H -antihistamines 2 5. Sigrist NE, Doherr MG, Spreng DE. Clinical findings and value of post-traumatic radiographs in Dexamethasone SP 0.05-0.1 mg/kg IV or IM Glucocorticoid dogs and cats with blunt trauma. J Vet Emerg Crit Care. 2004;14(4):259-268.

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6. Boag AK, Hughes D. Assessment and a predictor of gastric necrosis and initial treatment of perfusion abnormalities in the and subsequent plasma lactate values as emergency patient. Vet Clin North Am Small a predictor of survival in dogs with gastric Anim Pract. 2005;35(2);319-342. dilatation-volvulus: 84 dogs (2003-2007). J Vet 7. de Papp E, Drobatz KJ, Hughes D. Plasma Emerg Crit Care (San Antonio). 2011;21(1):36-44. lactate concentration as a predictor of gastric 12. Conti-Patara A, de Araújo Caldeira J, de necrosis and survival among dogs with gastric Mattos-Junior E, et al. Changes in tissue dilatation-volvulus: 102 cases (1995-1998). perfusion parameters in dogs with severe J Am Vet Med Assoc. 1999;215(1):49-52. sepsis/septic shock in response to goal- 8. Nel M, Lobetti RG, Keller N, Thompson PN. directed hemodynamic optimization at Prognostic value of blood lactate, blood admission to ICU and the relation to outcome. glucose, and in canine babesiosis. J Vet Emerg Crit Care (San Antonio). 2012;22(4): J Vet Intern Med. 2004;18(4):471-476. 409-418. 9. Lagutchik MS, Olgivie GK, Hackett TB, Wing- 13. Dowling PM. Anaphylaxis. In: Silverstein DC, field WE. Increased lactate concentrations in Hopper K, eds. Small Animal Critical Care ill and injured dogs. J Vet Emerg Crit Care. Medicine. St. Louis, MO: Elsevier Saunders; 1998;8(2):117-127. 2009:727-730. 10. Zacher LA, Berg J, Shaw SP, Kudej RK. 14. Waddell LS. Systemic anaphylaxis. In: Ettinger Association between outcome and changes SJ, Feldman EC, eds. Textbook of Veterinary in plasma lactate concentration during . 7th ed. St. Louis, MO: presurgical treatment in dogs with gastric Elsevier Saunders; 2010:531-534. dilatation-volvulus: 64 cases (2002-2008). 15. Sheikh A, Shehata YA, Brown SG, Simons FE. J Am Vet Med Assoc. 2010;236(8):892-897. (epinephrine) for the treatment of 11. Green TI, Tonozzi CC, Kirby R, Rudloff anaphylaxis with and without shock. Cochrane Database Syst Rev. 2008;4:CD006312. E. Evaluation of initial plasma lactate values as C

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