zbornik referatov xxviii. simpozija · 2018-01-03 · zbornik referatov xxviii. simpozij o...

Portorož, 9. – 11. april 2015

ZBORNIK REFERATOV

Univerza v LjubljaniVeterinarska fakulteta

XXVIII. SIMPOZIJAo aktualnih boleznih malih `ivali

ZBORNIK REFERATOV

XXVIII. SIMPOZIJA O AKTUALNIH

BOLEZNIH MALIH ŽIVALI

Portorož, 2015 http://www.zdruzenje-szvmz.si/

XXVIII. SIMPOZIJ O AKTUALNIH BOLEZNIH MALIH ŽIVALI ZBORNIK REFERATOV


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Izdalo: Slovensko združenje veterinarjev za male živali

Oblikovanje:AKTA DESIGNwww.aktadesign.si

270 izvodov

Vsebina

Silverstein D. Catching Your Breath: Approach and Treatment of The Patient with Respiratory Failure ..........................................................................................................................8

Pipan M. Ko se srce ustavi! “RECOVER Initiative” ........................................................................11

Silverstein D. Can You See It? SIRS/MODS/Sepsis: Recognition and Diagnosis ..............................14

Silverstein D. Can You Fix It? SIRS/MODS/Sepsis:Treatment and Monitoring ................................17

Pipan M. Ali grem v pravo smer? Monitoriranje tekočinske terapije .............................................21

Silverstein D. What are Your Goals? Goal directed therapy: How and Why? .................................23

Silverstein D. To Transfuse or Not to Transfuse? Transfusion Therapy in Critically Ill Patients ........28

Pipan M. Hmmm... le kaj je šlo narobe? Kako izboljšati oskrbo kritičnega pacienta? ...................31

Dombrowski SC. Bereavement Issues in Pet Loss ..........................................................................42

Dombrowski SC. Compassion Fatigue in the Veterinary Practitioner .............................................44

Seliškar A. Kaj moramo preveriti preden anesteziramo žival .........................................................46

Matko M. Priprava za kirurške posege ..........................................................................................48

Rostaher A. Klinični pristop pri garjavosti .....................................................................................50

Pavlin D. Internistične urgence ......................................................................................................53

Zakošek Pipan M, Plavec T. Rojstvo s carskim rezom – elektivni ali urgentni carski rez ................61

Frantar BE, Zupanc M. Epiduralna analgezija pri kritično bolnih psih ............................................61

Butinar J, Rejec A, Pilla T, Pečar J. Načrtovanje in izvedba resekcij tumorjev .................................61

Zemljič T. Perforativne poškodbe očesa .........................................................................................61

Pavlin D. Transsfenoidna hipofizektomija kot možnost zdravljenja Cushingove bolezni ................62

Jelovčan P, Mlakar N. Travmatska poškodba možgan: strel v glavo ...............................................62

Mlakar N, Domanjko Petrič A. Ultrasonografska diagnostika urgentnih abdominalnih in torakalnih stanj .............................................................................................................................62

Furman E. Zagotavljanje kakovosti laboratorijskih rezultatov „in-house“ veterinarskih laboratorijev ..................................................................................................................................63

Brložnik M, Mujagić E, Faraguna S, Švara T, Gombač M. Disgerminom jajčnika pri psici ...............63

Čurin A, Žel J, Divjak M. Ortotična oskrba psa po obsežni poškodbi tarzalnega sklepa.................63

Jagodič E, Žel J, Plavec T, Kovše M, Gombač M, Švara T, Zdovc I, Golob M. Piotoraks pri mački – kaj storiti, da bo zdravljenje uspešno? .............................................................................64

Luštrek U. Epiteliotropni limfom pri pritlikavem šnavcerju ............................................................64

Ostrouška M, Goruppi M. Policitemia rubra vera (primarna eritrocitoza) pri mački: predstavitev kliničnega primera in spremljanje zdravljenja s citostatikom hidroksiurea ...................................64

Trojner G. Kronično vnetje črevesja (za antibiotike dovzetna enteropatija) pri šarpeju .................65

Vasiljević M, Stanković S, Zrimšek P, Nemec Svete A, Krstić V, Seliškar A. Assessment of cardiac troponin I concentrations associated with medetomidine sedation in healthy dogs ....................65

Zakošek Pipan M. Znaki estrusa pri sterilizirani maltežanki ..........................................................66

Lukanc B, Žel J, Erjavec V. Dilatacija in zasuk želodca – naši izsledki pri kirurško oskrbljenih psih ...............................................................................................................................................66

ZBORNIK REFERATOV XXVIII. SIMPOZIJ O AKTUALNIH BOLEZNIH MALIH ŽIVALI


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Posebni pokrovitelji

Farmina in DJ Plus d.o.o., Tovarniška c. 15, 3312 Prebold

Vetpromet, Cesta na Brdo 100, 1000 Ljubljana

Simpozij so omogočili še

Bayer Animal Health, Bayer Croatia, Radnička cesta 80, 10000 Zagreb, Hrvaška

Dipros d.o.o., Gorenjesavska cesta 54a, 4000 Kranj

Elanco, zastopnik za Slovenijo: Iris mednarodna trgovina d.o.o., Cesta v Gorice 8, 1000 Ljubljana

EVG, molekularna diagnostika, Grajski trg 1, 2000 Maribor

Felivet, Nina Cizej s.p., Mladinska ulica 20, 2000 Maribor

Genera SI d.o.o., Parmova ulica 53, 1000 Ljubljana

Invitro, Rennweg 95, 1030 Wien, Avstrija

Idexx Laboratories Italia, Via Guglielmo Silva 36, 20149 Milano, Italija

Iris mednarodna trgovina d.o.o., Cesta v Gorice 8, 1000 Ljubljana

Kemofarmacija d.d., Cesta na Brdo 100, 1000 Ljubljana

Krka d.d., Šmarješka cesta 6, 8501 Novo mesto

Medical Intertrade d.o.o., Karlovška cesta 1, 1000 Ljubljana

Merck MSD AH, Intervet international B.V. Boxmeer, Podružnica Ljubljana, Šmartinska cesta 140, 1000 Ljubljana

MM Surgical d.o.o., Galjevica 81, 1000 Ljubljana

Salus, Veletrgovina, d.o.o., Litostrojska 46a, 1000 Ljubljana

Vetconsult Pharma d.o.o., Grebičeva 50, 1000 Ljubljana

Vetpet d.o.o., Letališka cesta 29, 1000 Ljubljana

Wellion, zastopnik za Slovenijo: Med Trust d.o.o., Litostrojska cesta 60, 1000 Ljubljana

Zoetis, zastopnik za Slovenijo: Iris Mednarodna trgovina d.o.o., Cesta v Gorice 8, 1000 Ljubljana



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ORGANIZACIJSKI IN UREDNIŠKI ODBOR SZVMŽ (UO SZVMŽ)

Doc. dr. Alenka Seliškar, dr. vet. med. (predsednica)

Prof. dr. Nataša Tozon, dr. vet. med. (podpredsednica – bodoča predsednica)

Igor Firm, dr. vet. med. (podpredsednik – prejšnji predsednik)

Barbara Celinšek, dr. vet. med. (tajnik)

Tjaša Pukl, dr. vet. med. (blagajnik)

Milan Matko, dr. vet. med. (član)

Doc. dr. Joško Račnik, dr. vet. med. (član)

ČASTNI ČLANI ZDRUŽENJA:

Prof. dr. Vjekoslav Simčič, dr. vet. med.

Prof. dr. Boyd R Jones, BVSc, FACVSc, DECVIM-Ca, MRCVS

Emil Mlinarič, dr. vet. med.

WORLD SMALL ANIMAL VETERINARY ASSOCIATION - WSAVA

OFFICERS

Prof. Colin Burrows, Executive Board Member, President

Prof. Jolle Kirpensteijn, Past President

Dr. Walt Ingwersen, President Elect

Dr. Shane Ryan, Executive Board Member, Vice-President

Dr. Siraya Chunekamrai, Honorary Secretary

Dr. Ellen van Nierop, Honorary Treasurer

Dr. Renée Chalmers Hoynck van Papendrecht, Executive Board Member

Dr. Nicola Neumann, Executive Board Member

FEDERATION OF EUROPEAN COMPANION ANIMAL VETERINARY ASSOCIATIONS - FECAVA

OFFICERS

Dr. Monique Megens, President

Dr. Jerzy Gawor, Vice President

Dr. Wolfgang Dohne, Secretary

Dr. Denis Novak, Treasurer

Dr. Simon Orr, Senior Vice-President



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ČETRTEK, 9. april 2015 PREDKONGRESNI DAN – Dermatološki seminarPokrovitelja IRIS in Elanco

Dermatologija hišnih ljubljenčkov: od novorojenčkov do mladih odraslih psov

08.30 – 09.30 PRIJAVA UDELEŽENCEV

09.30 – 11.00 Declercq J. Neonatalna in pediatrična dermatologija I

11.00 – 11.30 ODMOR

11.30 – 13.00 Declercq J. Neonatalna in pediatrična dermatologija II

13.00 – 14.30 KOSILO

14.30 – 14.50 Rostaher A. Spinosad – klinične izkušnje 14.50 – 16.00 Razprava: primeri predavateljev in udeležencev (moderatorica Rostaher A)

16.00 – 16.30 ODMOR

16.30 – 18.00 Declercq J. Dermatologija mladih odraslih psov

18.00 – 18.30 REDNA LETNA SKUPŠČINA DERMATOLOŠKE SEKCIJE

PETEK, 10. april 2015, plenarna dvorana 07.30 – 09.00 PRIJAVA UDELEŽENCEV08.45 – 09.00 OTVORITEV SIMPOZIJAModerator: Seliškar A09.00 – 09.45 Silverstein D. Catching Your Breath: Approach and Treatment of The Patient with Respiratory Failure09.45 – 10.30 Pipan M. Ko se srce ustavi! “RECOVER Initiative”

10.30 – 11.00 ODMOR (pokrovitelj Vetpromet)

Moderator: Pavlin D11.00 – 11.45 Silverstein D. Can You See It? SIRS/MODS/Sepsis: Recognition and Diagnosis11.45 – 12.30 Silverstein D. Can You Fix It? SIRS/MODS/Sepsis: Treatment and Monitoring

12.30 – 14.00 KOSILO

Moderator: Pavlin D14.00 – 14.45 Pipan M. Ali grem v pravo smer? Monitoriranje tekočinske terapije14.45 – 15.30 Silverstein D. What are Your Goals? Goal directed therapy: How and Why?

15.30 – 16.00 ODMOR

Moderator: Seliškar A16.00 – 16.45 Silverstein D. To Transfuse or Not to Transfuse? Transfusion Therapy in Critically Ill Patients16.45 – 17.45 Pipan M. Hmmm... le kaj je šlo narobe? Kako izboljšati oskrbo kritičnega pacienta?

18.00 – 19.30 SKUPŠČINA SZVMŽ 20.00 SVEČANA VEČERJA (pokrovitelj Farmina)

SOBOTA, 11. april 2015

Skupna predavanja za veterinarje in veterinarske tehnike, plenarna dvoranaModerator: Matko M09.30 – 10.15 Dombrowski SC. Bereavement Issues in Pet Loss 10.15 – 11.00 Dombrowski SC. Compassion Fatigue in the Veterinary Practitioner


Program za VETERINARJE, plenarna dvoranaModerator: Tozon N11.30 – 11.45 Zakošek Pipan M, Plavec T. Rojstvo s carskim rezom – elektivni ali urgentni carski rez11.45 – 12.00 Frantar BE, Zupanc M. Epiduralna analgezija pri kritično bolnih psih12.00 – 12.15 Butinar J, Rejec A, Pilla T, Pečar J. Načrtovanje in izvedba resekcij tumorjev12.15 – 12.30 Zemljič T. Perforativne poškodbe očesa

12.30 – 14.00 KOSILO

Moderator: Firm I14.00 – 14.15 Pavlin D. Transsfenoidna hipofizektomija kot možnost zdravljenja Cushingove bolezni 14.15 – 14.30 Jelovčan P, Mlakar N. Travmatska poškodba možgan: strel v glavo14.30 – 14.45 Mlakar N, Domanjko Petrič A. Ultrasonografska diagnostika urgentnih abdominalnih in torakalnih stanj14.45 – 15.00 Furman E. Zagotavljanje kakovosti laboratorijskih rezultatov „in-house“ veterinarskih laboratorijev

15.00 ZAKLJUČEK SIMPOZIJA

SOBOTA, 11. april 2015

Skupna predavanja za veterinarje in veterinarske tehnike, plenarna dvorana

Moderator: Matko M09.30 – 10.15 S. C. Dombrowski. Compassion Fatigue in the Veterinary Practitioner10.15 – 11.00 S. C. Dombrowski. Bereavement Issues in Pet Loss


Program za VETERINARSKE TEHNIKE, mala dvorana

Moderator: Firm I11.30 – 12.00 Seliškar A. Kaj moramo preveriti preden anesteziramo žival12.00 – 12.30 Matko M. Priprava za kirurške posege

12.30 – 14.00 KOSILO

Moderator: Rostaher A14.00 – 14.20 Rostaher A. Klinični pristop pri garjavosti14.20 – 14.30 Pipp J. Učinkovine za zatiranje ektoparazitov14.30 – 15.00 Pavlin D. Internistične urgence

15.00 ZAKLJUČEK SIMPOZIJA

POSTERJI1. Brložnik M, Mujagić E, Faraguna S, Švara T, Gombač M. Disgerminom jajčnika pri psici 2. Čurin A, Žel J, Divjak M. Ortotična oskrba psa po obsežni poškodbi tarzalnega sklepa 3. Jagodič E, Žel J, Plavec T, Kovše M, Gombač M, Švara T, Zdovc I, Golob M. Piotoraks pri mački – kaj storiti, da bo zdravljenje uspešno?4. Luštrek U. Epiteliotropni limfom pri pritlikavem šnavcerju 5. Ostrouška M, Goruppi M. Policitemia rubra vera (primarna eritrocitoza) pri mački: predstavitev kliničnega primera in spremljanje zdravljenja s citostatikom hidroksiurea

6. Trojner G. Kronično vnetje črevesja (za antibiotike dovzetna enteropatija) pri šarpeju 7. Vasiljević M, Stanković S, Zrimšek P, Nemec Svete A, Krstić V, Seliškar A. Assessment of cardiac troponin I concentrations associated with medetomidine sedation in healthy dogs 8. Zakošek Pipan M. Znaki estrusa pri sterilizirani maltežanki 9. Lukanc B, Žel J, Erjavec V. Dilatacija in zasuk želodca – naši izsledki pri kirurško oskrbljenih psih

PROGRAM XXVIII. SIMPOZIJA O AKTUALNIH BOLEZNIH MALIH ŽIVALIPortorož, 9. – 11. april 2015



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Catching Your Breath: APPROACH AND TREATMENT OF THE PATIENT WITH

RESPIRATORY FAILURE

Deborah Silverstein

The patient with respiratory distress always requires emer-gency attention and can prove frustrating and stressful for the veterinarian. These animals often have minimal respirato-ry reserves and even minor stress or gentle restraint can prove fatal (especially in cats!). The initial evaluation and therapeu-tic plan require keen physical examination skills, knowledge of common respiratory diseases, and an understanding of the risks and benefits associated with the various diagnostic and therapeutic options. In order to maximize the chance for a successful outcome, the clinician frequently must treat ani-mals based on minimal diagnostic tests. This presentation will review the initial evaluation of these patients, primary causes of respiratory failure, safest initial diagnostic approaches and emergent treatment strategies.

The clinical signs of dyspnea and possible respiratory fail-ure in dogs and cats commonly include tachypnea, cyano-sis and/or pale mucous membranes, open-mouth breathing, increased abdominal movement, and orthopnea. A careful physical examination is essential in the initial evaluation of a dyspneic animal, although stressed cats and some dogs may not tolerate restraint for a thorough examination. Many pa-tients will not show overt evidence of respiratory distress until they are transported, handled, or restrained. Some will signifi-cantly worsen upon presentation and progress to respiratory arrest.

By definition, ventilatory failure is the inability to eliminate carbon dioxide leading to hypercapnea, and oxygenation fail-ure is the inability to oxygenate the blood adequately. The primary cause of respiratory failure is hypoxemia, although hypercapnea and impending respiratory fatigue or arrest are also indications to act quickly and consider intubation and mechanical ventilation.

Hypercapnea is commonly caused by decreased minute ventilation due to central or peripheral nervous system disease (cervical spinal cord disease, polyradiculoneuritis, botulism,..), chest wall trauma (flail chest), pleural space disease (pneumo-thorax, diaphragmatic hernia), or upper airway obstruction (laryngeal paralysis, brachycephalic syndrome). If oxygen is not supplemented, hypoxemia will accompany hypercapnea in all animals, even if lung function is normal.

There are 3 basic causes of hypoxemia. One or more may play a role in a patient with respiratory failure:

1. Decreased fraction of inspired oxygen (FIO2): This is a problem at high altitudes or when animals are anesthetized and either the oxygen tank runs out of gas or the nitrous is inadvertently turned on without supplemental oxygen.

2. Hypoventilation: An increase in PaCO2 will cause an al-most equivalent decrease in PaO2. In most animals with hy-percapnea, oxygen supplementation will correct the hypox-emia, but the cause of the hypoventilation must be addressed (eg, pleural space disease, central nervous system depression, cervical spinal cord disease, neuromuscular diseases, chest wall injury, and upper airway obstruction). Endotracheal intu-bation and positive pressure ventilation is often required for severely affected animals.

3. Venous admixture: Venous admixture occurs when ve-nous blood enters the lungs and does not become oxygenat-ed, thus causing mixture of venous blood with arterial blood and lowering the oxygen content. Venous admixture may occur due to 1) low ventilation/perfusion, 2) no ventilation/perfusion, 3) shunt, or 4) diffusion impairment.

V/Q mismatch is the most common cause of hypoxemia. It occurs when there is uncoupling of normally matched al-veolar ventilation and pulmonary capillary flow, as seen with most pulmonary parenchymal diseases (eg, pneumonia, ede-ma, contusions,…). If there is “no V/Q,” the response to oxy-gen therapy is poor.

A brief history should be obtained while the initial exami-nation begins. The signalment and history may give important clues concerning the cause of respiratory compromise. Has the animal been coughing, had exercise intolerance, comor-bidities, recent vomiting, etc?

Deborah Silverstein, DVM, DACVECC Ryan Veterinary Hospital University of Pennsylvania 3900 Delancey Street Philadelphia, Pennsylvania, USA [email protected]



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The initial evaluation should pay special attention to the presence of inspiratory versus expiratory dyspnea, noises made while breathing, effort and speed of breathing (short, shallow versus slow with increased effort), and auscultation abnormalities over the trachea, lung fields, and heart. Since severely compromised felines often only display tachypnea and mild to moderate increases in effort, it is easy to under-estimate the degree of distress that a cat is truly experiencing.

Potential causes of an increase in respiratory effort in dogs and cats include large airway obstruction (e.g., pharyngeal masses such as polyps, hematomas, neoplasia, or foreign bodies, laryngeal edema, tracheal masses, or peripharyn-geal or peritracheal masses), lower airway obstruction (e.g., bronchoconstriction, luminal mucous or fluid accumulation), pulmonary parenchymal disease (e.g., cardiogenic or noncar-diogenic edema, infection/inflammation, neoplasia, hemor-rhage, fibrosis), pleural space disease (e.g., fluid accumulation due to blood, chyle, transudates, or exudates, pneumothorax, soft tissue masses, or a diaphragmatic hernia), chest wall dis-ease (e.g., open pneumothorax, flail chest/loss of chest wall rigidity, or neuromuscular disease), abdominal enlargement (e.g., gastric dilatation +/- torsion, pyometra, ascites), pulmo-nary thromboembolism, or “look-alike” diseases (e.g., stress, pain, excitement, hyperthermia, acidemia, hypotension, ane-mia, opioid agents, or pericardial tamponade).

Extrathoracic large airway obstruction is commonly asso-ciated with inspiratory stridor or stertor, while intrathoracic airway obstruction (e.g., asthma or bronchial disease) is more likely to cause expiratory dyspnea +/- expiratory noises such as wheezes or crackles. Pleural space disease is most com-monly recognized as a decrease in lung and heart sounds on auscultation of the chest. Decreased breath sounds may also be heard in normal cats with shallow respirations or obesity. A decrease in chest wall compliance may indicate a medi-astinal mass, diaphragmatic hernia, or other pleural space disease. Severe alveolar consolidation, thoracic masses, em-physema, or hyperinflation may also lead to decreased or ab-sent breath sounds upon auscultation. Pulmonary parenchy-mal disease typically leads to inspiratory crackles or crepitant sounds upon auscultation of the chest, although severe con-solidation may cause a decrease in breath sounds. The animal should be examined for evidence of jugular venous disten-tion which may suggest cardiac disease. A loss of chest wall rigidity often leads to paradoxical movement of a segment of the chest (“flail segment” with rib fractures) that moves inward during inspiration and outward during exhalation, in accordance with the changes in pleural pressure. Abdominal enlargement should be evident upon physical examination and “look-alikes” are typically diagnosed with the physical examination, via exclusion of other causes, or upon labwork analysis. Pulmonary thromboembolism might be suspected in animals with coexisting disease that might predispose the animal to a hypercoagulable state and when other potential causes of oxygen-responsive hypoxemia are not found.

The diagnostic plan depends primarily on the history, sig-nalment, and physical examination findings. A hemoglobin saturation measurement is a useful and relatively nonstressful means of assessing a cat’s oxygenation status. A hemoglobin saturation of less than 95% correlates to a PaO2 < 80 mm Hg (hypoxemia). However, it may be difficult to obtain accurate measurements in animals that are moving or have poor pe-

ripheral perfusion. Although an arterial blood gas might allow a more precise assessment of an animal’s ability to oxygen-ate, ventilate, and maintain acid-base status, it is not always practical in the dyspneic patient (especially cats and small dogs). Thoracocentesis is often diagnostic as well as thera-peutic in dogs or cats with dull breath sounds upon thoracic auscultation. Cytologic evaluation of any pleural fluid ob-tained +/- cultures and sensitivity testing, if indicated, should be performed. If the fluid appears whitish or milky, serum and pleural fluid triglyceride and cholesterol levels should be performed. If the fluid is grossly hemorrhagic, a packed cell volume and total solids should be compared to the periph-eral blood and further testing done if bleeding is suspected (coagulation times, platelet count, +/- anticoagulant roden-ticide screen). Once the animal is relatively stable, thoracic radiographs will provide additional valuable information. Lab-work is often helpful to diagnose metabolic derangements or coexisting disease that may cause secondary respiratory distress.

The goal of therapy in the dyspneic patient is to maximize oxygen delivery to the tissues and optimize carbon dioxide removal from the body. Oxygen administration via “flow by,” face mask, hood, or oxygen cage should be provided to all animals with an increased respiratory rate or effort. Some patients will respond favorably to oxygen administra-tion and minimal handling following presentation. If life-threatening dyspnea or impending fatigue is apparent, the dog or cat should be anesthetized, intubated, and ventilated with positive pressure (Ambu bag or mechanical ventilator). Obstruction of the large airway will require manual or sur-gical removal of the obstructive agent. A bypass maneuver using a small endotracheal tube, catheter/feeding tube and high-frequency jet ventilation, or tracheostomy may be re-quired in severe cases. Pharyngoscopy, laryngoscopy, retro-flex rhinoscopy, tracheoscopy, and/or bronchoscopy may be helpful in diagnosing the obstruction and obtaining biopsies if indicated. Animals with recurrent pleural space disease fol-lowing thoracocentesis (e.g., traumatic pneumothorax) may require a chest tube placement. An animal with a tension pneumothorax should not receive positive pressure ventila-tion until a chest tube has been placed or thoracotomy per-formed (in extreme situations) in order to prevent worsening of the disease process. Surgical exploration may be necessary in patients with persistent hemothorax, pyothorax, pneumo-thorax, or other pleural space diseases. Chest tubes should be placed and broad-spectrum antibiotics initiated in animals with evidence of a pyothorax. Computed tomography (CT) may be helpful in identifying the underlying cause of disease and guiding the surgical approach. Coagulation screening, d-dimer levels, thromboelastography, and a CT combined with angiography or nuclear scan may be helpful in diagnosing a PTE.

If asthma or bronchial disease is suspected based on physical examination and/or radiographs, a bronchodilator and injectable steroids (anti-inflammatory dose) should be ad-ministered. If bronchoconstriction is life threatening, a potent β2-adrenergic agonist should be given. The conventional sym-pathomimetics such as epinephrine, dopamine, dobutamine, isoproterenol, and ephedrine are quite effective bronchodila-tors, but do have undesirable systemic effects (tachycardia, premature ventricular contractions, systemic hypertension due to vasoconstriction). The more selective β2-adrenergic



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agonists may therefore be preferable. Examples include terb-utaline (3-5 mg/kg IV or 5-10 mg/kg IM), albuterol (2-5 mg/kg IV or 3-10 mg/kg IM), and metaproterenol (15-30 mg/kg IM) since they have less side effects, are not associated with as much rebound effect, are less likely to cause tachyphlaxis, and do not cross the blood brain barrier. These drugs may be given IV, IM, IT (into the trachea if intubated and no vascular access), or delivered into the mouth, nasal cavity, or conjunc-tival sac. If the patient is not experiencing life-threatening respiratory compromise, the weaker xanthine bronchodilator drugs (e.g., aminophylline [5-10 mg/kg IV]) may be beneficial with fewer side effects (especially if heart disease is also sus-pected). Glucocorticoids and antihistamines may be useful if there is an allergic component associated with the broncho-constriction. An endotracheal or transtracheal wash is often helpful in confirming a diagnosis.

If pulmonary edema secondary to heart failure is sus-pected, furosemide (1-4 mg/kg IV/IM [cat] or 2-8 mg/kg IV/IM [dog] every 1-4 hrs PRN) +/- topical nitroglycerin should be administered. Thoracocentesis may be required in animals with coexisting pleural effusion. Chest radiographs and/or an echocardiogram may be beneficial in diagnosing and as-sessing specific cardiac abnormalities in dogs and cats with congestive heart failure. Additional diagnostics that may be indicated if pulmonary parenchymal disease is identified in-clude endotracheal or transtracheal wash, coagulogram if hemorrhage is suspected, complete blood count, biochemical profile, and urinalysis. If lungworms are suspected, a Baer-mann fecal examination and zinc sulfate flotation should be performed and treatment with fenbendazole (25-50 mg/kg PO x 10-14 days) initiated when the animal is stable. Noncar-diogenic pulmonary edema is typically diagnosed using the history and evidence of caudodorsal pulmonary infiltrates on chest radiographs. Pulmonary contusions, pneumothoraces, and diaphragmatic hernias are often seen following trauma.

A penetrating chest wall injury should be explored and a chest tube placed. A flail chest should be treated with ade-quate analgesia +/- wrapping of the chest to prevent outward movement of the flail segment during exhalation. Placement of the patient on the affected side during the stabilization period may prove beneficial as well. Anesthesia, intubation, and positive pressure ventilation with the affected side up is palliative. Surgical stabilization may be required in animals with severely displaced fractures, and external stabilization may provide support in non-surgical patients.

Regardless of the cause of respiratory failure, the goal of stabilization is to prevent suffering and intubate BEFORE the animal arrests! Positive pressure ventilation does require a team of knowledgeable and skilled professionals, but can prove lifesaving and enable the clinician to perform valuable diagnostic tests and appropriate therapy to maximize success. Here are some guidelines to help the clinician decide when mechanical ventilation might be indicated:

1. If the PaCO2 is greater than 60 mmHg, or if the PaO2 is less than 60 mmHg while receiving oxygen supplementa-tion, the animal may benefit from mechanical ventilation.

2. If an animal is working very hard to breathe and is likely to become fatigued, mechanical ventilation may be the most humane way to relieve the work of breathing before the animal tires or arrests.

3. Following cardiac or respiratory arrest, most animals will benefit from at least temporary mechanical ventilation. This may help to stabilize the animal and prevent re-arrest while providing respiratory support and avoiding deleteri-ous hyoxemia or hyper- or hypocapnia.

4. Animals with confirmed or suspected intracranial hy-pertension (eg, traumatic brain injury) may benefit from mechanical ventilation to control the PaCO2 and keep it within the normal range, therefore prevent marked in-creases or decreases in cerebral blood flow secondary to hypercarbia or hypocarbia, respectively.

Two ventilator modes are used most commonly: Assist/control (AC), or Synchronous Intermittent Mandatory Ventila-tion (SIMV). The amount of ventilator support that is needed combined with the breathing effort of the patient determines which mode is chosen. Patients that require full support and are not able to put forth much effort on their own may benefit from AC, whereas those that need assistance by the ventilator, but are able to breathe on their own a portion of the time may do better with SIMV. Typically, we start patients with AC ventilation, then transition to SIMV when they are more stable and can tolerate a breathing challenge or are ready to wean from the ventilator.

Hypoxemic patients will usually benefit from positive end expiratory pressure (PEEP). PEEP applies positive pres-sure to the airway to prevent complete exhalation in order to increase functional residual capacity, increased alveolar size and recruitment, and prevent early closure of small airways. It maximizes gas transfer in alveoli that may have been collapsed due to pulmonary disease and typically enables the FiO2 to be decreased significantly. If high PEEP levels are necessary, however, it can decrease venous return to the heart, increase central venous pressure, and increase the mechanical work of breathing. PEEP is commonly started at 5 cm H20, and slowly increased until maximum oxygenation benefits are reached with minimal adverse effects on cardiovascular stability. The clinician must watch closely for the development of a pneu-mothorax since this can be rapidly fatal during mechanical ventilation. Careful attention to changes in thoracic ausculta-tion, peak inspiratory pressures, tidal volumes, and PaCO2 will enable the clinician to detect a pneumothorax quickly.

The animal in respiratory distress is often challenging to diagnose and treat. An understanding of common respiratory diseases in cats and dogs, combined with the history, signal-ment, and physical examination findings, is often sufficient for preliminary treatment. An assessment of response to ther-apy is also valuable in forming a presumptive diagnosis. Chest radiographs, echocardiogram, and labwork are often neces-sary to establish a more definitive diagnosis. Endotracheal in-tubation and positive pressure ventilation may be necessary in animals with life threatening respiratory failure.

References available upon request.



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KO SE SRCE USTAVI! “RECOVER Initiative”

Marko Pipan

Kljub napredku medicinske stroke v zadnjih desetletjih, ostaja preživetje z normalno nevrološko funkcijo po ne-nadnem in nepričakovanem zastoju srca na nezadovoljivo nizki ravni tako v humani kot v veterinarski medicini. Junija 2012 so bile v Journal of Veterinary Emergency and Critical Care objavljene prve klinične smernice za kardiopulmonalno oživljanje (KPO) psov in mačk (“REasesment Campaign On Veterinary Resuscitation - RECOVER”) (1). Smernice KPO so produkt temeljitega in sistematičnega pregleda znanstveno podprtih dokazov in védenja iz področja oživljanja tako pri živalih kot pri ljudeh. Smernice zatorej predstavljajo globalno sprejeto stališče glede varnega in učinkovitega oživljanja ob nenadnem poginu psov in mačk. Članek, ki sledi, je povzetek objavljenih smernic KPO in navaja najpomembnejše klinično aplikativne izsledke RECOVER iniciative.

Smernice poudarjajo pomen “verige preživetja”, sestav-ljene iz skupka postopkov, ki pacienta po nenadnem srčnem zastoju povezujejo s preživetjem. Prvi člen verige je zgodnje prepoznavanje srčnega zastoja in takojšen začetek zunanje masaže srca in umetnega dihanja. Končni člen verige je oskr-ba po oživljanju, kjer se osredotočimo na ohranjanje delovanja organov, pri čemer je v ospredju delovanje srca in možganov. Sledi opis postopkov, ki sestavljajo KPO.

Pripravljenost in preventiva

Sistematično in učinkovito izvajanje KPO je nujno potrebno za uspešen izid oživljanja. Hiter dostop do opreme in zdravil, ki jih pri reanimaciji potrebujemo (idealno na standardiziranem mestu v ustanovi oz. tam, kjer se bo oživljanje najverjetneje izvajalo), skrajša čas do začetka oživljanja in poveča verjetnost pozitivnega izida. Idealno je v ta namen opremiti voziček za reanimacijo, ki vsebuje intravenske katetre in orotrahealne tubuse različnih velikosti ter pribor za njihovo pritrditev, la-ringoskop, vrtalnik za intraosalni dostop, EKG, kapnometer, električni defibrilator, potrebna zdravila (adrenalin, vazopres-in, atropin, glukozo, amiodaron, lidokain, natrijev bikarbonat, kalcijev glukonat) ter kirurški set za urgentno torakotomijo in žilni dostop. Vidno postavljeni algoritmi oživljanja in seznam zdravil z ustreznimi odmerki so pri oživljanju v veliko pomoč. Nujno je periodično izobraževanje izvajalcev oživljanja in red-no izvajanje t.i. suhih treningov KPO. Ker gre pri oživljanju za timsko delo, pri katerem idealno sodelujejo trije ljudje ali več, je za učinkovito oživljanje potrebno ustrezno vodenje reani-macije in uigranost ekipe.

Temeljni postopki oživljanja

Temeljni postopki oživljanja (TPO) so ukrepi za vzdrževanje proste dihalne poti, podporo dihanju in krvnemu obtoku. Zajemajo prepoznavanje kardiopulmonalnega zastoja (KPZ), zunanjo masažo srca (ZMS) in vodeno predihavanje pacien-ta. Zelo pomembno je hitro prepoznavanja KPZ in takojšen pričetek kakovostne ZMS saj se s tem poveča verjetnost uspešne reanimacije. Preverjanje perifernega pulza za ugotav-ljanja prisotnosti ali odsotnosti krvnega obtoka je dokazano neobčutljiva in nenatančna metoda. Prav tako se ne priporoča uporaba Dopplerja za ugotavljanje KPZ razen, če se je nap-rava uporabljala za monitoriranje že pred srčnim zastojem. Tudi EKG lahko v določenih primerih zavaja (npr. električna aktivnost brez utripa (EABU), ventrikularna tahikardija brez utripa (VTBU)) in odloži začetek oživljanja. Zaradi navedenih dejstev se priporoča, da se z oživljanjem začne takoj pri vsaki neodzivni živali, ki ne kaže znakov življenja in ne diha oz. ne diha normalno (npr. agonalno dihanje). ZMS se izvaja v ne-prekinjenih 2-minutnih ciklusih, pri čemer je večina živali v lat-eralnem položaju. Frekvenca stisov prsnega koša je 100-120/min, globina stisov pa 1/3 do 1/2 globine prsnega koša. Med vsakim stisom pazimo, da se stena prsnega koša popolnoma sprosti in da se na prsni koš živali ne naslanjamo. Pri živalih priporočamo zgodnjo intubacijo (med intubiranjem ZMS ne prekinjamo) in vodeno predihavanje ob pravilno napihnjen-em zračnem mešičku (“cuff-u”), saj hipoksija in hiperkapnija zmanjšata verjetnost povratka spontanega krvnega obtoka (PSKO). Pravilnost intubacije preverimo z avskultacijo dihanja, palpacijo požiralnika, vidnim gibanjem prsnega koša med predihavanjem in kapnometrom. Predihavamo s frekvenco 10 vdihov/min, dihalnim volumnom 10 ml/kg in časom vpiha 1 sekunde. Ob učinkovitem predihavanju zaznamo med vdihom zmeren dvig prsnega koša. Izogibamo se hiperventilaciji, saj ta zmanjšuje uspešnost oživljanja. Med predihavanjem zunanje masaže srca ne prekinjamo. Glede na težavnost ustreznega monitoriranja vsebnosti kisika v krvi med KPO je nevarnost hipoksemije postavljena v ospredje in je zato uporaba 100% kisika upravičena. V kolikor možnost orotrahealne intubaci-je ne obstaja, začnemo z umetnim dihanjem “usta na nos” in izvajamo 2 hitra vpiha na 30 stisov prsnega koša (v času vpihov ZMS ne izvajamo). Na koncu vsakega 2-minutnega ciklusa TPO se izvajalec ZMS zamenja, da se prepreči utrujanje izvajalca in zagotovi ustrezna kvaliteta stisov prsnega koša. Prekinitev med ciklusi naj bo minimalna (5-10 sekund), kar naj zadostuje za oceno uspešnosti oživljanja in zamenjavo iz-vajalca ZMS.

Marko Pipan, dr. vet. med., Dipl. ACVECC [email protected]



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Dodatni postopki oživljanja

Kljub temu, da v teoriji ločimo TPO in dodatne postopke oživljanja (DPO), izvajamo pri bolnišnični reanimaciji vse post-opke istočasno. DPO zajemajo terapijo z vazopresorji, pozi-tivnimi inotropi in antiholinergiki, korekcijo elektrolitskih in kislinsko-baznih motenj, korekcijo hipovolemije in električno defibrilacijo. Če se TPO in DPO izvajajo pravilno, lahko dosežemo PSKO v 58% (2).

Vazopresorji so esencialen del KPO. Adrenalin se aplicira v odmerku 0,01mg/kg IV (t.i. nizka doza) na samem začetku oživljanja, nakar aplikacije ponavljamo na 3-5 minut. Vi-soka doza adrenalina (0,1 mg/kg IV) se lahko uporabi pri neuspešnem, dalj časa trajajočem oživljanju. Vazopresin se priporoča kot alternativa adrenalinu ali v kombinaciji z njim; odmerek 0,8 U/kg IV apliciramo v razmakih 3-5 minut. Kljub pomanjkanju dokazov o koristnosti uporabe atropina med oživljanjem, se aplikacija atropina v odmerku 0,04 mg/kg IV priporoča pri KPZ zaradi prekomerne vagalne stimula-cije. Zdravila apliciramo po intravenski ali intraosalni poti, saj takšna aplikacija omogoča dokazano večje preživetje. V ko-likor to ni mogoče lahko za aplikacijo uporabimo intratraheal-no pot. Odmerek zdravil v tem primeru povečamo (2-10x), razredčimo s fiziološko raztopino ali sterilno vodo za redčenje zdravil in apliciramo po katetru, ki je daljši od vstavljenega tubusa.

Električna defibrilacija se uporablja pri KPO, ko gre za prekatno migetanje (t.i. ventrikularna fibrilacija -VF) ali VTBU. Bifazni defibrilatorji omogočajo, v primerjavi z monofaznimi, uspešno defibrilacijo že pri nižji energiji defibrilacije s čimer se zmanjša poškodba miokarda. Po novem defibrilacije ne ponavljamo več 3x zapored, ampak po enkratni neuspešni defibrilaciji ponovno takoj začnemo z ZMS. Uspešnost defi-brilacije preverimo šele po 2-minutnem ciklusu TPO. Prekor-dialni udarec (t.j. udarec z dlanjo nad srcem) se je kot oblika mehanske defibrilacija izkazal za minimalno učinkovitega pri VF. Kljub superiornosti električne defibrilacije se prekordialni udarec lahko uporabi v primeru VF, ko električni defibrilator ni na voljo.

Uporaba antiaritmikov - pri VF in VTBU, ki ne odgovori na električno defibrilacijo lahko uporabimo amiodaron ali lidokain, čeprav je učinkovitost slednjega vprašljiva. Namreč, uporaba lidokaina pri defibrilaciji z monofaznim defibrilator-jem lahko zviša količino potrebne energije za uspešno defi-brilacijo. Rutinska uporaba magnezijevega sulfata se pri KPO ne priporoča več.

Ostale intervencije - antagoniziranje uporabljenih seda-tivov in narkotikov se svetuje pri KPO povezanem z anest-ezijo. Korekcija dokazane hipokalciemije med KPO je in-dicirana, rutinska uporaba intravenske aplikacije kalcija med oživljanjem pa se ne priporoča. Priporoča se korekcija dokumentirane hiperkalemije. Rutinska uporaba kortikoster-oidov se med oživljanjem ne priporoča. Uporaba ITD ventila (“impedance treshold device”) je smotrna pri teži nad 10 kilogrami, čeprav dokazov o večji uspešnosti oživljanja z upo-rabo te naprave še nimamo. Pri oživljanju daljšem od 10-15 minut se lahko odločimo za aplikacijo natrijevega bikarbona-ta v odmerku 1 mmol/kg. Agresivna tekočinska terapija med KPO normovolemičnega pacienta je povezana z zmanjšano prekrvljenostjo koronarnega žilja, zato se rutinska uporaba in-travenskih tekočin med oživljanjem ne priporoča. Pri živalih v

hipovolemiji tekočinska terapija v obliki intravenskega bolusa najverjetneje koristi in se zato v tem primeru priporoča. Ur-gentna torakotomija in notranja masaža srca je učinkovitejša metoda oživljanja v primerjavi z ZMS in se priporoča pri vs-akem daljšem neuspešnem oživljanju, velikih psih, tamponadi srca, diafragmatski herniji, zlomu reber, penetrirajoči poškodbi prsnega koša, plevralnem izlivu, pnevmotoraksu, abdominalni krvavitvi, KPO pri katerem točen čas zastoja srca ni znan in anesteziranih pacientih s posegi v prsnem košu ali abdomnu. Pri tem se moramo zavedati zahtevnosti tega načina oživljanja in intenzivnosti oskrbe, ki jo bo tak pacient potreboval po uspešni reanimaciji.

Monitoriranje med oživljanjem

Nenadno povišanje EtCO2 med oživljanjem je indika-tor PSKO. Vrednosti EtCO2 >15 mm Hg pri psih in > 20 mm Hg pri mačkah kažejo na učinkovito izvajanje masaže srca in lahko povečajo možnost PSKO. Esencialen del monitoriranja med oživljanjem je EKG, saj omogoča spremljanje aktivnosti srca in vodenje DPO (odločanje glede aplikacije različnih zdravil in uporabe električne defibrilacije). Izvajanje ZMS vp-liva na EKG zapis zato se interpretacija srčnega ritma izvaja ob koncu 2-minutnih ciklusov TPO in po električni defibrilaciji. Kot že omenjeno je preverjanje perifernega pulza nezanesljiva metoda ugotavljanja PSKO.

Oskrba po oživljanju

Oskrba pacienta po PSKO predstavlja pomemben člen “verige preživetja” KPO. Nenaden srčni zastoj in s tem neza-dostna prekrvljenost tkiv povzroči generalizirano sistem-sko hipoksijo, katere posledice se pokažejo v obdobju po uspešnem začetnem oživljanjanju. Odpovedovanje organov, kardiogeni šok, poškodba možganov in posledice prima-rne bolezni so najpomembnejši vzroki za visoko umrljivost v tem obdobju. Podatek, da kar 85% psov in muc ne preživi uspešnega začetnega oživljanja (3), in da jih večina v nekaj urah pogine zaradi ponovnega srčnega zastoja (4) potrjuje pomembnost intenzivnega monitoriranja in zdravljenja po začetnem PSKO. Nujna je optimizacija dihanja z vzdrževanjem normoksije (PaO2 80-100 mm Hg, SpO2 94-98%) in nor-mokapnije (psi PaCO2 32-43 mm Hg, mačke PaCO2 26-36 mm Hg). Podpora dihalne funkcije v obliki manualnega ali mehaničnega predihavanja je pogosto potrebna v tem obdob-ju. Ustrezna prekrvljenost miokarda in možganov se zagotovi s hemodinamsko optimizacijo, katera vključuje zagotavljanje normotenzije ali blage hipertenzije z uporabo intravenskih tekočin, vazopresorjev in pozitivnih inotropov. Kontinuiran EKG, neinvazivno merjenje krvega tlaka, pulzna oksimetrija, plinska analiza krvi z laktatom in saturacija kisika v centralni venski krvi (ScvO2) so temeljni parametri monitoriranja v tem obdobju. Ciljne vrednosti so CVP 0-10 mm Hg, srednji arteri-jski tlak 80-120 mm Hg, ScvO2 ≥ 70% in laktat < 2,5 mmol/l. Vzdržujemo normoglikemijo. Preprečujemo hipertermijo in hipotermične živali postopno segrevamo po 0,25-0,5°C/uro do normotermije. Ob anemiji je ciljna vrednost hema-tokrita po transfuziji okrog 25%. Ob neustrezni nevrološki funkciji uvedemo nevroprotektivno terapijo (t.j. terapevtska hipotermija pri komatoznih stanjih; hiperozmotska terapija z manitolom ali hipertonično fiziološko raztopino ob sumu povišanega znotrajlobanjskega tlaka; zdravljenje epileptičnih napadov). Terapevtska hipotermija (telesna temperatura 32-



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34°C) v trajanju 24-48 ur po uspešnem oživljanju pri koma-toznih pacientih izboljša nevrološko in srčno funkcijo, vendar zahteva visoko stopnjo intenzivnega zdravljenja z mehanskim predihavanjem. Rutinska uporaba kortikosteroidov se po uspešnem začetnem oživljanju ne priporoča. V primeru rela-tivne adrenalne insuficience oz. pri pacientu, ki kljub pravilne-mu intravenskemu tekočinskemu zdravljenju in uporabi va-zopresorjev in inotropov ostaja hemodinamsko nestabilen, lahko z uporabo hidrokortizona (1 mg/kg na 6 ur) izboljšamo hemodinamsko stanje. Razume se, da je zdravljenje v obdob-ju po PSKO prilagojeno posameznemu pacientu in njegovim specifičnim potrebam. Po uspešnem oživljanju se priporoča premestitev živali v veterinarsko ustanovo, ki omogoča 24-urno intenzivno terapijo in nego.

Literatura:

1. Fletcher DJ, Boller M, Brainard BM, et all: RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 7: Clinical guidelines, J Vet Emerg Crit Care 22(S1):102-131,2012.

2. McIntyre RL, Hopper K, Epstein SE:Assessment of cardiopulmonary resuscitation in 121 dogs and 30 cats at a university teaching hospital (2009-2012), J Vet Emerg Crit Care 24(6):693-704,2014.

3. Hofmeister EH, Brainard BM, Egger CM, et all: Prognostic indicators for dogs and cats with cardiopulmonary arrest treated by cardiopulmonary cerebral resuscitation at a university teaching hospital, J Am Vet Assoc 235(1):50-57,2009.

4. Kass PH, Haskins SC: Survival following cardiopulmonary resuscitation in dogs and cats, J Vet Emerg Crit Care 2(2):57-65,1992.



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SIRS, MODS AND SEPSIS: RECOGNITION AND DIAGNOSIS

Deborah Silverstein

The systemic inflammatory response syndrome (SIRS) de-scribes the clinical condition seen with widespread activation of the inflammatory system secondary to an infectious or non-infectious insult. It is well known that a localized inflammatory response normally occurs at a site of tissue damage or injury in order to protect the host. In patients with SIRS, however, severe inflammation leads to an “overflow” of mediators into the systemic circulation and results in numerous global abnor-malities that may have life threatening consequences. If not recognized quickly and diagnosed accurately, SIRS may result in multiple organ dysfunction syndrome (MODS) and death. The distinction between SIRS and sepsis is based upon the presence or absence of infection as described below.

DEFINITIONS

• Systemic Inflammatory Response (SIRS): the clinical syndrome of systemic inflammation which results from either an infectious or non-infectious insult (ie septic or nonseptic SIRS).

• Sepsis: the clinical syndrome of systemic inflammation which results from infection (bacterial, viral, protozoal or fungal).

• Severe Sepsis: sepsis complicated by dysfunction in one or more organs.

• Septic Shock: acute circulatory failure and persistent arterial hypotension despite adequate volume resuscita-tion associated with sepsis.

• Multiple organ dysfunction syndrome (MODS): physiologic derangements in endothelial, coagulation, cardiopulmonary, renal, nervous, endocrine, and gastro-intestinal systems associated with the systemic inflamma-tory response syndrome.

PATHOGENESIS OF SIRS & MODS

The pathophysiologic mechanisms responsible for the generation of the SIRS are complex and incompletely under-stood. The initial insult that stimulates SIRS can come from a variety of sources such as trauma, burns, aspiration, pan-creatitis, or infectious agents (eg products of gram-positive

or gram-negative bacteria. The induction of systemic inflam-mation may initially start locally (i.e. an abscess localized to a limb) but can lead to systemic signs when “mediators” enter the circulation causing global activation of inflammation. Al-though mediators such as platelets, polymorphonuclear leu-kocytes, and the endothelium also play a role, it appears that the stimulation of macrophages and the release of inflamma-tory cytokines are pivotal in the generation of SIRS.

During gram-negative sepsis, the lipid A portion of li-popolysaccharide (LPS), the glycolipid component of the cell wall, binds to LPS binding protein (LBP). This LPS-LBP complex binds to membrane bound CD14 on macrophages. This bind-ing leads to activation of macrophages and initiates intracellu-lar signaling to start transcription of inflammatory cytokines. The cytokines that are generated include tumor necrosis fac-tor (TNF), IL-1, IL-6, IL-8 and interferon-gamma. In addition to pro-inflammatory mediators, the response also generates anti-inflammatory cytokines such as IL-4, IL-10, IL-13, and transforming growth factor-beta. This compensatory anti-in-flammatory response is often referred to as CARS. In addition to LPS, low oxygen tension, acidosis, extracellular adenosine triphosphate (ATP), and pro-inflammatory molecules such as thrombin that result from tissue injury and stress can also re-sult in the activation of macrophages.

While cytokines trigger a beneficial inflammatory re-sponse that promotes local coagulation to confine tissue damage, the excessive production of these pro-inflammato-ry cytokines can be even more dangerous than the original stimulus, overcoming the normal regulation of the immune response and producing the clinical signs notably seen in pa-tients with SIRS. When the immune system is fighting patho-gens, these cytokines signal immune cells, such as T-cells and macrophages, to travel to the site of infection. In addition, cytokines activate these recruited immune cells stimulating them to produce even more cytokines. This production of a “cytokine storm” and global activation of white blood cells ultimately overwhelms the compensatory anti-inflammatory response and is a key component in the pathogenesis of SIRS.

In addition to systemic activation of white blood cells, other pathologic effects of inflammatory mediators include: increased capillary permeability, vasodilation, activation of coagulation, myocardial dysfunction, and mitochondrial dys-function. These pathologic effects of systemic inflammation can lead to the syndrome of multiple organ dysfunction or MODS.

MODS is characterized by abnormalities in organs that were not affected by the original insult and is associated




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with a high morbidity and mortality rate. Organs at risk for dysfunction include: lungs, cardiovascular (heart and vascula-ture), kidneys, gastrointestinal tract, endocrine, nervous, and coagulation systems. Mitochondrial dysfunction leading to a reduction in cellular ATP is thought to be an important player in the development of organ dysfunction and/or failure. The failure of mitochondria is thought to occur secondary to tis-sue ischemia that results from circulatory collapse, microcir-culatory changes, and hypoxemia. In addition, mitochondria may be damaged (or inhibited) by reactive nitrogen and oxy-gen species. However, in the lungs, acute respiratory distress syndrome (ARDS) is thought to result directly from inflamma-tion not from mitochondrial dysfunction. The resulting organ damage may be permanent or may resolve once the underly-ing cause of inflammation has been cured.

CLINICAL SYNDROME & DIAGNOSIS

Clinical manifestations of SIRS and sepsis are often non-specific and will vary depending on the underlying disease process. Historical findings will also differ and may be non-specific such as a loss of appetite and depression. Physical examination findings such as fever, brick red mucous mem-branes, tachypnea, tachycardia, and bounding pulses may be common in patients in the hyperdynamic phase of SIRS and sepsis. However, as disease progresses, the patient may develop hypotension, pale mucous membranes, and hypo-thermia. It is important to note that dogs and cats differ in their manifestations of SIRS. Cats do not develop red mucous membranes and are more likely to have a relative bradycardia and hypothermia.

Patients in which SIRS and/or sepsis is suspected should have complete blood count, biochemistry analysis, urinalysis, and coagulation testing performed. In veterinary patients, the most common hematologic abnormalities noted with sepsis include leukocytosis, leukopenia, increased percentages of bands, toxic neutrophils, thrombocytopenia and coagulation abnormalities. Cats are frequently anemic whereas dogs will often have an elevated hematocrit reflecting hemoconcen-tration secondary to volume depletion, splenic contraction or a combination of both. Changes in the serum biochemistry panel are typically reflective of the underlying disease pro-cess. With progression of disease, the biochemical profile may reveal progressive organ dysfunction. Variable abnormalities in blood glucose in dogs with sepsis are reported. Decreased serum albumin is a common finding. This is likely due to loss of albumin (either lost from the body or into interstitial spaces resulting from vascular permeability), hepatic dysfunction or preferential synthesis of acute phase proteins by the liver. Hyperbilirubinemia is also a common finding in small animal patients with sepsis. This is thought to occur secondary to cholestasis in dogs and may be secondary to hemolysis in cats. Coagulation testing may reveal abnormalities associ-ated with disseminated intravascular coagulation (DIC) such as prolonged prothrombin time and partial thromboplastin time, and elevated d-dimers and fibrinogen degradations pro-ductions (FDP’s). Additional diagnostic evaluation of a patient with suspected SIRS/sepsis should include venous or arterial blood gas measurements, blood pressure, ECG, and pulse oximetry to assess for hypoxemia. Many patients will have a metabolic acidosis reflecting poor tissue perfusion secondary to hypovolemia and increases in lactate.

Criteria proposed for the diagnosis of SIRS has been ex-trapolated from the human medical literature for use in dogs and cats. In one veterinary study of both septic and non-sep-tic dogs, criteria that had the greatest sensitivity for the di-agnosis of SIRS were determined (Table 1). In cats, proposed criteria for SIRS were derived from a retrospective study of cats with severe sepsis identified at necropsy (Table 1). In this study, bradycardia was identified in 16% of cats, highlighting the difference between the dog’s and the cat’s physiologic response to sepsis. Patients must have two of the four criteria present in order for the diagnosis of SIRS to be made (3/4 is preferred in cats).

Table 1. Proposed criteria for the diagnosis of SIRS in dogs and cats

Dogs Cats

Temperature (oF) <100.6 or >102.6 <100 or >104

Heart Rate (beats/minute) >120 <140 or >225

Respiratory Rate (breaths/minute) >20 >40

WBC (x103/ul ); <6 or >16; >19 or <5 % bands >3%

In addition to the above criteria, other parameters which may support the presence of systemic inflammation include: altered mental status, interstitial edema, alterations in blood glucose (ether hyperglycemia in the absence of diabetes or hypoglycemia). Patients with septic shock are often hemo-dynamically unstable and will have continued arterial hypo-tension despite volume resuscitation, elevated mixed venous oxygen saturation (supporting mitochondrial dysfunction) and evidence of persistent hyperlactatemia.

A diagnosis of sepsis can be made once infection is docu-mented and the patient fulfills at least two of the four criteria listed in Table 1 for SIRS. The patient’s history and physical examination may initially help to determine where to start looking for the source of infection. In addition, thoracic and abdominal imaging (radiography and ultrasonography) should be performed in all patients with suspected SIRS or sepsis. Samples, if it is safe, should be collected for culture and sensitivity testing to identify the cause of sepsis and to direct anti-microbial therapy. Blood, urine, peritoneal or tho-racic effusion, joint fluid, CSF, endotracheal or bronchoalveo-lar wash fluid, or organ aspirates could all be considered as possible sources of samples to be cultured. Gram-negative enteric bacteria are the most commonly implicated organisms in sepsis in dogs and cats. However, mixed infections and gram-positive infections have also been described.

STAGING SEPSIS

The clinical syndromes of SIRS and sepsis are inherently difficult to define. This lead to the adoption of PIRO (Table 2), a method developed in order to describe the clinical manifes-tations of infection and the host’s response to it. This method was developed during the 2001 International Sepsis Defini-tions Conference. In this method, PIRO is an acronym for predisposition, infection, response and organ dysfunction. PIRO provides a framework in which patient factors are incor-porated along with the microbial insult in order to stage the



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disease process and identify factors that may contribute to morbidity and mortality. Although this method was originally developed for use in septic human patients it can be adapted for use on veterinary patients.

Table 2: PIRO system for staging sepsis

PIRO Present Future

Predisposition Age, Species, gender, breed, concurrent illness Genetic susceptibility of the host to an abnormal or inappropriate inflammatory response and enhanced understanding of the host response to infection

Insult or Infection Culture and sensitivity of infecting organisms Detection of microbial products (i.e. LPS, bacterial DNA)

Response SIRS, clinical and clinicopathologic signs of Markers of inflammation (CRP, IL-6) sepsis and septic shock Host responsiveness (ICAM-1, cortisol, LBP) Specific targets of therapy (APC)

Organ Dysfunction Clinicopathologic abnormalities suggesting Measures of cellular response to insult organ dysfunction or infection (cytopathic hypoxia, apoptosis) Number of failing organ systems

APC: Activated protein C, CRP: C-reactive protein, ICAM-1: intracellular adhesion molecule-1, IL-6: interleukin-6, LBP: lipopolysaccharide binding protein, LPS: lipopolysaccharide. From: Mittleman Boller E, Otto CM. Sepsis. In: Silverstein DC, Hopper K (eds). In: Textbook of small animal critical care medicine, Saunders, St. Louis, 2009.

Once a patient has been diagnosed with clinical signs of SIRS or sepsis, it is paramount that rapid treatment is initiated to correct the underlying disease process. Time is of the essence and any delay in appropriate therapy can adversely affect sur-vival rates.




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SIRS, MODS AND SEPSIS: TREATMENT OPTIONS

Deborah Silverstein

Timely treatment and intensive monitoring of patients suffering from SIRS, MODS, or sepsis is of utmost importance for maximizing survival. Patients with evidence of cardiovas-cular shock require emergent therapy in order to minimize further tissue ischemia and cellular damage. Although there is no “magic bullet” for the treatment of patients suffering from SIRS, MODS, or sepsis, and it is likely that an individ-ual patient’s genetic predisposition plays an important role in determining the inflammatory response of these patients, aggressive empiric treatment and supportive care are crucial. The primary aims of treatment include rapid circulatory sup-port, antimicrobial therapy (if appropriate), and goal-directed supportive measures.

FLUID THERAPY

Patients suffering from SIRS, MODS, and/or sepsis com-monly have subjective and objective evidence of poor perfu-sion. Optimization of cardiovascular function is therefore a primary goal in the management of these patients in order to maximize oxygen delivery to the tissues and minimize cellular ischemia/organ damage. Early, aggressive fluid therapy is the cornerstone of treatment to increase preload and thus cardiac output. However it is also important to avoid fluid overload! Isotonic crystalloids, hypertonic crystalloid solutions, synthetic colloids and blood component therapy may be used during intravascular fluid resuscitation and maintenance of the pa-tient with SIRS, MODS, or sepsis. The choice of fluid type(s) depends on the overall clinical picture, but general guidelines can be helpful.

Isotonic crystalloid solutions remain the cornerstone of treatment for patients with SIRS, MODS, or sepsis. For ani-mals with evidence of cardiovascular shock (non-cardiogenic), a dose of up to one blood volume (also known as the shock dose) of isotonic crystalloid solution (90 mL/kg in the dog and 50 mL/kg in the cat) can be given. Generally, 1/3-1/2 of the shock dose is administered as quickly as possible, followed by additional boluses as indicated by clinical parameters and re-peated physical examination. Following administration, there is rapid distribution of the crystalloids into the extracellular fluid compartment so that only ~25% of the delivered vol-

ume remains in the intravascular space by 30 minutes after in-fusion. Routine fluid therapy is also important for animals that are cardiovascularly stable in order to maintain an adequate level of hydration and perfusion. It is important that excessive fluid volumes are not administered to avoid volume overload, especially in patients that may have vascular leak syndromes.

Hypertonic (7.0-7.5%) sodium chloride administration may be useful for the treatment of cardiovascular instability in animals that do not have interstitial dehydration. Hyper-tonic saline causes a transient osmotic shift of water from the extravascular to the intravascular compartment. It is ad-ministered in small volumes (5 mL/kg) intravenously over ap-proximately 10 minutes. In addition to pulling fluid into the intravascular space, there is evidence that it may also be ben-eficial to reduce endothelial swelling, increase cardiac con-tractility, cause mild peripheral vasodilation, and modulate the inflammatory response. Due to the osmotic diuresis and rapid redistribution of the sodium cations that ensue follow-ing the administration of hypertonic saline, the intravascular volume expansion is transient (<30 minutes) and additional fluid therapy (either isotonic crystalloids or synthetic colloids) must therefore be used with hypertonic saline.

Colloids are large molecules (molecular weight >10-20,000 daltons) that do not readily sieve across the vascular membrane and may therefore be especially useful in hypo-proteinemic animals with SIRS, MODS, and sepsis. These flu-ids are hyperoncotic to the normal animal and therefore pull fluid into the vascular space. They cause an increase in blood volume that is greater than that of the infused volume and help to retain this fluid in the intravascular space (assuming normal capillary permeability). Hydroxyethyl starch solutions, primarily hetastarch solutions, are most commonly used in small animal patients and are suspended in an isotonic crys-talloid solution. Tetrastarch solutions have been more recent-ly studied in humans and animals and are purported to have less side effects. The recommended dose of most synthetic colloids is up to 20 mL/kg in the dog and up to 10 mL/kg in the cat for the treatment of shock. Continuous rate infu-sions of 1-2 mL/kg/hr can be used to increase oncotic pres-sure in animals that are hypoproteinemic. Excessive volumes of synthetic colloid solutions can lead to volume overload, co-agulopathies, hemodilution, and possible kidney injury (only reported in humans).

Synthetic colloids can also be used with isotonic crystal-loids to maintain adequate plasma volume expansion with lower interstitial fluid volume expansion and to expand the intravascular space with smaller volumes over a shorter time period. Despite multiple clinical studies in humans, there is no




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definitive documentation that the use of colloids is superior to the use of crystalloids for resuscitation, and the price of colloids is significantly greater than that of crystalloids. The use of synthetic colloids in critically ill human patients has dra-matically decreased, or even ceased in some countries, due to concerns of acute kidney injury from these solutions. Evi-dence for this relationship in small animals is lacking at this time, but caution should be exercised.

Animals suffering from cardiovascular instability can also be given a combination of hypertonic saline and a synthetic colloid in order to prolong the effect of bolus fluid therapy. A 1:2.5 ratio of 23.4% sodium chloride with a synthetic colloid will make a ~ 7.5% saline mixture (44 mL of 23.4% NaCl in 106 mL of a hydroxyethyl starch). This may be useful as a small volume resuscitation fluid, especially in large animals or those with evidence of intracranial hypertension and shock.

The need for blood products in patients with SIRS, MODS, and/or sepsis is often dependent on the patient’s disease process and clinical picture. Animals with recent blood loss that are unresponsive to fluid therapy alone may benefit from red blood cell administration, especially if the hematocrit has fallen below 25-30% and venous oxygen saturation remains <65-70% despite volume resuscitation. However, excessive increases in hematocrit should be avoided since this will in-crease blood viscosity. In addition, many of these animals are coagulopathic and should be treated with fresh frozen plasma if the clotting times are outside of the normal range.

Packed red blood cells and fresh frozen plasma are ad-ministered at a dose of 10-15 mL/kg and fresh whole blood at a dose of 20-25 mL/kg. Platelets are only present in fresh blood within 24 hours of collection and their use is indicated in animals with thrombocytopenia/pathia-induced bleeding disorders or massive hemorrhage (eg severe ITP-induced hem-orrhage). Plasma products are most commonly used in ani-mals with severe hypoalbuminemia, profound blood loss, or a coagulopathy. Its ability to increase colloid osmotic pressure is limited compared to the hyperoncotic synthetic colloids.

Animals with SIRS, MODS, and/or sepsis that have severe hypoalbuminemia may benefit from treatment with 25% hu-man albumin. Albumin is crucial in the transport of drugs, hormones, chemicals, toxins, and enzymes. Preliminary stud-ies in dogs showed that human albumin administration in dogs increased circulating albumin concentrations, total sol-ids, and increase colloid osmotic pressure, although the effect on mortality remains unknown. More recent data, however, has described sensitization, acute and delayed reactions, and potentially lethal complications from human albumin admin-istration to normal dogs. The product is therefore only recom-mended in critically ill animals that are severely hypoproteine-mic and have anticipated ongoing losses or are at high risk for complications due to marked hypoalbuminemia. The recent use of canine albumin solution provides an exciting new pos-sibility for the use of species-specific, natural colloid resuscita-tion. However, problems with manufacturing and recalls have limited its use in recent years. Further research is warranted.

VASOPRESSOR AND INOTROPE THERAPY

SIRS, MODS, and sepsis can all lead to hypotension de-spite intravascular volume resuscitation (shock), therefore ne-cessitating the use of vasopressor and/or inotrope therapy. Since both cardiac output and systemic vascular resistance affect oxygen delivery to the tissues, therapy for hypotensive patients includes maximizing cardiac function with fluid ther-apy and inotropic drugs and/or modifying vascular tone with vasopressor agents. Commonly used vasopressors include catecholamines (epinephrine, norepinephrine, dopamine) and the sympathomimetic drug phenylephrine. In addition, vasopressin, corticosteroids, and glucagon have been used as adjunctive pressor agents.

Dopamine has various potential actions on adrenergic and dopaminergic receptors. Primarily dopaminergic effects are seen at low intravenous doses (1-5 mcg/kg/min), mainly beta-adrenergic effects are seen at moderate doses (5-10 mcg/kg/min), mixed alpha- and beta- adrenergic effects are present at high doses (10-15 mcg/kg/min), and primarily alpha-adren-ergic effects are seen at very high doses (15-20 mcg/kg/min). The actual dose response relationship is unpredictable in a given patient because it is dependent on individual variability in enzymatic dopamine inactivation, receptor down regula-tion, and the degree of autonomic derangement. Dopamine can be used as a single agent therapy to provide both ino-tropic and pressor support in animals with vasodilation and decreased cardiac contractility. Despite dopamine’s beneficial effects on cardiac output and blood pressure, it may have del-eterious effects on renal, mesenteric, and skeletal blood flow.

Norepinephrine (NE) has mixed alpha and beta-adrenergic receptor agonism with preferential alpha- receptor activity. Therefore, the effects on heart rate and contractility are mild, and NE is commonly used as a pressor agent in animals with normal or increased cardiac output states. The vasopressor dose of NE in humans (and extrapolated to dogs) is 0.05-0.5 mcg/kg/min intravenously.

Epinephrine (epi) is a potent pressor with mixed alpha- and beta-agonist activity. Although epi is thought to have more potent beta-agonist effects than NE, individual re-sponse is quite variable in patients with systemic inflamma-tory diseases and hypotension. Epi may significantly impair splanchnic blood flow compared to other vasopressor drugs. The vasopressor dose of intravenous epi is 0.01-0.1 mcg/kg/min and for primarily beta-agonist effects is 0.005-0.02 mcg/kg/min. Epi is rarely used as a sole first-line vasopressor agent due to it s potential side effects, but may be necessary in criti-cally ill animals.

Phenylephrine is a pure alpha agonist drug that causes profound vasoconstriction. It has been shown to cause an increase in cardiac output and blood pressure, presumably due to increased venous return to the heart and activation of alpha-1 receptors in the myocardium. Phenylephrine is typi-cally used in patients that are unresponsive to other sympa-thomimetics, although it can be used as a sole first-line agent in vasodilated, hypotensive animals. Since phenylephrine has no beta-agonist activity, it is the least arrhythmogenic of the sympathomimetic pressor drugs and is therefore desirable in animals that develop tachyarrhythmias in response to other pressor agents. The intravenous dose range is 0.5-3 mcg/kg/min.



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Dobutamine is a beta-agonist with no alpha effects. It increases cardiac output, oxygen delivery, and oxygen con-sumption without causing vasoconstriction. It is therefore useful in animals with cardiac insufficiency. Dobutamine may worsen or precipitate tachyarrhythmias and may precipitate seizure activity in cats. The intravenous dose range is 1-5 mcg/kg/min in cats and 2.5-20 mcg/kg/min in dogs.

Vasopressin is a non-adrenergic vasopressor agent. It has both direct and indirect effects on the vascular smooth muscle via the V1 receptors and induces vasoconstriction in most vascular beds. In vitro, vasopressin is a more potent va-soconstrictor than phenylephrine or NE. At low doses, this drug causes vasodilation in renal, pulmonary, mesenteric, and cerebral vasculature in an attempt to maintain perfusion to these vital organs. Low flow states secondary to hypovolemia or septic shock are associated with a biphasic response in en-dogenous serum vasopressin levels. There is an early increase in the release of vasopressin from the neurohypophysis in re-sponse to hypoxia, hypotension, and/or acidosis, which leads to high levels of serum vasopressin. This plays a role in the sta-bilization of arterial pressure and organ perfusion in the initial stages of shock. There appears to be a subsequent decrease in circulating vasopressin levels, most likely due to a depletion of hypothalamic stores. The use of vasopressin in animals in the later stages of shock, especially those that exhibit vaso-dilation and are refractory to catecholamine therapy, may therefore be beneficial. The drug also enhances sensitivity to catecholamines and therefore may allow the dose of con-current catecholamine therapy to be lowered. Experimental studies in dogs have demonstrated an increase in blood pres-sure and cardiac output with minimal side effects. A clinical case series using vasopressin at 0.5-5 mU/kg/min found an increase in blood pressure following vasopressin therapy as well. This drug will require further investigation, but may be considered in animals with catecholamine resistant vasodila-tory shock, as is commonly seen in animals with SIRS, MODS, and sepsis.

The incidence of relative adrenal insufficiency in small ani-mals suffering from SIRS, MODS, and/or sepsis has not been clearly elucidated, but some animals with refractory hypoten-sion may benefit from physiologic steroid treatment.

ANTIMICROBIAL THERAPY

Early and appropriate antibiotic therapy is crucial for the treatment of patients with proven or suspected sepsis, espe-cially those with clinical evidence of SIRS or MODS. Blood, urine, respiratory secretions (collected by endotracheal wash, transtracheal wash or bronchoscopy) and/or other available body fluids (i.e., pleural or peritoneal fluid) should be ob-tained for analysis and culture, as indicated, prior to initiat-ing antimicrobial therapy. Broad-spectrum antibiotic therapy should be administered pending culture and sensitivity re-sults. Empirical antibiotic choices should be effective against gram-positive and negative organisms, as well as anaerobes. Initial combinations might include ampicillin (22 mg/kg IV q6-8h) and enrofloxacin (15 mg/kg IV q24 h in dogs, 5 mg/kg IV q24h hours in cats), ampicillin and amikacin (15 mg/kg IV q24 h), cefazolin (22 mg/kg IV q8h) and amikacin, ampicillin and ceftazidime (22 mg/kg IV q8h), or clindamycin (10 mg/kg IV q8-12h) and enrofloxacin. Single agents such as ticarcillin/

clavulanic acid (50 mg/kg IV q6h), cefoxitin (15-30 mg/kg IV q4-6h), or meropenem (24mg/kg IV q24h if bacterial resist-ance is suspected) could be used initially as well.

GASTROINTESTINAL PROTECTION

Stress-related mucosal disease (SRMD) and subsequent upper gastrointestinal (GI) bleeding are frequently seen in critically ill humans with SIRS, MODS, and sepsis and may also occur in dogs and cats. Clinical signs of hematemesis, hema-tochezia, or melena should alert the clinician to potentially se-rious GI hemorrhage. Hypoperfusion of the upper GI mucosa, excessive gastric acid secretion and impaired mucosal defense mechanisms (mucous secretion, production of growth fac-tors) contribute to the development of SRMD. The incidence of SRMD in veterinary patients is unknown and therefore no guidelines exist for its management.

The initial strategy in critically ill dogs and cats should be to ensure adequate GI perfusion and employ early enteral nutrition. High-risk patients should receive pharmacologic prophylaxis for stress-related GI hemorrhage. Based on the currently available evidence in human medicine, it appears that proton pump inhibitors (PPI) are superior to histamine-2 receptor antagonists (H2RA), which are superior to sucral-fate in the prevention of SRMD in adult critical care patients. Drugs available include omeprazole (PPI) 0.7-1.0 mg/kg PO q24h, pantoprazole (PPI) 0.7-1.0 mg/kg IV q24h, famotidine (H2RA) 0.5-1.0mg/kg IV q12-24h, PO, ranitidine (H2RA) 0.5-4 mg/kg IV q8-12h and sucralfate (protectant) 0.25-1gm/25kg PO q6-8h. Recent evidence suggests that ranitidine does not decrease acid production in dogs at clinically recommended doses, but further research would be helpful.

NUTRITION

Following initial stabilization of the patient with SIRS, MODS, and/or sepsis, nutritional status should be addressed. Adequate nutrition is critical in patients with secondary hy-permetabolic states such as sepsis. The enteral route (orally or via nasoesophageal, esophagostomy, gastrostomy, or je-junostomy tube) is preferable if the animal is normotensive, not vomiting, and alert. Parenteral nutrition should be admin-istered if the enteral route is not feasible or contraindicated. If the blood glucose falls below 60 gm/dL, 0.5 mL/kg of 50% dextrose should be diluted 1:1 with sterile water and admin-istered intravenously over 1-2 minutes. The fluids should also be supplemented with dextrose as needed (2.5-7.5%). Hyper-glycemia should be avoided since it has been associated with an increased likelihood of infection and a poorer prognosis.

MONITORING

Septic patients should be closely monitored since minute-to-minute changes in the animal’s condition may require con-tinuous adjustments or interventions. Frequent physical ex-aminations, body weight, PCV/TS, blood glucose, electrolytes, blood gas values, coagulogram, urine output, blood pressure, EKG, pulse oximetry, and central venous pressure should be closely followed and repeatedly assessed. Below are some general guidelines to maximize tissue perfusion and prevent organ ischemia:



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1. Maintain PCV >25% in animals with acute anemia secondary to loss or lysis of red blood cells.

2. Keep colloid osmotic pressure >16 mmHg or total solids >4.5 gm/dL (45g/L) in animals with acute hypoproteinemia. Consider the use of synthetic colloids +/- plasma therapy in these patients.

3. Maintain clotting times within the normal range with plasma administration as needed.

4. Keep the blood glucose within the normal range, if possible. Supplemental dextrose or insulin therapy may be necessary.

5. Keep electrolytes within the normal range, if possible.

6. Ensure a mean arterial pressure of 70 mmHg (not higher than 130 mmHg).

7. Aim for a heart rate of 70-120 beats per minute (may be breed dependent). Treat arrhythmias as needed.

8. Watch closely for evidence of an increase in respiratory rate or effort since this is often the first sign of volume overload/pulmonary edema.

9. Ensure a urine output of at least 1-2 mL/kg/hour.

10. Keep hemoglobin saturation (pulse oximeter reading) above 93% or PaO2 greater than 80 mmHg using oxygen supplementation needed. Inspired oxygen concentrations of <60% should be used, if adequate, to prevent oxygen toxicity.

11. Keep central venous pressure between 0-10 cm H2O.

12. Aim to normalize lactate, if elevated, as soon as possible.

13. Keep ScvO2 greater than 70%

CONCLUSION

Prognosis in patients with SIRS, MODS, and sepsis de-pends on the underlying disease process and the stability of the cardiovascular system. Regardless, sepsis and SIRS is as-sociated with a very high morbidity rate, with mortality rates in humans ranging from 20-40%. Novel therapies have been researched, including anti-endotoxin antibodies, anti-TNF an-tibodies, and substances that affect the coagulation system, with mostly negative outcomes. Recently, activated Protein C, involved in the fibrinolysis arm of the coagulation cascade, has shown promise in improving overall mortality in septic people, but its use in animals is not well delineated.

Sepsis and SIRS may result in severe cardiovascular ab-normalities, coagulation disturbances, multiple organ failure, acute lung injury, and death. Immediate recognition of the clinical presentation is vital to the success of treatment of affected patients. Aggressive and immediate fluid resuscita-tion to provide adequate tissue perfusion and oxygenation improves the outcome in these critically ill patients. The un-derlying cause must be diagnosed early, as many cases re-quire emergent surgical intervention once the cardiovascular system has been stabilized, and correction of anemia, coagu-lopathy, acid/base disturbances, and electrolyte imbalances have been attempted. Prognosis must be considered guarded in patients with septic shock and SIRS, especially if organ fail-ure or acute lung injury is present. Depending on the underly-ing cause, early and aggressive treatment with fluids, colloids, plasma, antibiotics, and resection of infected tissue can result in full recovery.




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ALI GREM V PRAVO SMER? MONITORIRANJE TEKOČINSKE TERAPIJE

Marko Pipan

Tekočinsko zdravljenje predstavlja pomemben del zdrav-ljenja hospitaliziranih, urgentnih in kritičnih pacientov. Hitrost nadomeščanja, količina tekočin in tip izbrane tekočine so odvisni od osnovne bolezni, tekočinskega primanjkljaja in tipa izgubljene tekočine. Vedeti moramo ali želimo nado-mestiti znotrajžilni, intersticijski ali znotrajcelični primanjkl-jaj tekočine. Hipovolemija in hipotenzija (oz. različne oblike šoka), korekcija dehidracije, zagotavljanje dnevnih potreb po vodi in elektrolitih, nadomeščanje izgubljene tekočine (npr. bruhanje, driska, poliurija, obsežne opekline, izguba tekočin v tretji prostor), uravnavanje kislinsko-baznega ravnovesja (npr. hipokloremična presnovna alkaloza, laktatna acidoza) in elektrolitske motnje (npr. hipo- in hipernatriemija, hipo- in hiperkaliemija) so pogoste indikacije za uporabo intraven-skega tekočinskega zdravljenja. Zaradi različnih razlogov za uporabo tekočinske terapije je poznavanje načinov moni-toriranja tovrstnega zdravljenja zelo pomembno pri obravnavi urgentnega in kritičnega pacienta, pri čemer je spremljanje odgovora organizma na tekočinsko zdravljenje najzanesljivejši pokazatelj ustrezne uporabe intravenskih tekočin. Zavedati se moramo, da agresivna infuzija kristaloidov lahko vodi do ede-ma organov (npr. pljučni edem, možganski edem), zmanjšane motilitete črevesja, trebušne hipertenzije, zmanjšane kontrak-tilnosti srca, zmanjšanja tkivne oksigenacije, elektrolitskih ner-avnovesij, anemije, hipokoagulabilnosti, hipoproteinemije ter povečane obolevnosti in smrtnosti (1,2).

Hipovolemija in hipotenzija

Zanesljivih kliničnih kazalcev zadostne napolnjenosti ožilja na žalost ni. Barva sluznic, hitrost kapilarnega polnjenja, frekvenca srčnega utripa, kvaliteta arterijskega pulza, stanje zavesti ter toplina tačk in uhljev so osnovni klinični kazalci hemodinamske stabilnosti in ustreznosti periferne prekr-vavitve. Prekomerna polnjenost jugularnih ven lahko kaže na srčno popuščanje. Neinvazivno merjenje arterijskega krvnega tlaka, prisotnost arterijske hipotenzije (t.j. sistolični tlak < 90 mmHg, srednji tlak < 60 mm Hg) in povišan laktat (> 2,5 mmol/l) pripomorejo k diagnozi neustrezne prekrvljenosti tkiv, šoka in tkivne hipoksije. Pri zdravljenju hipovolemije in hipo-tenzije spremljamo tudi vrednosti centralnega venskega tlaka, produkcijo urina, saturacijo centralne venske krvi (ScvO2) in EKG zapis. Optimalni volumen potrebne tekočine (ki v večini primerov ni maksimalni šokovni odmerek) lahko ugotovimo

le z rednim spremljanjem vseh teh parametrov in ugotavljan-jem kliničnega odziva pacienta na začetni tekočinski bolusni odmerek. Ena najpomembnejših in najtežjih nalog pri zdrav-ljenju kritičnega pacienta je nadomeščanje znotrajžilnega tekočinskega primanjkljaja s pravo mero. Pri tekočinskem zdravljenju moramo upoštevati tudi primarno bolezen in pridružene poškodbe; ob kontuziji pljuč bomo morali biti s tekočinami zelo previdni, saj lahko z agresivno tekočinsko ter-apijo dihalno funkcijo poslabšamo. Pri aktivni krvavitvi v abdo-men je bolje uporabiti bolj restriktiven protokol tekočinskega zdravljenja in vzdrževati arterijski krvni tlak na spodnji meji normalnega. Pri poškodbi možganov in povišanem znotra-jlobanjskem tlaku, ravno nasprotno, stremimo k višjemu ar-terijskemu tlaku, zato da zagotovimo ustrezen možganski prekrvavitveni tlak. Pri obsežnem peritonitisu se pogosto zgodi, da velike količine tekočine uhajajo v abdomen, kar mo-ramo pri vodenju tekočinske terapije upoštevati.

Dehidracija

Pri ugotavljanju stopnje intersticijske dehidracije si pomag-amo z vlažnostjo sluznic, prožnostjo kožne gube, vlažnostjo roženice in vdolbenostjo oči. Na žalost je to dokaj nenatančna in subjektivna metoda in služi zgolj za grobo oceno stopnje dehidracije. Slinjenje lahko prekrije suhe sluznice, atropin pa sluznice izsuši in potencira oceno stopnje dehidracije. Na oce-no turgorja vpliva starost živali - pri mladičkih je delež vode v intersticiju večji kar prožnost kožne gube poveča, medtem ko se s starostjo elastičnost kože manjša. Minimalna sto-pnja dehidracije, ki jo lahko ocenimo je 5%, maksimalna pa 12%. Dehidracija višja od 10% povzroči znake hipovolem-ije in zmanjšane prekrvljenosti tkiv. Poznavanje telesne teže pred boleznijo nam lahko pomaga pri oceni dehidracije, saj akutno izgubo teže v klinični praksi enačimo z izgubo vode. Pri določanju dehidracije nam je v pomoč tudi določanje specifične teže urina, saj je ob dehidracij in ustrezni funkciji ledvic urin vedno močno koncentriran.

Po začetni oceni dehidracije in začetku tekočinskega zdravljenja ocenimo uspešnost rehidracije v 6-24 urah. Hitrost korekcije dehidracije je odvisna od bolezenskega stanja; npr. pri akutni poškodbi ledvic se priporoča hitrejša korekcija dehi-dracije. Dnevno tehtanje živali je učinkovit in enostaven način spremljanja tekočinske terapije, saj se uspešna rehidracija odraža v porastu telesne teže. Primerjavo količine apliciranih intravenskih tekočin in tekočin izločenih iz telesa (količina urina, tekočine iz drenaž, driska, bruhanje, hude opekline) pri kritičnih pacientih opravimo na 12-24 ur in tako ovrednotimo

Marko Pipan, dr. vet. med., Dipl. ACVECC [email protected]



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zadostnost tekočinske terapije. Redno spremljanje hema-tokrita (Hct) in skupnih proteinov (SP) nam prav tako pomaga pri spremljanju zadostnosti tekočinske terapije, saj višanje vrednosti Hct in SP pogosto pomeni tekočinski primanjkljaj. Padanje vrednosti sečnine in kreatinina ter ugotavljanje manj koncentriranega urina (ob odsotnosti ledvične patologije) kaže na ustreznost tekočinske terapije. Produkcija urina pri živali, ki prejema intravensko tekočinsko zdravljenje mora biti vsaj 1-2 ml/kg/uro.

Ob sistemskem vnetnem odgovoru in/ali hipoalbumine-miji se lahko z agresivno tekočinsko terapijo zaradi večje pre-pustnosti žilja in nižjega koloidnega ozmotskega tlaka pojavi periferni edem. Pri spremljanju tekočinske terapije zato redno avskultiramo pljuča, spremljamo frekvenco dihanja, napor ob dihanju in stanje zavesti. Znaki tekočinske preobremenitve so serozni nosni izcedek, edem konjuktive, prekomerna pol-njenost jugularnih ven, intersticijski edem okončin, povišana frekvenca in napor dihanja, inspiratorni pljučni poki in srčni galop (mačke).

Kislinsko bazno ravnovesje

Najpogostejša kislinsko bazna motnja, ki jo zdravimo s tekočinsko terapijo je presnovna acidoza (npr. laktatna acido-za, diabetična ketoacidoza, uremična acidoza). Uspešnost ter-apije pri laktatni acidozi lahko spremljamo z rednim merjenjem (na 2-6 ur) plazemskega laktata, kar ima tudi prognostično vrednost. Normalizacijo uremične acidoze spremljamo z vred-notenjem padca sečnine in kreatinina. Pri hipokloremični me-tabolni alkalozi, ki je prisotna pri obstrukciji tankega črevesja, uporabljamo 0,9% raztopino NaCl z dodatkom kalija, saj so ti pacienti zaradi bruhanja velikokrat tudi hipokaliemični. Pri mačku z obstrukcijo uretre, azotemijo in uremično presnovno acidozo lahko uporabimo uravnotežen kristaloid (npr. Hart-mannova raztopina) ali 0,9 % NaCl (3). Velike količine 0,9 % NaCl vodijo v razvoj hiperkloremične presnovne acidoze, medtem ko velike količine Ringer laktata lahko povzročajo presnovno alkalozo, saj se laktat v jetrih presnavlja v bikar-bonat. Najboljši način spremljanja uspešnosti zdravljenja kis-linsko baznih motenj je seveda plinska analiza venske ali ar-terijske krvi.

Elektrolitske motnje

Korekcija hiponatriemije in hipernatriemije zahteva zelo rigorozno spremljanje vrednosti serumskega natri-ja (na začetku zdravljenja na 2 uri) in poglobljeno znanje tekočinskega zdravljenja. Prenizek ali previsok natrij normal-iziramo s hitrostjo 0,5-1,0 mmol/l/uro. Centralna pontina mielinoliza je lahko posledica prehitre korekcije hiponatriem-ije, možganski edem pa se lahko pojavi ob prehitri korekciji hipernatriemije. Pri kritičnem pacientu se vrednost natrija med tekočinskim zdravljenjem lahko zelo spreminja, zato je potrebno budno spremljanje njegove vrednosti. Pri hipoka-liemiji v intravenske tekočine dodamo ustrezno količino ka-lijevega klorida in kalij višamo s hitrostjo 0,5 mmol/kg/uro (ob diabetični ketoacidozi in nizkem kaliju lahko ob stalnem spremljanju srčne funkcije in diureze kalij korigiramo hitreje in sicer 1-1,5 mmol/kg/uro). Zdravljenje hiperkaliemije zajema redčenje kalija v krvi z infuzijo kristaloidov brez kalija, aplikaci-jo inzulina z glukoznim kritjem, uporabo natrijevega bikar-bonata, uporabo β2-adrenergičnih agonistov (npr. terbutalin, albuterol) in pri hudi hiperkaliemiji tudi stabilizacijo srčne mišice s kalcijevim glukonatom. V začetni fazi zdravljenja me-rimo kalij na 2-4 ure. Za korekcijo hipokloremije uporabljamo

tekočine bogate s klorom (npr. 0,9% raztopino NaCl). Tudi hipomagneziemija in hipofosfatemija zahtevata intravensko nadomeščanje magnezija in fosfata.

Literatura:

1. Silverstein DC, Santoro-Beer K. Daily intravenous fluid therapy. In: Silverstein DC, Hopper K, eds. Small animal critical care medicine. St. Louis, Missouri. Elsevier Saunders, 2015: 316-321.

2. Cotton BA, Guy JS, Morris JA, et all. The cellular, metabolic, and systemic consequences of agressive fluid resuscitation strategies. Shock 2006; 26: 115-121.

3. Drobatz KJ, Cole SG. The influence of crystalloid type on acid-base and electrolyte status of cats with urethral obstruction. J Vet Emerg Crit Care 2008; 18: 355–361.



23

GOAL DIRECTED THERAPY

Deborah Silverstein

Introduction

Traditionally, the treatment of patients suffering from cardiovascular shock has focused on the improvement of physical examination parameters and blood pressure meas-urements. There was no specific time factor, but it seemed logical to aim for normalization of perfusion parameters sooner than later. However, the concept of correcting as many measureable variables within the first 6 hours has be-come an intensive area of recent study. There have been few treatment strategies that have significantly improved survival in emergent or critically ill patients until the past decade, as the concept of early goal directed therapy has repeatedly and consistently shown a marked decrease in morbidity and mor-tality.

Perfusion Parameters

Shock most frequently results from decreased tissue perfusion and ultimately leads to inadequate cellular energy production. Regardless of the underlying cause of shock, de-creased perfusion and a subsequent decrease in oxygen deliv-ery leads to an increase in cellular oxygen extraction, resulting in a decrease in central venous (ScvO2) or mixed venous (SvO2) oxygen saturation. This increase in oxygen extraction is the body’s attempt to match systemic oxygen demands. When oxygen extraction exceeds 50-60% of delivery, anaerobic metabolism ensues and lactate is produced. This delivery-dependent hypodynamic phase of shock results in an inverse relationship between lactate concentrations and oxygen de-livery or ScvO2/SvO2.

Initially, vital signs may remain normal, also known as “occult shock” and it may be difficult for even the astute clinician to detect the severity of illness at this early compen-satory stage. If left unrecognized and untreated, however, cardiopulmonary collapse and organ dysfunction may ensue. This state is especially characteristic of patients with sepsis and we commonly see a hyperdynamic phase that develops after resuscitation. A patient with compensated systemic in-flammatory response syndrome (SIRS) or sepsis is character-ized by an elevated ScvO2/SvO2 and normal lactate. The lactate subsequently increases and the elevated ScvO2/SvO2 denotes pathologic delivery dependence or delivery independence

(see figure below), and is associated with increased mortality in human patients. The apparent failure of the body to in-crease oxygen extraction and thus oxygen consumption may be secondary to either microcirculatory derangements or mi-tochondrial dysfunction.

Therefore, the reliance on using multiple examination pa-rameters, cardiovascular measurements and laboratory evalu-ation in order to create a “bundle” of items to monitor and normalize might enable the clinician to recognize and treat abnormalities quickly in order to maximize the chance for suc-cess.

The Resuscitation Bundle Concept

The resuscitation bundle is not actually a novel strategy for resuscitation. In 1976, Wilson et al. wrote several expert opinions that included the basic tenets of early sepsis manage-ment (i.e., early recognition, source control, antibiotic therapy and early hemodynamic optimization of oxygen delivery). In the popular publication of 2001, similar “early goal directed therapy” (EGDT) was tested against standard care in a rand-omized control trial and resulted in a mortality benefit greater than 16% (see figure below). Over the last decade, the com-ponents of EGDT and the “resuscitation bundle” have been examined, validated and incorporated into evidence-based human guidelines (e.g., Surviving Sepsis Guidelines 2012).

What kind of patient should receive EGDT?

Patients that show clinical evidence of poor perfusion based on hypotension (systolic BP<90 mmHg) or a lactate level >4 mmol/L should receive GDT as soon as possible. Im-provement in the blood pressure and level of hyperlactatemia are associated with a better outcome in dogs. The study de-sign for Rivers study is below:




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Rivers et al, NEJM 2001

Goal Directed Therapy

Once a patient is identified as high risk, the suspicion of sepsis should be raised unless another obvious cause of hy-potension and hyperlactatemia is suspected. Early administra-tion of antimicrobials, source control and appropriate cultures should be obtained. The combination of antibiotics and early hemodynamic optimization is ~3-6 hours in order to maxi-mize success in most studies.

Although the accuracy of central venous pressure (CVP) monitoring in the assessment of volume status has been questioned recently, similar outcomes are seen when com-pared to pulmonary artery catheter usage for guiding fluid therapy in people with acute lung injury. It appears that the issue may actually be time sensitive: early, aggressive fluid therapy using CVP monitoring is useful, but late aggressive fluid therapy is not. This has yet to be proven in veterinary medicine, however.

Source Control

Most patients with noncardiogenic shock have suspected sepsis as a possible cause of the clinical signs at some point in their workup. Rapid identification of the source of inflamma-tion is therefore essential to initiate appropriate, timely thera-py. This workup typically involves full labwork and urinalysis, urine culture, thoracic radiographs, abdominal ultrasound, cytologic evaluation and fluid analysis (+/- biochemical evalu-ation) of any peritoneal or pleural fluid, and/or arthrocentesis or central spinal fluid analysis. Animals with severe gastroin-testinal ulceration or bleeding may also suffer from bacterial translocation. Cutaneous or subcutaneous infections should

be ruled out via careful physical examination. Any sources of sepsis that require surgical intervention should be addressed as soon as the patient is stabilized.

Early Antimicrobial Therapy

Animals with confirmed or highly suspected sepsis should receive appropriate antimicrobial therapy as soon as possible. Mortality rates escalate for every hour of delay in administra-tion of antimicrobials in human patients with septic shock. Ideally, samples for culture and sensitivity testing should be obtained prior to starting antimicrobial therapy, they should not delay treatment. Intravenous, bactericidal antimicrobial drugs that target the organisms and site of infection should be used; inappropriate antimicrobial selection is associated with a 5-fold increase in death in humans with septic shock. Results of culture and sensitivity testing should be used when changing therapy in order to de-escalate the spectrum to de-crease the incidence of resistant organisms.

Mean Arterial Pressure

The target mean arterial pressure (MAP) is somewhat controversial; one human study found that a MAP< 60-65 mmHg during the first 24-48 hours was most predictive of 30 day mortality and organ function. This endpoint should be achieved using fluid and vasopressor therapy, as appropri-ate, although fluid administration is preferred to vasopres-sor use within the first six hours, especially since hypotension tends to be more refractory to fluid therapy in the later stages of disease presentation. Another human study showed that targeting a MAP >70 mmHg using vasopressor therapy may increase mortality. Although Rivers et al used a target MAP



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>65 mmHg, most patients exceeded this value greatly. A ret-rospective feline study found that a Doppler blood pressure <90 mmHg was associated with decreased survival.

Central Venous Pressure (CVP)

Although the accuracy of a CVP measurement stands in question, equivalent outcomes have been observed when compared to the pulmonary artery catheter for assessment of fluid status in certain groups of critically ill patients. CVP measurements have shown significant association with 30 day mortality in humans, although some research has sug-gested a negative impact on survival when CVP is used to guide fluid management. The key to maximize the usefulness of CVP measurements appears to be timing: early, aggres-sive fluid resuscitation to target CVP values is associated with improved outcomes, but late aggressive fluid therapy is not. It is therefore important to use CVP monitoring in context and early in the course of treatment. The clinician must watch for trends and recognize that the absolute value may be influ-enced by several factors. The Surviving Sepsis Campaign rec-ommends a CVP ≥8 mmHg within 6 hours of therapy. The use of hydroxyethyl starch for resuscitation in patients with sepsis is no longer recommended, although it is unknown whether veterinary patients suffer the same nephtrotoxic effects as their human counterparts. Hydroxyethyl starches are there-fore still a reasonable resuscitative fluid, but caution should be exercised.

Central venous tissue saturation

The central venous (from the cranial vena cava) or mixed venous (from the pulmonary artery) oxygen saturation (ScvO2

or SvO2, respectively) can readily detect imbalances between oxygen delivery and oxygen consumption in the delivery de-pendent phase of the curve (above), even in the face or nor-mal physical examination parameters. There is an absolute difference between ScvO2 (from cranial vena cava) and SvO2 (from pulmonary artery) of ~5% (normal is >72% for ScvO2 and >75% for SvO2), but either can be used clinically and it has proven to be the single most significant prognostic indica-tor (there is some controversy regarding correlations between two values in septic shock states). The ScvO2 has also proven to be a valuable predictor of survival upon admission to the ICU in dogs with sepsis/septic shock due to pyometra. The clini-cian must either increase oxygen delivery or decrease oxygen consumption in an attempt to normalize the ScvO2 or SvO2 to >65% or 70%, respectively. Failure to increase ScvO2 within 6 hours is associated with a 14% increase in mortality in peo-ple. Therefore, this value becomes the trigger for providing supplemental oxygen, administering red blood cell transfu-sions, treatment with positive inotrope drugs and initiation of positive pressure ventilation. There are limitations to the use of venous oxygen saturation that will be discussed.

Red Blood Cell Transfusions

Animals suffering from hypoperfusion secondary to SIRS or sepsis commonly present with or develop anemia second-ary to the pre-existing disease, volume resuscitation and dilu-tion, impaired bone marrow response and possible decrease in sensitivity of the erythropoietin receptors. A compensa-tory increase in systemic oxygen extraction occurs to main-tain oxygen needs, but may not be adequate. Red blood cell transfusions may therefore be warranted during this delivery dependent state if the lactate is elevated and the ScvO2/SvO2

decreased. One human study found that an ScvO2 of 69.5% was a useful transfusion trigger in order to maximize survival. Although the use of red blood cells in these patients has been controversial over the years, a large observational human study recently found that red blood cell transfusions were as-sociated with decreased mortality rates. Although 10mg/dL of hemoglobin is the current transfusion trigger for people with septic shock, the best trigger for small animals remains unknown.

Inotrope Therapy

Myocardial dysfunction in people and animals with SIRS or sepsis is common. Patients treated with EGDT had 12.9% greater frequency of (early recognition of) myocardial dys-function requiring inotropic therapy. Research has shown that neither the physical examination nor the ScvO2 can predict systolic dysfunction. The surviving sepsis campaign guidelines recommend the use of dobutamine in human patients that have ongoing evidence of hypoperfusion despite adequate intravascular volume and mean arterial pressure.

Ventilatory Support

Animals with severe hypoxemia, hypercarbia, or impend-ing respiratory fatigue are most likely to benefit from me-chanical ventilation. A persistently low ScvO2/SvO2 may signal cardiopulmonary decompensation and the need for ventilator support, especially since the work of breathing consumes 20-40% of systemic oxygen delivery. Although the use of neuro-muscular blocking agents has not been extensively studied in small animals with acute respiratory distress syndrome, early administration of these drugs has been shown to improve outcome and decrease duration of mechanical ventilatory support in humans.

Base Excess

The amount of base or acid (in millimoles) that is required to titrate the blood pH to 7.4 at 37ºC and a PaO2 of 40 mm Hg is referred to as base excess (BE). This value often serves as a marker of a metabolic acidosis. In critically ill patients, a lactic acidosis should be suspected, although azotemia, ketoacido-sis, bicarbonate loss or hyperchloremia may also contribute. A more negative BE has been associated with increased mortal-ity in people and is also associated with a worse prognosis in DKA patients and is predictive of SIRS in dogs with pyometra. Although it appears to have prognostic significance, its use in guiding therapy is unknown. If BE remains low despite ag-gressive resuscitation, this should flag the clinician to search for the underlying cause.

Lactate and Lactate Clearance

Type A lactic acidosis is associated with tissue hypoxia and anaerobic energy production. The clearance of elevated lac-tate seems to be more important than a single value; the use of lactate clearance as a marker of global hypoxia dates back to the 1960s. However, a normal lactate level does not neces-sarily mean that oxygen delivery is normal. Type B lactic acido-sis may also be present in septic patients due to microvascular shunting, mitochondrial dysfunction, and/or dysregulation of pyruvate dehydrogenase activity. However, the recent study in dogs with sepsis due to pyometra found a significant de-crease in lactate over time in survivors. Another study evaluat-ing EGDT and lactate in 8 critically ill dogs showed that death was more likely if the animal’s lactate failed to decrease by at



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least 50% during the first 6 hours of aggressive treatment. Human studies have found a correlation between early lac-tate clearance and a decrease in pro- and anti-inflammatory biomarkers, improved organ function and reduced mortality. In some studies, resuscitation based on CVP, MAP and lactate clearance of 10% was as effective as resuscitation based on CVP, MAP and ScvO2/SvO2 >70%. This remains controversial, however, since lactate exceeds clearance only when the criti-cal oxygen extraction ratio has been reached, a less sensitive indicator of impending tissue hypoxia compared to ScvO2/SvO2.However, studies examining the use of lactate clear-ance as the primary resuscitation endpoint have shown not only a mortality benefit, but also a decrease in organ failure, duration of catecholamine therapy, and length of mechani-cal ventilation. However, it is important to remember that an elevated lactate in septic patients may indicate more than just poor tissue perfusion (e.g., cytopathic hypoxia, microcirculatory dysfunc-tion), and conversely a normal lactate does not exclude the possibility of tissue hypoperfusion. Therefore, a bundle ap-proach is most logical in order to most effectively treat patients based on early indices of perfusion abnormalities.

Urine Output

Although it appears that acute kidney injury is more frequently ap-preciated in human ICUs, small animal patients are also at risk. Acute kidney injury ranges in severity from minor changes in renal function or indices of damage to the need for renal replacement therapy. Urine output is a rather crude, but often simple, measurement of renal perfusion and for-mation of ultrafiltrate. Animals that are well hydrated should make at least 0.5-1 ml/kg/hr of urine and those re-ceiving aggressive fluid therapy should concord-antly make more. If urine output is low in a critically ill patient that is thought to be volume loaded, sources of inappropriate loss (e.g., peritoneal effusion, pleural effusion, GI losses) or fluid retention should be evaluated. If the patient is hypotensive or has reduced cardiac output, urine production is not expected to be nor-mal as well. Judicious fluid therapy (e.g., 5-20 ml/kg isotonic crystalloid bolus) should be attempted in order to normalize urine output if no other cause can be found; overhydration should be avoided. The use of hydroxyethyl starch solutions

has not been associated with nephrotoxicity in small animals, although future research may further investigate a possible link.

If placement of a urinary catheter is not possible or deemed undesirable, urine weight can be measured from bedding or diapers and the bladder can be measured using ultrasound at frequent intervals. Body weight changes can also yield valuable information; a gain of 5-10% of body weight is indicative of a positive fluid balance in hydrated pa-tients (keeping in mind that large volumes of stool or urine in the bladder, as well as third-spaced fluids, can also increase body weight). Diuretic therapy (e.g., furosemide), or hemodi-alysis/renal replacement therapy, may be necessary in select patients. An overview of patient management from Rivers at al study is below:

Rivers et al, NEJM 2001

The Resuscitation Bundle

In general, veterinary patients present in the later stages of disease than their human counterparts. Therefore the idea of “early” GDT is relative, although standardized goals should still be attempted based on the evidence based recommen-dations. One human study showed a survival benefit up of GDT to 18 hours after admission, although earlier resuscita-tion was better. Although the goals, or bundles, used may



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vary according to the monitoring capabilities and resources within a given hospital, the underlying logic and physiology behind goal directed therapy remains. Optimization of CVP, MAP, hemoglobin and urine output has been adequate in hu-man medical ICUs and not only led to a decrease in mortality, but also a shortened length of hospitalization, duration of mechanical ventilation and antimicrobial treatment duration. In addition, patients resuscitated with specific standardized goals had a more rapid reversal of shock and less delayed vasopressor administration. The ideal bundle in veterinary pa-tients is yet to be determined, but preliminary studies suggest that the lactate/lactate clearance, MAP, CVP and ScvO2/SvO2

deserve further study. The guidelines from the Surviving Sep-sis Campaign 2012 are shown below:

Surviving Sepsis Campaign Care Bundles 2012

Why Does GDT Work?

It is well known that global tissue hypoxia and inflamma-tion are closely associated. ScvO2/SvO2 is significantly related to mitochondrial function; inflammatory mediators can alter mitochondrial function in people with sepsis. Persistence of global tissue hypoxia correlates with inflammatory mediators, as shown by Rivers et al. Therefore, the use of GDT enables alteration of the inflammatory cascade (e.g., lower IL-8 lev-els) and prevents the second hit phenomenon of multi-organ failure and worsening inflammation. It remains to be seen whether adjunctive therapies, in combination with GDT, may further enhance the beneficial effects of this approach. Ad-ditionally, the influence of GDT on the microcirculation is still under investigation, but likely offers another benefit of GDT.

Conclusion

GDT is the recommended way to treat emergent patients, especially those with suspected or confirmed sepsis. More than 10 years after Rivers’ publication suggested the benefits of GDT, multiple human (and a few) veterinary studies have not only validated this approach, but also shown that it mod-ulates the inflammatory response, decreases the incidence and progression of organ failure, and decreases the cost of treatment for all patients. EGDT saves 1 out of every 6 human patients suffering from sepsis and septic shock. Although there have been more recent studies in 2014 (ProCESS and ARIES trials) questioning the true value of EGDT, the basic the-ory behind the strategy of “stabilizing the patient as soon as possible” remains. It may be argued that the “conventional” quality of care has improved so much that it is harder to prove

the benefit of an investigational protocol if the standard of care is also excellent.

Busy veterinary hospitals may not always have adequate staffing to properly follow GDT to the letter, but mortality reduction has been found even with suboptimal compliance rates of 51% in human hospitals. The days of looking for a magic bullet are over; GDT using bundle therapies may be one of the most effective interventions for the management of shock, especially in patients with sepsis. When simplified, it merely reinforces the notion that “time is of the essence” for these patients.

Suggested reading:

1. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345(19):1368-1377.

2. Conti-Patara A, de Araujo CJ, Mattos-Junior E, et al. Changes in tissue perfusion parameters in dogs with severe sepsis/septic shock in response to goal-directed hemodynamic optimization at admission to ICU and the relation to outcome. J Vet Emerg Crit Care (San Antonio ) 2012;22(4):409-418.

3. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med 2013;39(2):165-228.

4. Stevenson CK, Kidney BA, Duke T, et al. Serial blood lactate concentrations in systemically ill dogs. Vet Clin Pathol 2007;36(3):234-239.

5. Butler AL. Goal-directed therapy in small animal critical illness. Vet Clin North Am Small Anim Pract 2011;41(4):817-38, vii.

6. Puskarich MA, Trzeciak S, Shapiro NI, et al. Prognostic value and agreement of achieving lactate clearance or central venous oxygen saturation goals during early sepsis resuscitation. Acad Emerg Med 2012;19(3):252-258.

7. Hayes GM, Matthews K, Boston S, et al. Low central venous oxygen saturation is associated with increased mortality in critically ill dogs. JSAP 2011;(52):433-440.

8. The ProCESS Investigators. A Randomized Trial of Protocol-Based Care for Early Septic Shock. NEJM 2014;370:1683-1693.

9. The ARISE Investigators and the ANZICS Clinical Trials Group. Goal-Directed Resuscitation for Patients with Early Septic Shock. NEJM 2014; 371:1496-1506.



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TO TRANSFUSE OR NOT TO TRANSFUSE: TRANSFUSION THERAPY IN CRITICALLY ILL PATIENTS

Deborah Silverstein

The administration of species-specific blood components can prove life-saving in critically ill patients. However, they do have potential adverse effects and may be costly to the own-er. In order for the clinician to make the best decision possible for each patient, an individualized approach to the question, “To transfuse, or not to transfuse?” should be determined. The following information will hopefully assist you in making the most appropriate choice for your critical patients.

Reasons to Transfuse a Dog or Cat

The need for blood products in the critically ill animal is dependent on the patient’s disease process. Many severely ill small animals suffer from anemia and/or a coagulopathy sec-ondary to consumption, loss, dilution, and hepatic dysfunc-tion. However, not all animals require a transfusion. There are 3 primary reasons to give a blood transfusion: 1) severe ane-mia or an acute decrease in PCV of ≥50%, 2) coagulopathy or active uncontrollable bleeding, or 3) symptomatic blood component deficiency (e.g. severe hypoalbuminemia). Since every treatment has potential risks, these must always be weighed against the expected benefit of giving a transfusion. In general, the product that is transfused should supply exact-ly what the patient needs in order to decrease potential side effects, maximize resources and most efficiently correct the problem at hand. Potential risks of administering allogenic blood products include transfusion related immunomodula-tion (TRIM), transfusion associated cardiac overload (TACO) and transfusion related acute lung injury (TRALI). Additional specific transfusion reactions and clinical signs are described following the specific products below.

Blood Products and Their Uses

Fresh Whole Blood

Fresh whole blood contains red blood cells, clotting fac-tors and functional platelets. It is used to treat thrombocyto-penia-induced bleeding disorders or massive hemorrhage (or if it is all you have!).The blood should be collected from the donor and administered to the recipient within 6-8 hours for

maximal effectiveness, but platelet activity is maintained to some degree for up to 24 hours. Transfusion of fresh whole blood is unlikely to raise the platelets counts much, and the half-life of the platelets is very short in the circulation (a mat-ter of hours), but they will help form platelet plugs in bleeding animals.

Packed Red Blood Cells (PRBCs)

Packed red blood cells are most commonly used for the treatment of severe anemia or acute decreases in PCV of ≥50%. Although there is no precise “transfusion trigger” in veterinary medicine, the clinician should assess the anemic patient for evidence of anemia-related clinical signs (heart rate, mentation, lactate, etc) and treat the number if deemed clinically necessary.

When assessing the need for PRBCs, the PCV and total solids should be assessed simultaneously to determine wheth-er the animal is more likely to be suffering from red cell loss (ie hemorrhage) or lysis of red blood cells (the total solids does not change in this case). In animals with acute hemorrhage, the PCV may have a gradual decline during isotonic crystalloid resuscitation. Animals suffering from blood loss may need a combination of PRBCs and plasma, or other products such as fresh whole blood (discussed later), following crystalloid resuscitation. Leukoreduced RBCs have the white blood cells removed from the red blood cells prior to storage. This may reduce nonhemolytic febrile reactions.

Fresh Frozen Plasma

Fresh frozen plasma is frozen within 6 hours of collection at -70ºC and is stable for 1 year. It contains clotting factors and albumin, but not red blood cells or platelets. It is useful for treatment of coagulopathic, animals with clinical evidence of bleeding or those with abnormal clotting parameters that require surgical intervention. Plasma is not an efficient on-cotic agent, but does help to maintain or increase the colloid osmotic pressure and albumin concentration of the recipient. However, it takes approximately 40 ml/kg to raise the albumin 1g/dl (or 10 g/L), therefore the administration of hyperoncotic synthetic colloids or concentrated human or canine albumin is more effective for increasing the oncotic pressure or albumin levels, respectively (discussed further below).

Refrigerator Stored or Frozen Plasma

Refrigerator stored or frozen plasma is more than 1 year old (but less than 4 years old) no longer contains platelets or the labile coagulation factors (V, VIII, and vonWillebrand’s




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factor). These products can be used for albumin support or the replacement of vitamin K-dependent coagulation factors (early in the bleeding process, before other factors are defi-cient).

Cryoprecipitate

When fresh frozen plasma is thawed to the point that its consistency is slushy, it is then centrifuged and the top 80% of the supernatant is removed. The remaining precipi-tate is termed cryoprecipitate. Cryoprecipitate contains rela-tively high concentrations of fibrinogen, fibro¬nectin, factor VIII, XIII, and von Willebrand’s factor and is the preferred treatment for bleeding dogs with these plasma protein de-ficiencies. The recommended dose is 15ml per 10kg of body weight.

Cryopoor (or cryosupernate) Plasma

This is the supernatant that remains after preparation of cryoprecipitate and contains the stable coagulation factors II, VII, IX, X, anticoagulant and fibrinolytic factors, and albumin. It can be useful for the treatment of specific coagulation fac-tor deficiencies that do not require vWf, fibrinogen or factor VIII.

Albumin Therapy

The treatment of critically ill animals with severe hypoal-bumemia can prove challenging. Although albumin is noto-rious for its role as an oncotic agent in the blood, it serves many other important roles including the transport of drugs, chemicals, toxins, bilirubin and enzymes, as well as modula-tion of coagulation and inflammation. Dogs and cats with clinically significant hypoalbuminemia or those with severe ongoing losses may benefit from treatment with concentrat-ed albumin products. Human serum albumin is available for use in dogs; one 50-ml bottle of 25% human serum albumin is equivalent to approximately 3 units of plasma. There is a proven risk for both an immediate and delayed allergic reac-tion, and repeated use is not recommended. Naturally occur-ring anti-human serum albumin antibodies have been found in dogs that have never received HSA transfusions. These an-tibodies have also been shown to develop in dogs following a single infusion of human serum albumin. Human serum albu-min should not be used in healthy patients or those with mild, asymptomatic disease. Lyophilized canine albumin is now on the market in the US, and early evidence suggests that it is safe and effective for the treatment of severe hypoalbumine-mia in dogs. Its expense and contamination issues have lim-ited use thus far, however.

Platelets

Frozen platelet concentrate and lyophilized canine plate-let concentrate are available in some countries for treatment of severe, symptomatic thrombocytopenia with life-threaten-ing bleeding. Fresh whole blood or platelet rich plasma are the most effective methods to deliver platelets that are func-tional and likely to stop thrombocytopenia-induced bleeding, however. The frozen and lyophilized products deserve further study before definitive use can be recommended.

Autologous Blood

In animals with excessive hemorrhage into the pleural or peritoneal cavity, autotransfusion of whole blood should be considered. The blood is gently aspirated, anticoagulated,

and filtered prior to administration. Hemorrhage due to neo-plastic or septic processes should not be autotransfused.

DONOR AND RECIPIENT SCREENING RECOMMENDATIONS

All canine blood donors should be typed for dog erythro-cyte antigen (DEA) 1, and all cats should be typed for the AB blood groups. Potential blood donors should be young (≤6 years old), in good body condition, and receive preventative health care and vaccinations. These dogs and/or cats should have comprehensive health examination at least twice a year which includes a complete physical examination, complete blood count, serum chemistry, urinalysis, fecal and infectious disease testing as dictated by the location. The dogs should weigh more than 25 kg and the cats more than 5 kg (ideal body weight). If a hospital chooses to have an in-house feline blood donor program, the cats should have adequate envi-ronmental enrichment and a limited time for donation prior to adoption. The American College of Veterinary Internal Medicine has published blood donor screening recommenda-tions.

A blood type should be performed on any patient that will receive red blood cells; cats should also have a cross match performed prior to any transfusion. The canine species does not harbor alloantibodies prior to sensitization; therefore a single transfusion in a naïve patient without blood typing is reasonable if the patient is unstable. It is best to only uti-lize DEA 1 negative canine blood, although all donors can be used as long as typing is performed. Any cat that will receive a red cell transfusion should be blood typed, as administration of the wrong blood type to a cat can cause a fatal transfu-sion reaction. There are three feline blood types: A, B and AB. Type A is the most common blood type in domestic cats worldwide. Cats with type B blood have significant anti-A al-loantibodies and should never receive type A blood. A more recently discovered red blood cell antigen, termed the Mik antigen, has been identified in domestic shorthair cats. It is possible that cats lacking this Mik antigen produce alloan-tibodies that can lead to destruction of transfused red cells containing the antigen.

Many hospitals with a large emergency caseload maintain their own blood donor program, comprised mostly of com-munity or staff animals. There are also several animal blood banks in certain countries that can safely send blood com-ponent therapy rapidly (often overnight if needed). If whole blood is to be collected for administration to a patient in the clinic, the blood must be aseptically drawn into a collection system and appropriately anticoagulated. Blood collection systems with citrate-phosphate-dextrose-adenosine (CPDA) are most commonly recommended, using a ratio of whole blood to CPDA is 1 mL CPDA to 9 mL whole blood collected. A total of 40–55 mL of whole blood is commonly collected from feline blood donors. Subcutaneous or intravenous iso-tonic crystalloid fluids are frequently given to replace the col-lected blood. The maximum amount of blood that can safely be removed from a canine blood donor is 20 mL/kg (no more than every 4-6 weeks; iron therapy may be beneficial, espe-cially if anemia develops.) Sedation is typically given to help the donor cooperate and to minimize stress.



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CALCULATIONS AND ADMINISTRATION

Pretreatment is generally not recommended. Red blood cells that are stored in the refrigerator do not require warm-ing and this is discouraged as it may accelerate aging of the red blood cells and promotes bacterial growth. Fresh frozen plasma should be thawed in a designated warm water bath until liquefied prior to administration. An appropriate filter should be used for delivery of all blood products (at least 170 microns). If dilution of flushing of products with red blood cells or whole blood is necessary, 0.9% NaCl is the preferred fluid.

When determining the amount of blood to transfuse, general guidelines are as follows:

• For every 1% increase in PCV, give 1.5ml/kg of PRBCs or 2-3 mls/kg of FWB

• To treat prolonged clotting times: 10-15ml/kg plasma (FFP or FP); repeated dosing may be necessary

• To raise the albumin by 1g/dl (or 10g/L), 30-40 ml/kg should be administered (this does not take into account ongoing losses), or concentrated albumin as below

• Platelet concentrate: 1 unit/10 kg (100 mL/10 kg)

• Cryoprecipitate: 1 unit/10kg

• Concentrated albumin: 1-2 gm/kg over 6-12 hours

Baseline vital signs should be obtained and monitored every 15-30 minutes during the transfusion. All transfused products, especially RBC, should be administered slowly for the first 30 minutes, unless bolus therapy is required to save the patient’s life, to try and detect a possible transfusion reac-tion early (see below). If a reaction is suspected (most com-monly fever or vomiting), the transfusion should be stopped or the rate greatly reduced. Diphenhydramine (1–2 mg/kg IM or IV) can be administered and the transfusion re-initiated. Dexamethasone SP (0.25 mg/kg IV) can also be administered once prior to re-initiation of the transfusion if deemed clini-cally necessary. A single bag should not be administered over >4 hours to decrease the risk of bacterial contamination.

If anaphylaxis occurs, although rare, rapid treatment with epinephrine should ensue and a sample of the bag retained for testing.

Potential Side Effects

Infused blood products should always be filtered (mini-mum 170 microns) and the recipient monitored for signs of transfusion reaction. These might include febrile non-hemo-lytic reactions, restlessness, vomiting or diarrhea, acute col-lapse, wheezing, dyspnea, urticaria, hemoglobinemia or he-moglobinuria, and/or hypotension. The transfusion should be stopped immediately if any of these reactions are observed. Further adverse effects of blood transfusions include pulmo-nary emboli and respiratory distress syndrome due to red cell, white cell, or platelet clumps, heparinization if large amounts of heparin are administered, acidosis and/or hypocalcemia if large amounts of citrate anticoagulants are administered.

ADDITIONAL CONSIDERATIONS

Leukoreduction

The use of leukoreduced blood components is an area of active research and becoming more mainstream in veterinary medicine. The use of a leukoreducing filter allows 99.99% of white blood cells to be removed from the whole blood unit prior to processing and separating it into component therapy. Although blood products can also be administered through a leukoreduction filter, prestorage leukoreduction is preferable to prevent the release of cytokines from white blood cells dur-ing storage. The only real down sides to performing leukore-duction routinely are the additional expense of the filter and added labor.

Storage time

Despite the fact that advances in the storage procedure of pRBC has extended the shelf-life up to 42 days (with certain additives), there is increased awareness of the detrimental ef-fects of storage time on the quality of the blood transfused Serious transfusion related complications can occur, and transfusion of aged red blood cells (>2 weeks old) may have deleterious effects on clinical outcome when compared to transfusion with fresh red blood cells. This is likely due to pro-gressive biochemical and biomechanical changes that occur in the function and structure of the cells, collectively referred to the red blood cell storage lesion. Some of the storage re-lated changes in pRBCs include a loss of RBC deformability, shape and membrane, oxidative injury to lipids and proteins, decreased oxygen affinity and delivery, increased adhesion to endothelial cells, decreased life span, accumulation of lactate, potassium and free hemoglobin, shedding of active proteins, lipids and microparticles, bacterial contamination and adverse coagulation effects.




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HMMM… LE KAJ JE ŠLO NAROBE? KAKO IZBOLJŠATI OSKRBO KRITIČNEGA PACIENTA ?

Marko Pipan

V klinični praksi se veterinarji redno srečujemo z urgentni-mi pacienti. V prispevku opisujem uspešen pristop k urgentne-mu in kritičnemu pacientu, ki kaže znake hemodinamske nestabilnosti, prizadetosti centralnega živčevja, dihalne stiske ali znake presnovnih motenj. V kolikor se s tovrstnimi pacienti ne srečujemo redno se lahko zgodi, da pri diagnostičnem pro-cesu in zdravljenju nehote pozabimo na “korake”, ki lahko odločajo o preživetju kritično bolne živali.

Pomembnost kliničnega pregleda

Ocena dihalne funkcije, hemodinamske stabilnosti in nevrološke funkcije je temeljni del pregleda vsakega urgent-nega in kritičnega pacienta. Klinični pregled omogoča oceno začetne klinične slike, pravilno izbiro diagnostike in zdrav-ljenja ter spremljanje odziva različnih organskih sistemov na zdravljenje. Redno spremljanje klinične slike je zaradi nesta-bilnosti kritičnega pacienta bistvenega pomena za uspešnost zdravljenja in osnova pri odločanju o nadaljnjih postopkih di-agnostike in zdravljenja.

Neinvazivno merjenje arterijskega krvnega tlaka

Neinvazivno merjenje arterijskega krvnega tlaka (AKT) pomaga pri potrditvi diagnoze cirkulacijskega šoka in spreml-janju odziva kardiovaskularnega sistema na tekočinsko zdrav-ljenje. V kompenzirani fazi in na začetku faze dekompen-zacije hipovolemičnega šoka je arterijski tlak zaradi delovanja kompenzatornih mehanizmov telesa še vedno normalen. Vsak sistemsko prizadet urgenten pacient in vsak kritičen pacient zahteva redno merjenje AKT in vzdrževanje normotenzije (srednji arterijski tlak 80-120 mm Hg).

Uporaba pulznega oksimetra

Pulzni oksimeter omogoča hitro, neinvazivno in kon-tinuirano oceno oksigeniranosti arterijske krvi oz. zasičenosti hemoglobina s kisikom (SpO2) in predstavlja nepogrešljiv del začetne diagnostike dihalne stiske in monitoriranja kritično bolne živali. Pri pacientu, ki vdihuje zrak iz okolja pulzni ok-simeter omogoča oceno ustreznosti izmenjave kisika v pljučih. Možnost, da nam aparat ne pokaže realne vrednosti SpO2 ob-

staja pri pigmentaciji sluznice, periferni vazokonstrikciji, hipo-tenziji, hudi anemiji, pretiranem tresenju živali ter prisotnost MetHb ali COHb v krvi. Vrednosti SpO2 pod 95% pomenijo hipoksemijo in vrednosti pod 90% kažejo na hudo hipoksem-ijo. Med anestezijo, ko žival vdihuje obogaten zrak s kisikom ali 100% kisik, je pulzni oksimeter pozen pokazatelj neus-trezne izmenjave kisika v pljučih in pljučne patologije.

Minimalna krvna preiskava

Pri večini urgentnih pacientov želimo vedeti vsaj vrednosti hematokrita (Hct), skupnih proteinov (SP), sečnine in glukoze. Poleg tega, lahko s pregledom krvnega razmaza ocenimo ustreznost različnih krvnih celic. Nizke vrednosti Hct in SP najpogosteje kažejo na izgubo krvi, medtem ko povišane vrednosti obeh parametrov kažejo na hemokoncentracijo. Nizek Hct z normalnimi ali visokimi SP kaže na hemolizo ali neustrezno produkcijo kostnega mozga. Sečnina je povišana pri dehidraciji, neustrezni ledvični funkciji, vseh oblikah šoka, obstrukciji sečnice, uroabdomnu in gastrointestinalnem kr-vavenju. Hipoglikemija se pogosto pojavi pri mladičih in malih psih, portosistemskem šantu, nezadostni funkciji jeter, sepsi, hipoadrenokorticizmu in inzulinomu. S pregledom razmaza krvi ugotavljamo prisotnost leukocitoze, leukopenije, trom-bocitopenije, aglutinacijo eritrocitov, prisotnost sferocitov, ocenimo regenerativnost anemije in včasih lahko celo potrdi-mo prisotnost znotrajceličnih povzročiteljev bolezni (npr. ba-bezija, anaplazma, hemobartonela) oz. parazitov (mikrofilarije dirofilarije).

Plinska analiza krvi, kislinsko-bazno ravnovesje in laktat

Plinska analiza krvi z oceno kislinsko-baznega ravnovesja je za resno obravnavo kritično bolne živali nenadomestljiva! V klinični praksi za oceno kislinsko-baznega ravnovesja zados-tuje preiskava venske kri, medtem ko je arterijska kri potreb-na, ko nas zanima natančna ocena oksigeniranosti arterijske krvi. Ugotavljanje ustreznosti pljučne ventilacije in oksigenaci-je krvi, prisotnosti presnovne acidoze (laktatna acidoza, diabetična ketoacidoza, uremična acidoza, zastrupitev z etilen glikolom) in drugih kislinsko-baznih motenj (npr. presnovna alkaloza pri obstrukciji tankega črevesja) so nekatere indikaci-je za uporabo plinske analize. Povišan laktat (> 2,5 mmol/l) je pokazatelj tkivne hipoperfuzije in hipoksije. Hiperlaktatemija je najpogosteje povezana s sistemsko hipoperfuzijo tkiv oz. šokom, kjer višje vrednosti laktatat pomenijo obsežnejšo Marko Pipan, dr. vet. med., Dipl. ACVECC

[email protected]



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hipoksijo tkiv. Laktat se je izkazal kot prognostični indikator pri zasuku želodca z dilatacijo (1), babeziozi (2), septičnem peritonitisu (3) in sistemsko bolnih psih (4) pri čemer je bolj kot začetna vrednost laktata pomemben njegov padec po začetku zdravljenja. Velja omeniti, da je v začetni fazi šoka laktat lahko normalen.

Uporaba AFAST in TFAST ultrazvočne preiskave

“Abdominal focused assessment with sonography for trauma” (AFAST) je hiter sistematičen pregled abdomna z ultrazvokom v katerem iščemo prosto tekočino, ki jo lahko aspiriramo in diagnostično ovrednotimo (npr. septični ab-domen, hemoabdomen, uroabdomen, biliarni peritonitis). Čeprav je bila preiskava v prvotnem smislu namenjena začetni oceni poškodovanih živali, se je njena uporaba hitro razširila in predstavlja danes pomemben del začetne diagnostike vsakega huje prizadetega urgentnega pacienta (5). S TFAST (“Thoracic focused assessment with sonography for trauma“) gledamo na prisotnost proste tekočine v prsnem košu in osrčniku ter na prisotnost pneumotoraksa (6). Z ultrazvokom lahko zaznamo nabiranje proste tekočine v abdomnu in toraksu v zelo ma-jhni količini, kar omogoča hitro diagnostiko abdominalne in torakalne patologije.

Tekočinska terapija pri hipovolemiji

Ena najpomembnejših in najtežjih nalog pri zdravljen-ju kritičnega pacienta je nadomeščanje intravaskularnega tekočinskega primanjkljaja s pravo mero. V zadnjih letih je prišlo do korenite spremembe na področju šokovnih odmerk-ov intravenskih tekočin, ki se jih uporablja pri pacientih v šoku. Trenutno se priporoča zaporedna aplikacija manjših bolusnih odmerkov. Začnemo z 1/4 ali 1/3 celotnega šokovnega odmer-ka, ki je za kristaloide 90 ml/kg pri psu in 60 ml/kg pri mački. Določen odmerek tekočine apliciramo v 10-15 minutah. Po bolusu ponovno preverimo klinične kazalce prekrvljenosti tkiv (barva sluznic, čas kapilarne polnitve, frekvenca srca, kvaliteta arterijskega pulza, toplina uhljev in tačk, stanje zavesti, arteri-jski krvni tlak, centralni venski tlak) in glede na odgovor telesa na prvi bolus po potrebi bolus ponovimo. Najboljši pokazatelj ustreznosti tekočinske terapije je sam odgovor kardiovasku-larnega sistema na tekočinsko zdravljenje. Klinične izkušnje kažejo, da pri večini hipovolemičnih živali zadostuje aplikacija 2/3 celotnega šokovnega odmerka, kar pa ne velja za žival v septičnem šoku, kjer so potrebe po intravenskih tekočinah pogosto večje. Zavedati se moramo, da agresivna infuzija kristaloidov lahko vodi do edema organov (npr. pljučni edem), zmanjšane motilitete črevesja, povečanega intraabdominal-nega tlaka, zmanjšane kontraktilnosti srca in tkivne hipoksije (7).

Diagnostična in terapevtska punkcija proste telesne tekočine

Vsakdo, ki se srečuje z urgentnimi pacienti mora biti vešč v izvedbi diagnostične in terapevtske torakocenteze, abdomi-nocenteze, perikardiocenteze in artrocenteze. Pri punkciji tekočine si lahko pomagamo z ultrazvokom. Področje punkcije obrijemo, umijemo in razkužimo. Medtem ko je diagnostična punkcija del diagnostičnega procesa, s terapevtsko punk-

cijo pacienta stabiliziramo in ga pripravimo na nadaljnje diagnostične in terapevtske posege. Pri sistemsko prizadetih živalih za izvedbo punkcije običajno zadostuje že blaga se-dacija (uporaba benzodiazepinov) z uporabo lokalnega an-estetika ali opioidnega analgetika (npr. butorfanol). V kolikor je pri nestabilnem pacientu potrebno vstavljanje torakalnega drena, se zaradi možnosti dihalnega zastoja priporoča orotra-healna intubacija pacienta in vodeno predihavanje.

Rentgensko slikanje prsnega koša

Rentgensko slikanje prsnega koša je del začetne diagnos-tike vsakega kritičnega pacienta, pri katerem bo potrebno večdnevno agresivno bolnišnično zdravljenje. Odkrivanje vz-roka dihalne stiske, aspiracijske pljučnice pri neambulatornih in nevroloških pacientih oz. kroničnem bruhanju ter ugotav-ljanje pljučnih metastaz pri geriatričnih živalih, so le nekateri izmed razlogov zakaj je preiskava potrebna. Odsotnost vidne patologije pljuč, normalna silhueta srca in ustrezna polnjenost venskega žilja potrdijo primernost pacienta za agresivno tekočinsko zdravljenje. Začetno rentgensko slikanje poleg tega omogoča diagnostiko intratorakalne patologije, ki se razvije med samim bolnišničnim zdravljenjem (npr. aspiraci-jska pljučnica, akutni respiratorni distresni sindrom, pljučna tromboembolija, pljučni edem ob tekočinski preobremenitvi ali srčnem popuščanju).

Stabilizacija kritičnega pacienta pred kirurškim posegom

Anestetiki in hipnotiki lahko zmanjšajo krčljivost srčne mišice, frekvenco srčnega utripa in tonus perifernega žilja, kar lahko vodi v hipotenzijo, zmanjšano prekrvljenost tkiv in generalizirano hipoksijo. Pogosto se zgodi, da kritični pa-cienti, ki sicer delujejo hemodinamsko stabilni pred pose-gom, postanejo hudo hipotenzivni med anestezijo. Kritično bolne živali, ki potrebujejo urgenten kirurški poseg (npr. zasuk želodca z dilatacijo, septični abdomen, hemoabdo-men, obsežne inficirane ugrizne rane s sistemskim vnetnim odgovorom, politravma, absces trebušne slinavke), moramo pred posegom zadostno stabilizirati. Z agresivno tekočinsko terapijo, transfuzijo, uporabo vazopresorjev in inotropov, ko-rekcijo elektrolitskih odstopanj in kislinsko-baznega ravnoves-ja ter ozmotsko terapijo za normalizacijo intrakranialnega tlaka kritičnega pacienta ustrezno pripravimo na poseg in zmanjšamo možnost intraoperativnih in pooperativnih komp-likacij.

Uporaba kortikosteroidov

Kortikosteroidi se pri urgentnem kritičnem pacientu up-orabljajo selektivno! Pri poškodovani živali, travmi glave in hipovolemiji se kortikosteroidov NE poslužujemo zaradi nji-hovih negativnih učinkov (t.j. gastrointestinalna razjeda in kr-vavenje, poslabšanje hiperglikemije, upočasnjeno celjenje ran, oslabljen imunski odgovor, zmanjšana prekrvljenost ledvic). Študija opravljena pri ljudeh s travmatsko poškodbo glave je pokazala, da je bila umrljivost pri pacientih, ki so bili zdravljeni s kortikosteroidi višja (8). Pri septičnem šoku jih uporabljamo le, če arterijskega krvnega tlaka ne uspemo normalizirati z ustrezno tekočinsko terapijo in uporabo vazopresorjev in inotropov oz. ob dokazani relativni adrenalni insuficienci. V



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tem primeru se priporoča aplikacija hidrokortizona (1 mg/kg na 6 ur). Pri anafilaktičnem šoku kortikosteroidi v akutni krizi ne igrajo pomembne vloge, saj imajo zapoznel učinek in ne vplivajo na kardiovaskularne efekte anafilakse.

Ko je uporaba kortikosteroidov indicirana (imunsko pogo-jena hemolitična anemija ali trombocitopenija, nekrotizirajoči encefalitis, steroidno odzivni meningitis-arteritis), uporabimo imunosupresiven odmerek deksametazona (0,2-0,6 mg/kg/24 ur parenteralno) ali prednizolona (1-2 mg/kg/12 ur peroralno) (9).

Uporaba nesteroidnih analgetikov pri kritičnem pacientu

Uporaba nesteroidnih analgetikov (NA) pri hemodinamsko nestabilnem pacientu ni primerna v začetnih urah zdravljenja oz. dokler ne dosežemo normovolemije, normalnega krvnega tlaka, popolne rehidracije in ustrezne produkcije urina. Zaradi neustrezne prekrvljenosti gastrointestinalnega trakta in led-vic ob prisotnosti hipovolemije oz. šoka je možnost ulcero-genega delovanja in akutne poškodbe ledvic ob uporabi NA večja. Pri hemodinamsko nestabilnih pacientih, ki potrebujejo protibolečinsko terapijo se odločimo za opioidne analgetike oz. multimodalno analgezijo.

Povišana telesna temperatura

Pri povišani telesni temperaturi moramo ločiti med vročino in hipertermijo. Vročina je posledica višje nastavitve termoreg-ulacijskega centra (TC) v hipotalamusu zaradi delovanja pred-vsem notranjih a tudi zunanjih pirogenov in je najpogosteje znak vnetja ali infekcije v telesu. Povišana temperatura telesa je v tem primeru koristna, saj ustvarja nelagodno okolje za razmnoževanje mikrobov in tumorskih celic, krepi vnetni in imunski odgovor telesa in lahko celo poveča učinkovitost an-timikrobikov (10). Iz teh razlogov hlajenje živali z vročino in nižanje telesne temperature z antipiretiki v večini primerov ni potrebno.

Pri hipertermiji se telesna temperatura dvigne brez spremembe v TC zaradi visoke temperature v okolju in nezmožnosti hlajenja živali (zaprta žival v avtu), tvorbe top-lote v telesu ob prekomerni mišični aktivnosti (npr. epileptični status, hipokalcemična tetanija, pretirana telesna aktivnost), motenj v oddajanju toplote (npr. paraliza larinksa), reak-cije na anestezijo (npr. maligna hipertermija) ali kombinacije naštetih vzrokov. Pri telesni temperaturi višji od 41,0 °C je nujno takojšnje ohlajanje živali s hladno vodo, uporabo venti-latorja in polaganjem vrečk ledu na velike telesne vene. Da se izognemo iatrogeni hipotermiji z ohlajanjem prenehamo, ko dosežemo temperaturo 39,4 (10).

Literatura:

1. Beer KA, Syring RS, Drobatz KJ. Evaluation of plasma lactate concentration and base excess at the time of hospital admission as predictors of gastric necrosis and outcome and correlation between those variables in dogs with gastric dilatation-volvolus: 78 cases (2004-2009). J Am Vet Med Assoc 2013; 242 (1):54-58.

2. Nel M, Lobetti RG, Keller N, et all. Prognostic value of blood lactate, blood glucose, and hematocrit in canine babesiosis. J Vet Intern Med 2004; 18(4): 471-6.

3. Cortellini S, Seth M, Kellett-Gregory LM. Plasma lactate concentrations in septic peritonitis: A retrospective study of 83 dogs (2007-2012). J Vet Emerg Crit Care (San Antonio) 2014 Sep 11. doi: 10.1111/vec.12234.

4. Stevenson CK, Kidney BA, Duke T, et all. Serial blood lactate concentrations in systemically ill dogs. Vetrinary Clinical Pathology 2007; 36:234–239.

5. Lisciandro GR. Abdominal and thoracic focused assessment with sonography for trauma, triage, and monitoring in small animals. J Vet Emerg Crit Care 2001; 21(2): 104-122.

6. Lisciandro GR, Lagutchik MS, Mann KA, et all. Evaluation of a thoracic focused assessment with sonography for trauma (TFAST) protocol to detect pneumothorax and concurrent thoracic injury in 145 traumatized dogs. J Vet Emerg Crit Care 2008; 18(3): 258-269.

7. Cotton BA, Guy JS, Morris JA, et all. The cellular, metabolic, and systemic consequences of agressive fluid resuscitation strategies. Shock 2006; 26: 115-121.

8. Roberts I, Yates D, Sandercock P, et all. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomized placebo-controlled trial. Lancet 2005; 364: 1321-1328.

9. Cohn LA. Acute hemolytic disorders. In: Silverstein DC, Hopper K, eds. Small animal critical care medicine. St. Louis, Missouri. Elsevier Saunders, 2015: 586-590.

10. Miller JB. Hyperthermia and fever. In: Silverstein DC, Hopper K, eds. Small animal critical care medicine. St. Louis, Missouri. Elsevier Saunders, 2015: 55-59.



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42

ISSUES IN PET BEREAVEMENT AND CLIENT COMMUNICATION

Stefan C. Dombrowski

Issues in pet bereavement and client communication

This presentation will discuss issues in pet bereavement and how to communicate with human clients who are facing the prospect of losing a beloved pet. Of any medical profes-sional veterinary practitioners, particularly those in oncology and emergency/critical care, have the most tangible experi-ence with death and dying. However, these professionals may not have been trained to understand the issues associated with the bereavement process including how to communicate with caregivers. Veterinary practitioners may have acquired this experience over time and through practice, but the vet-erinarian’s and veterinary technician’s role as a medical pro-fessional is primary. Issues regarding bereavement and client communication may not have been covered within academic training programs in veterinary medicine. This presentation reflects a starting point for the veterinary practitioner who wishes to better understand a number of topics including the intensity of the human-animal bond; complicated grief; the social, emotional, physical and behavioral sequelae of grief; special bereavement issues involving children and the elderly; and how to appropriately communicate with clients when they must be faced with end of life decisions for their pets.

The Human-Animal Bond

The human-animal bond for many people can be more profound and powerful than a connection with other humans (Gosse & Barnes, 1994; Lagoni, Butler & Hetts, 1994). Because of the intensity of this bond, the loss of a pet can be devastat-ing to the human client. Many countries around the world do not fully recognize the death of a pet in the same way that they acknowledge the death of a human (Ross & & Baron-Sorenson, 1998). Evidence of the profundity of the human-animal bond can be seen throughout history. Humans tend to anthropomorphize their pets by extending the same value and belief system to those pets that they extend to humans (Fogle, 1992). For instance some religions debate whether animals have souls and may gain entrance into heaven. An-

cient societies from antiquity even buried their owner’s pets with them to assist or accompany the deceased owner on their journey after death. The issue of bereavement may be even more complicated when associated with an older per-son. The pet may be a symbol of a connection to a deceased loved one or may be the only friend with whom the elder had a connection. The pet may also motivate the older person to take care of the pet, permitting the older person to get out of the home to visit the pet store, the veterinarian’s office, the groomer, and take the pet for a walk on a daily basis. The loss of the older person’s pet then represents the loss of potential exercise and social contact with the outside world.

Veterinary Grief Support including Complicated Grief

The death of a pet can be significant and painful with intense grief and loss consistent with that experienced when a close friend or family member dies. Gage and Holcomb (1994) conducted a survey of 200 couples who had reported the death of a pet within the past three years. These couples viewed the death of the pet as less stressful than the death of a human member of the immediate family but more stress-ful than the death of other human relatives. There is rela-tively little information available for veterinary teams wishing to learn how to support grieving pet owners and help them cope with end-of-life decisions (Pilgrim, 2010). Yet, veterinary practitioners are often the first point of contact with clients who experience the loss of their pets. In some respects the veterinary practitioner has the most experience with grief and loss of any medical professional. However, there is often in-sufficient room in veterinary training programs to offer cover-age of grief support including what grief looks like and how to properly communicate bad news with clients. Grief issues become even more complicated by the lack of recognition by society and one’s family and friends. As an example, there are generally not memorial services associated with the loss of a pet or time off from work for pet bereavement.

What does Grief Look like?

Grief carries with it a host of physical, social, emotional, behavioral, cognitive and spiritual sequelae (Lagoni & Dur-rance, 2011). This information will be discussed and is impor-tant for the veterinary practitioner to recognize as the veteri-nary team and its front administrative staff is often the point of first contact with the bereaved individual and would be well-served by knowing the typical expressions of grief.

Stefan C. Dombrowski, Ph.D. Professor & Director School Psychology Program Department of Graduate Education, Leadership & Counseling Rider University, Lawrenceville, NJ 08648 [email protected]



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Disenfranchised grief will also be presented and dis-cussed. Disenfranchised grief reflects the type of grief that is paradoxical. In some cultures, pets are viewed by society as members of the family. However, society does not does not afford the same policies and rights to the bereaved pet owner such as time off from work, the attendance of a funeral, or acknowledgment of the loss via a card or flowers. This is fur-ther complicated by factors associated with guilt regarding the need for pet owners to make an active decision to end their pet’s lives via euthanasia.

Resources for the Veterinary Practitioner

Resources for the veterinary team will be presented includ-ing how to provide effective grief support. It is not expected that the veterinary practitioner assume the role of therapist. This is not the veterinary professional’s role, but the veteri-nary practitioner should understand how to properly commu-nicate with clients and provide emotional support protocols. Common scenarios will be presented including how to help children with their loss, euthanasia decision-making, deliver-ing of bad news, helping seniors, and communicating with intellectually/emotionally disabled clients. Generic guidelines for communication including what should be stated and what should not be stated (e.g., do not use clichés such as “time heals all wounds” or “everything happens for a reason”) will also be presented.

References

Lagoni, L., Butler, C & Hetts, S. (1994). The human-animal bond and grief. Philadelphia: W. B. Saunders.

Fogle, Bruce (1992). If your cat could talk. London: Dorling Kindersley

Gage, G. & Holcomb, R. (1991). Couples perceptions of the stressfulness of the death of the family pet. Family Relations, 40, 103-106.

Lagoni, L. & Durrance, D. (2011). Connecting with grieving clients, Second Edition. Lakewood, Colorado: American Hospital Association Press.

Pilgrim, M. D. (2010). Communicating social support to grieving clients: The veterinarian’s view. Death Studies, 34, 699-714.

Ross, C. B. & Baron-Sorenson. (2007). Pet loss and human emotion: A guide to recovery. New York: Routledge.



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Stefan C. Dombrowski, Ph.D. Professor & Director School Psychology Program Department of Graduate Education, Leadership & Counseling Rider University, Lawrenceville, NJ 08648 [email protected]

COMPASSION FATIGUE IN THE VETERINARY PRACTITIONER

Stefan C. Dombrowski

The field of veterinary medicine is rewarding and affords opportunity to heal animals. The work environment, however, can be intensely pressured and highly emotional. Veterinary practitioners (i.e., veterinarians and veterinary technicians/nurses) work long hours under stressful conditions where the practice of saving animals often supersedes the process of acknowledging intense feelings and promoting self-care. Unfortunately, it is the combination of a stressful work en-vironment, a lack of self-care, and the lack of processing of emotions and feelings that often contributes to compassion fatigue.

What is compassion fatigue?

People working in the profession of veterinary medicine are generally highly dedicated, compassionate individuals who are excited about making improvements in the lives of animals. Over time the veterinary professional may become disenchanted and disillusioned and see their dedication and interest wane. This disillusionment may extend to other as-pects of life and adversely impact their relationships and general life functioning. Chronic exposure to death, dying, grief, and emotionally intense environments can lead to dif-ficulty with relationships, both at home and at the office, and feelings of anger, frustration, loneliness, cynicism, and even suicide (Bartram & Baldwin, 2010). When practitioners expe-rience such deterioration in interpersonal, occupational and emotional functioning then they may be suffering from com-passion fatigue (Ayl, 2013).

Definition

Compassion fatigue involves the emotional, physical, mental, social and spiritual changes that occur as a result of engaging empathetically with and around people who are experiencing a traumatic event such as death and dying (Ayl, 2013). Compassion fatigue is much more than stress and burnout created by a hectic work environment. It is associated with the deep awareness of the suffering of others coupled with the desire to relieve that suffering (Penson et al., 2000). Compassion fatigue has also been defined as secondary trauma or vicarious trauma (Keidel, 2002).

Stress involves too much work with too many hours, and too high of expectations. Burnout is related to feelings of depletion, emptiness, apathy, and a lack of motivation. Fre-quently, time away from the job such as a holiday or vacation can resolve stress and burnout and reinvigorate one’s motiva-tion and passion for work.

Compassion fatigue is similar to but much more deleteri-ous than stress and burnout. It is sometimes associated with a restriction in feelings or becoming numb to one’s feelings. Compassion fatigue is a very real problem in veterinary medi-cine and in any profession that faces long term exposure to suffering, loss, and difficult clients. Because of the continu-ous demands that are placed on veterinary professionals it is no wonder compassion fatigue ensues. The person who is experiencing compassion fatigue may be devastated by the repeated exposure to the pain and trauma of others or to chronic exposure to death and dying. This chronic exposure to difficult clients, grief, and trauma may leave the professional feeling overwhelmed, angry, exhausted and maybe even un-able to care about anything. When left untreated compas-sion fatigue can lead to career dissatisfaction, high turnover rates, substance abuse and even suicide (Batram & Baldwin, 2010; Collins & Long, 2003). Additional symptoms may in-clude changes in personality and behavior. Some veterinary professionals may feel like they are a different person or that they no longer recognize themselves. Compassion fatigue may result in interpersonal difficulties where practitioners are short-tempered with friends, family, co-workers and people that the professional does not even know. The person suffer-ing from compassion fatigue may even become disillusioned with his or her profession. He or she has lost the joy that was once experienced practicing veterinary medicine. Precise sta-tistics regarding the prevalence of compassion fatigue in the field of veterinary medicine is generally unavailable. Research on this topic is needed.

What contributes to Compassion fatigue?

There are a number of factors and situations that may contribute to compassion fatigue. This includes the stress of dealing with difficult clients who project their anger and grief onto the veterinary professional and their staff. Com-passion fatigue may also emerge when dealing with death or dying on a frequent, if not daily, basis. This exposure can be extremely stressful particularly when involving children and the elderly. Additionally, there is the complexity and stress of navigating the decision to euthanize a beloved pet. The human client may not understand the process and may re-ject the explanation offered by the veterinary professional



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leading to prolonged and seemingly unnecessary suffering of the animal. Additionally, the human client may be under significant stress and trauma when the client is faced with the prospect of making an active decision regarding the death of their pet via euthanasia. Human clients may be less accus-tomed to dealing with death and dying and may superimpose a human-like value system upon an animal where euthanasia is to be eschewed. The nearly daily contact with client’s grief and the prospect of death and dying can increase risk for compassion fatigue. Other factors which may contribute to compassion fatigue include the client’s inability or unwilling-ness to pay for a medical procedure that can save the animal’s life. This can increase the veterinary professional’s feelings of guilt in some circumstances, and anger and disgust in others.

The Worst Outcome of Compassion Fatigue: Suicide

People who take their lives do so for many reasons. There are biological and environmental contributions. Compassion fatigue may work in combination with these other factors to increase risk for suicidality among veterinary professionals. Suicide may well represent an extreme manifestation of com-passion fatigue. However, the veterinary profession works in a milieu where euthanasia is often advocated to alleviate the suffering of pets and the process of euthanasia is normalized. Veterinary professionals must often encourage, justify, and explain euthanasia to clients. This may well normalize lower inhibitions toward suicide and may be seen as a viable so-lution for dealing with their own problems (Kirwin, 2005). Bartram and Baldwin (2008) conducted a study in the UK and found that the suicide rate was four times the general population and two times that of other health professionals. Certainly these factors may contribute to the increased risk of suicide in the profession. This connection is alarming and makes it essential that the veterinary professional increase emphasis on self-care.

Symptoms of Compassion Fatigue

Although working in the field of veterinary medicine can be extremely rewarding it can also be emotionally intense and often exhausting. Chronic exposure to difficult clients, trauma, and death and dying is emotionally draining. The vet-erinary professional who once found her job rewarding now may find it thankless and devoid of meaning. The professional may encounter feelings of guilt, sorrow, anger, and rage on an intermittent or continuous basis. Sometimes emotions may erupt, and can often be negative. The professional may even become short-tempered over even the smallest of issues.

Treating Compassion Fatigue

It is critically important that the professional does not ignore the feelings and difficult emotions that arise as part of his or her role. These feelings and emotions will need to be processed and released rather than buried and ignored. If not, then the professional may find that multiple aspects of their lives are impacted, from professional to personal.

The love for animals or the desire to help them is a mo-tivating factor for individuals to enter the field of veterinary medicine. The field is generally honored to have such com-passionate individuals. However, compassion fatigue can erode ones passion and compassion for the field if it remains unrecognized or ignored. There is hope, though not necessar-ily a magic pill, for resolving compassion fatigue. Treatment options are possible and will be discussed within this presen-tation. This includes treatment options for both the individual veterinary practitioner and the veterinary practice. Treatment options range from self-care programs to professional help at both the individual and veterinary practice level. Some of these options will be briefly discussed. In totality, this presen-tation offers an introduction to the topic of compassion fa-tigue in the veterinary practitioner and furnishes suggestions for treatment and self-care.

References

Bartram, D. J. & Baldwin, D. S. (2010). Veterinary surgeons and suicide: A structured review of possible influences on increased risk. Veterinary Record, 166, 388-397.

Collins, S. & Long, A. (2003). Too tired to care? The psychological effects of working with trauma. Journal of Psychiatric Mental Health Nursing, 10, 17-27.

Keidel, G. C. (2002). Burnout and compassion fatigue among hospice caregivers. American Journal of Hospice and Palliative Care, 19, 200-205.

Kirwan, A. P. (2005). Mankind and other animals. Unpublished Thesis. Open University

Penson, R. T., Dignan, F. L., Canellos, C. L., Picard, C. L. and Lynch, T. J. (2000). Burnout: Caring for the caregivers. Oncologist, 5, 425-434.



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KAJ MORAMO PREVERITI PREDEN ANESTEZIRAMO ŽIVAL

Alenka Seliškar

Anamneza in klinični pregled sta najpomembnejša dela predanestezijskega pregleda, ki ga opravimo pri vseh živalih. To velja tako za stare in bolne kot za mlade, navidezno zdrave živali pred elektivnimi kirurškimi posegi. Lastnika mo-ramo pred anestezijo seznaniti z anestezijskim tveganjem, neželenimi učinki anestetikov in analgetikov ter morebitnimi zapleti med anestezijo. Pred anestezijo obvezno pridobimo pisno soglasje za poseg. Pred anestezijo stehtamo žival, vzam-emo izčrpno anamnezo in opravimo temeljit klinični pregled, podatke pa zabeležimo v kartoteko, ali še bolje, anestezijski zapisnik. Lastnika vprašamo naslednje:

Kdaj je žival nazadnje jedla in pila?

Psi in mačke lahko pijejo vodo do posega. Pasjih in mačjih mladičev do šestega meseca starosti ne postimo pred anest-ezijo. Še posebej pazimo, da post ni predolg pri miniaturnih pasmah psov, pri katerih lahko že po nekaj urah posta pride do hipoglikemije. Odrasli psi lahko zaužijejo manjši obrok lahko prebavljive hrane še 3 do 4 ure pred anestezijo, post daljši od 12 ur pa je celo škodljiv, saj pri daljšem postu pride med anestezijo do zatekanja želodčne vsebine v požiralnik in posledično do ezofagitisa. Odraslih mačk prav tako ne postimo več kot 12 ur. Post je izjemoma daljši pri posegih na zgornjih prebavilih, kjer bi prisotnost hrane ovirala preiskavo (npr. pri gastroskopiji) ali poseg (npr. pri resekciji želodca) oziroma pri nekaterih boleznih (npr. megaezofagus), kjer lahko med uvo-dom v anestezijo pride do zatekanja želodčne vsebine v žrelo in posledično do aspiracije vsebine v zgornje dihalne poti.

Ali žival vsakodnevno dobiva zdravila (katera, ko-likokrat dnevno, koliko časa)?

Nekatera zdravila lahko potencirajo delovanje anestetikov ali povzročijo zaplete med anestezijo, zato je dobro vedeti, katera zdravila je žival dobila v zadnjem tednu dni oziroma vsaj v zadnjih 24 urah. Na primer, zdravila za zniževanje krvnega tlaka iz skupine inhibitorjev angiotenzin-konvertaze ali ACE inhibitorji (enalapril), lahko pri sočasni uporabi feno-tiazinskih pomirjeval (acepromazin) povzročijo hipotenzijo, ki jo je težko odpraviti.

Ali je žival zadnji mesec kazala kakršnekoli znake bolez-ni (neješčnost, driska, bruhanje, kihanje, kašelj, izcedek iz nosnic ali oči, krvavitev iz nosnic itd.)?

Ali je žival imela kdaj epileptični napad oziroma če je epileptik, katera zdravila jemlje za nadzor epilepsije in kdaj nazadnje je zaužila ta zdravila?

Ali je žival kdaj padla v nezavest, težko dihala, kašljala, se hitro utrudila na sprehodu?

Oteženo ali pospešeno dihanje in hitro utrujanje med fizično aktivnostjo živali je lahko znak bolezni srca. Ena od pogostejših bolezni srca pri majhnih in srednje velikih pasmah psov je miksomatozna bolezen mitralne zaklopke, katero večina psov sorazmerno dobro kompenzira in lastniki dolgo ne vedo, da ima pes okvarjeno srčno zaklopko. Izgube zav-esti zaradi bolezni srca ne smemo zamenjati z izgubo zavesti zaradi hipertermije (toplotnega udara) ali epilepsije.

Ali žival normalno odvaja vodo in blato, kdaj je šla naz-adnje na vodo in blato?

Ali je bila žival cepljena teden dni pred anestezijo?

Anestezija in kirurški poseg sta stresna dejavnika in zavira-ta delovanje imunskega sistema, zato se elektivnim posegom v splošni anesteziji izogibamo vsaj teden dni po cepljenju. Izjema so nujni posegi.

Ali je žival breja oziroma v laktaciji?

Pri brejih živalih se moramo izogibati zdravilom, ki so po-tencialno škodljiva za plod (npr. nesteroidni analgetiki). Upo-raba zdravil med brejostjo ali laktacijo je indicirana le, kadar korist zdravila za mater odtehta tveganje neželenih učinkov pri plodovih oziroma mladičih.

Ali je žival imela kdaj reakcijo na zdravila oziroma je lastnik opazil kakršnekoli neželene učinke pri jemanju zdravil. Kako je žival prenesla morebitne prejšnje an-estezije?

Ob sprejemu živali se z lastnikom dogovorimo, kdaj bo žival predvidoma odpuščena v domačo oskrbo. Nekateri last-niki v pretirani skrbi za svojo žival poskušajo z različnimi pritiski vplivati na našo odločitev. Zavedati se moramo, da mi nosimo odgovornost za morebitne zaplete po anesteziji. Lastnik sam ni sposoben pravilno interpretirati kliničnih znakov, ki kažejo, da utegne priti do zapletov po anesteziji, niti teh zapletov ni sposoben sam reševati. Prav tako se moramo zavedati, da no-simo odgovornost za morebitne zaplete, do katerih bi lahko prišlo zaradi lastnikovih posebnih želja (npr. odklanja britje dlake na mestu, kjer nameravamo vstaviti intravenski kateter).

Osnovni klinični pregled pred anestezijo vključuje mer-jenje telesne temperature, frekvence dihanja in frekvence perifernega pulza, ki jo primerjamo s frekvenco srca (ugotav-ljamo prisotnost pulznega deficita). Preverimo barvo sluznic,

Doc. dr. Alenka Seliškar, dr. vet. med Univerza v Ljubljani, Veterinarska fakulteta, Klinika za kirurgijo in male živali, Gerbičeva 60, 1000 Ljubljana, [email protected]



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beloočnic, čas periferne polnjenosti kapilar (CRT), otipamo periferne bezgavke ter preverimo kožni turgor (ocenimo sto-pnjo hidracije živali). Z avskultacijo srca preverimo delovanje vseh štirih srčnih zaklopk in ugotavljamo morebitno prisot-nost srčnih šumov ali nepravilnosti srčnega ritma. Avskulti-ramo tudi pljuča in ugotavljamo odstopanja od normalnih dihalnih šumov.

Na osnovi kliničnega pregleda in anamneze po potrebi odredimo dodatne preiskave (hematološke, biokemijske pre-iskave krvnega seruma, rentgensko slikanje prsnega koša, ultrazvočni pregled srca, EKG), s katerimi lahko odkrijemo odstopanja od fizioloških vrednosti in ustrezno prilagodimo anestezijski protokol ali celo odložimo poseg.

Pri psih, ki prihajajo na elektivne kirurške posege, je zaradi razširjenosti anaplazmoze v Sloveniji in morebitne subklinične trombocitopenije priporočljivo preveriti število trombocitov. Običajno pri vseh psih pred posegom (izjema so urgent-na stanja, kjer je žival treba takoj anestezirati in pa manjši kirurški posegi) naredimo hemogram z diferencialno belo krvno sliko. Pri starejših psih običajno preverimo še delovanje ledvic (sečnina, kreatinin) in jeter (ALT, alkalna fosfataza), saj se večina anestetikov presnavlja v jetrih in izloča prek led-vic. V primeru spremenjenih vrednosti izpeljemo dodatne diagnostične postopke ter ustrezno prilagodimo anestezijski protokol in odmerke posameznih zdravil.

Podobno velja za mačke, kjer smo še toliko bolj pozorni na prisotnost kroničnega obolenja ledvic, ki ga mačke na začetku bolezni dobro kompenzirajo. Zato pri vseh mačkah starejših od pet let, kljub temu da so navidezno zdrave, preverimo delovanje ledvic (sečnina, kreatinin) ter naredimo hemogram z diferencialno belo krvno sliko. Odvisno od zdravstvenega stanja živali, odredimo še druge preiskave (npr. FeLV/FIV test), katerih rezultati bi lahko vplivali na izbiro anestezijske tehnike.

Ameriško združenje anesteziologov (ASA iz angl. Ameri-can Society of Anesthesiologists) je na osnovi ocene zdravs-tvenega stanja živali pripravilo klasifikacijo zdravstvenih stanj, s katero razvršča živali v pet kategorij:

• ASA 1: zdrave živali brez zaznavnih bolezni (npr. mlada, zdrava mačka ali psica, ki prihaja na elektivno ovariek-tomijo)

• ASA 2: živali z manjšimi do zmernimi sistemskimi bolezn-imi, ki vidno ne ogrožajo zdravja (npr. 8 let stara psica s tumorjem mlečne žleze, brez drugih znakov bolezni, naročena na mamektomijo)

• ASA 3: živali z manjšimi do zmernimi sistemskimi bolezn-imi, ki kažejo manjše do zmerne znake bolezni (npr. 10 let star srednji koder z miksomatozno boleznijo mitralne zaklopke, zdravljen s furosemidom in antihipertenzivi, ki prihaja na multiplo ekstrakcijo zob zaradi paradontalne bolezni)

• ASA 4: živali s hudimi sistemskimi boleznimi, ki ogrožajo njihovo življenje (npr. toksemična psica z zaprtim gnojnim vnetjem maternice, pri kateri je treba čimprej opraviti ovariohisterektomijo; maček z obstrukcijo sečnice in hiperkalemijo s K nad 8 mmol/l)

• ASA 5: moribundne, umirajoče živali, pri katerih ne pričakujemo preživetja naslednjih 24 ur, če ne bodo op-erirane (npr. sindrom razširitve in zasuka želodca pri psu).

Nujne primere dodatno označimo s črko E (iz angl. emergen-cy).

Na osnovi ASA klasifikacije, izkušenosti in znanja kirurga in anestezista ter opremljenosti klinike določimo stopnjo anest-ezijskega tveganja ter izberemo ustrezno anestezijsko tehniko in raven monitoriranja. Živali v večini primerov bolj intenzivno nadziramo med splošno anestezijo, medtem ko je nadzor nad sediranimi živalmi žal slabši. Sedirane živali običajno niso opremljene z monitorji, zaradi prisotnosti grlnega refleksa niso intubirane, kar zveča tveganje za aspiracijo izbruhane ali regurgitirane želodčne vsebine in ne omogoča asistiranega oziroma vodenega predihavanja. Sedirane živali sicer lahko oksigeniramo prek obrazne maske, asistirano predihavanje pa je na ta način do neke mere mogoče le pri mačkah in kuncih, bistveno manj uspešno je pri psih.

Ne smemo pozabiti, da smo s tem, ko smo žival sprejeli v obravnavo, odgovorni za varen in uspešen potek anestezije in da, neglede na lastnikove želje ali potrebe, samostojno spre-jemamo odločitve v zvezi z zdravljenjem živali in posledice, ki iz tega izhajajo. In pri tem ne pozabimo na znani rek »Ni var-nih anestetikov ali varnih anestezijskih tehnik, so samo varni anestezisti«.

Reference

Grimm KA, Tranquilli WJ, Lamont LA, editors. Essentials of small animal anesthesia and analgesia, 2nd ed. Chichester: John Wiley & Sons , 2011: 3-15.

Hall LW, Clarke KW, Trim CM. Veterinary anaesthesia, 10th ed. Edinburgh: WB Saunders, 2001: 1-26.

Seymour C, Butcher R. Anestezija in analgezija (FECAVA izobraževalni moduli, slovenska izdaja). Ljubljana: SVZ, 2005: 77 str.



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PRIPRAVA ZA KIRURŠKE POSEGE

Milan Matko

Širok je dežnik, ki pokriva postopke do kirurškega posega. Zajema štiri osnovne postavke, mejnike; kirurško osebje (kirur-gi, asistenti-pomočniki, anestezisti), pacienta ter predkirurško in kirurško sobo. Za vse štiri pa veljata dva različna kriterija: Kirurški poseg bo, če bo pacient sprejet, torej, če bodo v pos-topkih sprejema izpolnjeni kriteriji, ki dovoljujejo splošno ali drugo anestezijo in operacijo, in če je operacija po pregledu urgentno sprejetega pacienta ali predhodno naročenega pa-cienta potrebna. Drugi kriterij soosebje z ustreznim znanjem, predkirurška in kirurška soba z opremo in instrumenti, vse to pa mora biti vedno pripravljeno v obsegu pričakovanega dela. Tok celotne poti pacienta od sprejema do kirurške sobe je fokusiran na preprečitev infekcije med postopki, striženje, optimalno dezinfekcijo operacijskega polja in na pripravo ter vodenje anestezije in tekočinske oskrbe. Odnos do skrbnika, pristop in delo s pacientom pri sprejemu, v času priprave ter anestezije mora biti korekten in v prijaznih okvirih, brez ne-pravilnih, grobih manipulacij.

Osebje:

• Anestezisti,

• Kirurgi

• Asistenti (veterinarski pomočniki - veterinarski tehniki)

V opisanih postopkih je delo veterinarskih pomočnikov avtonomno, vendar je pričakovano odgovorno in pošteno do ostalih udeležencev (lastniki, sodelavci) in do pacienta. V stat-utu angleškega združenja veterinarjev je člen , ki eksplicitno zahteva od zaposlenih veterinarskih pomočnikov, da delajo odgovorno in izključno po navodilih in pod kontrolo veteri-narjev. Nikakor ni pričakovano odstopanje ali neupoštevanje navodil kirurga in anestezista, ki vodita dva različna med sabo odvisna postopka, ki se začneta s sprejemom pacienta v am-bulanti in naprej v predkirurški sobi do kirurgije. Delo vseh veterinarskih pomočnikov mora biti usklajeno med njimi in z anestezisti ter kirurgi, od sprejema pacienta do kirurške mize. Glede na vrsto kirurškega posega morajo pomočniki, po ustnih navodilih, ali vnaprej predpisanih protokolih pri-praviti in ves čas spremljati pot pacienta. Pričakovano je, da

različni pomočniki sodelujejo pri sprejemu pacienta v ambu-lanti in nato v predkirurški sobi. Veterinarski pomočniki, ki so v kirurški sobi, sprejmejo pacienta šele v njej in so z njim predvidoma do zaključka operacije in po pravilu kirurške sobe med posegom ne zapuščajo.

Pri, delu v predkiruški in kirurški sobi, mora biti osebje us-trezno zaščiteno zaradi preprečitve kontaminacije: Prevleke za obuvala, maske, kape, rokavice in odvisno od zahtevnosti načrtovanega kirurškega posega tudi sterilna obleka. S tem se prepreči prenos infekcije med pacienti in tudi od os-ebja na pacienta in obratno. Noben nepotreben sprehod v kirurško sobo pred in med posegom ni upravičen. Število pomočnikov v kirurški sobi mora biti limitirano na potreben minimum. Pomočniki pomagajo pri sterilnem oblačenju ki-rurga. Vsi kirurški instrumenti so sterilizirani in pakirani ter zloženi v omarah. Potrebne instrumente za načrtovano opera-cijo pomočnik pripravi pred posegom po ustnih navodilih ali napisanih protokolih.

Pacient:

• Naročen za poseg.

• Urgentno sprejet v stanju, ko lahko pričakujemo kirurški poseg.

1. Sprejem pacienta (tešč: 6, 12, 18 ur, pije lahko do ½ ure pred posegom)

2. Klinični pregled z oceno stanja, merjenje triasa (T,P,D)

3. Odvzem krvi: Osnovne preiskave: Ht, skupni pro-teini, urea…

4. Pri pregledu moramo upoštevati, da je pes v okolju, ki se ga običajno boji in mu je neznan, zaradi tega lahko zelo spremeni svoje obnašanje in se lahko nekateri klinični parametri spremenijo in niso za objektivno presojo..

5. Triaža: Sprejem za kirurški poseg ali odločitev o potrebnih dodatnih postopkih in dodatnih pre-iskavah je lahko odvisna od: Starosti, pasme, nefiziološke debelosti, znanih kroničnih obolenjih, ki lahko ali pa nimajo povezave s pričakovanim pose-gom, kliničnega stanja: Šok, anemija, nenormalna temperatura, utrujenost, odsotnost, konstantna bolečina, pareza, paraliza, meteorizem, povračanje, driska, spremenjen pulz, dispneja…

Milan Matko DVM Toplica-center za zdravljenje živali Topolšica 15, 3326 www.toplica-vet.net



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6. Obseg krvnih in drugih preiskav (slikovna diagnos-tika, specialistični pregledi – ortopedski, nevrološki, endoskopski…) je odvisen od fiziološkega stanja pacienta in kriterijev, ki so narekovali kirurški poseg ter pričakovane težavnosti posega.

7. Upoštevati se morajo tudi objektivni parametri presoje izvidov (npr.: Pes, ki ima zaporo črevesja povrača, vendar bo vseeno operiran, da se zapora sanira).

Predkirurška soba:

Tu se pacientu vstavljajo intravaskularni katetri. Za vstav-ljanje arterijskih in centralnih je obvezna uporaba sterilnih rokavic. Doda se infuzijski sistem in trakovi za fiksacije, ki pacienta spremljajo do zaključka posega, nato se zavržejo. Po potrebi se pacientu izprazni zadnji del črevesa in se ga kateterizira. Začne se ustrezna anestezija po protokolu za predvideni kirurški poseg. Z monitoringom se spremljajo vi-talni parametri. Opravi se striženje operacijskega polja in širše sesanje pacienta. Za zahtevnejše posege se psa dan preje okopa. Opravi se prva dezinfekcija operacijskega polja.

Kirurška soba:

Naj bo velika s čim več naravne svetlobe, skoraj obvezno z nadtlakom. Dezinfekcija zraka in prostora se lahko oprav-lja z baktericidnimi lučmi. V kirurško sobo sprejmejo pacienta pomočniki, ki so samo v kirurški sobi. Tu se opravi ponovna, dokončna dezinfekcija. Operacijsko polje se pred posegom popolnoma izolira od ostale površine telesa.

Pred in med posegom mora biti gibanje v kirurškem pros-toru omejeno in umirjeno. Izogibamo se nepotrebnega go-vorjenja. Oseba izdiha v povprečju 3.000 do 50.000 bakterij v minuti, več med govorjenjem. Govorjenje naj bo omejeno na nujno kirurško komunikacijo. Za vsak kirurški poseg se men-jajo kirurške maske.

Sterilni instrumenti se dodajajo kirurgu po fazah operacije.

Po končanem posegu prevzamejo pacienta zunanji pomočniki. V kirurški sobi se pripravi za novega pacienta. Vse kar se je uporabljalo pri prejšnjem se odstrani, vključno z infuzijskimi sistemi. Kirurška miza se pripravi za naslednjega pacienta z mehanskim čiščenjem in dezinfekcijo. Tla se brišejo v izjemnih slučajih, ko je prišlo da večjega onesnaženja.

ZAKLJUČEK

Postopki od sprejema pacienta do začetka kirurškega posega, ki je vdor v integriteto organizma, zahtevajo odgo-vorno in dosledno delo. Vsak korak in postopek veterinarskih pomočnikov morata biti premišljena, da se prepreči kontami-nacija, ki grozi s petih strani: Iz pacienta, od osebja, iz vode, ki služi za čiščenje, iz okolja (zraka, predmetov…), iz kon-taminiranih dezinficiensov in direktno iz rok pri manipulaciji s pacientom, pri dajanju katetrov, priklapljanju infuzijskih sis-temov in pri striženju ter dezinfekciji. Pomočniki morajo imeti ustrezno znanje, da ne spregledajo odmikov od normale pri vodenju anestezije in tekočinske oskrbe in tudi v tem seg-mentu omogočijo čim večjo optimizacijo poti od sprejema pacienta do kirurškega posega.



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KLINIČNI PRISTOP PRI GARJAVOSTI

Ana Rostaher

Clinico-pathological descriptions of dermatoses caused by mite

Canine demodicosisCan be localized (picture 1) or generalized with >3 areas affected (picture 3). The adult parasites are cigar shaped and have

8 legs.

Canine sarcoptic mange

The main clinical sign is severe pruritus, erythema and papules (picture 1), with time skin become very thickened and crusted (picture 2). The parasites are oval to round with short legs (8) on microscopical examination.

Feline sarcoptic mangeThe main clinical signs is severe pruritus with crusting, usually on the head (picture 1) or the limbs (picture 2). On microscopy

one can find eggs, fecal pellets (scybala) and round to oval adult mites with short legs.

Ana Rostaher, dr.vet.med., Dipl ECVD University of Zurich, Vetsuisse Faculty [email protected]



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CheyletiellosisThe main clinical feature is scaling (picture 1), sometimes one can see moving scales, therefore the expression ‘walking

dandruff’. Usually the dorsum is affected (picture 2). On the microscopical examination (picture 3) the mites are saddle shaped and have an indentation in the middle of the body (*) and the tipical hook-like mouth parts called palpi (arrow)

Otodectes

The main typical sign is aural pruritus, which can be elicited by manipulation (Pinal-pedal reflex as in sarcoptic mange; pic-ture 1). The ears are usually filled with a dark brown dry material, similar to coffee grounds (picture 2). If one is very attentive at the start of the otoscopic examination, they can be visible as whitish moving points running away from the light source (picture 3). Microscopically they show a large body and 8 legs which are very long in comparison to other mites (picture 4).

Trombiculosis

The dermatoses with these mites are usually seen in autumn. These mites live in decaying vegetation’s, so the skin lesions usually develop on body areas with close contact with the ground like feet (picture 1), abdomen or head. The larve are having 3 pairs of legs and are oval shaped and can be visible by nacked eye (picture 1)

References

Miller HW, Griffin CE, Campbell KL. Parasitic skin disease. In: Muller & Kirk’s Small Animal Dermatology, eds. Elsevier (Missouri, USA), 2013: 284-342.



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INTERNISTIČNE URGENCE

Darja Pavlin

Povzetek

V prispevku je opisanih nekaj najpogostejših laboratori-jskih odstopanj, ki lahko predstavljajo življenje ogrožujoče stanje pri psih in mačkah. To so zlasti hiper- in hipokalemi-ja, hiper- in hipokalcemija in hipoglikemija. Zanje je nujno, da jih prepoznamo hitro oziroma takoj odreagiramo, saj je lahko vsakršno odlašanje z ustreznim zdravljenjem usodno za našega pacienta.

HIPERKALEMIJA (kritična vrednost K > 7 mmol/L) (1)

Kako jo prepoznamo? Žival kaže znake oslabelosti mišic (ko kalij preseže 7,5 mmol/l), predvsem pa hiperkalemijo lahko prepoznamo po tipičnih odstopanjih na EKGju.

Možni vzroki: pseudohiperkalemija (trombocitoza, lev-kocitoza, hemoliza med jemanjem krvi), metabolna acidoza, nekontrolirani DM, masivna travma tkiv, predoziranje digi-talisa, dehidracija (blaga hiperkalemija), oligurična, anurična odpoved ledvic, urinarna obstrukcija, ruptura urinarnih poti, hipoadrenikorticizem (Addisonova bolezen), pseudohipoad-renokorticizem (infestacija s Trichuris sp.)

Princip zdravljenja: Hiperkalemija ima v prvi vrsti kardiotoksične učinke in povzroča podaljšano depolarizacijo prevodnega sistema miokardija in s tem bradikardijo. Zdrav-ljenje hiperkalemije poteka preko treh različnih mehanizmov, odvisno od stopnje hiperkalemije in izraženosti kliničnih zna-kov:

• razredčitev serumskega kalija, izboljšanje ledvične prekr-vitve in povečanje izločanja K preko ledvic z uporabo infuzijskih raztopin, ki vsebujejo malo ali nič K (Ringer laktat, 0.9% NaCl, 0.45% NaCl);

• prerazporeditev K iz izvenceličnega prostora intracelu-larno (Na bikarbonat, glukoza, inzulin, terbutalin);

• preprečevanje direktnih kardiotoksičnih učinkov (Ca glukonat);

HIPOKALEMIJA (kritična vrednost K < 3 mmol/L) (1)

Kako jo prepoznamo? Posledice hipokalemije lahko razde-limo v 4 kategorije: metabolne, nevromuskularne, ledične in kardiovaskularne. Hipokalemija privede do oslabelosti skel-etnih mišic in v hujših primerih disfunkcije dihalnih mišic in diafragme, saj je kalij potreben za vzdrževanje mirovnega membranskega potenciala celic. Tipična je ventrofleksija vratu in glave, trda hoja, lahko se pojavi paralitični ileus in atonija želodca (ko kalij pade pod 2,5 mmol/l). Odstopanja na EKGju, povezana s hipokalemijo, so atrijske in ventrikularne tahiarit-mije in ventrikularna fibrilacija.

Možni vzroki: anoreksija, bruhanje, driska, vnos večjih količin infuzijskih raztopin z majhno vsebnostjo K, hipoter-mija, hiperinzulinemija, aplikacija diuretikov, Cushingov sin-drom, preveliki odmerki mineralokortikoidov, ledvičnabolezen (poliurija/polidipsija), postostobstrukcijska diureza, poliurija, hipomagnezemija.

Princip zdravljenja: Pri zdravljenju moramo najprej na-domestiti deficit kalija, nato pa rešiti primarno bolezen, ki je privedla do hipokalemije. Kalij vedno apliciramo počasi, zaradi možne kardiotoksičnosti.

Tabela: okvirna navodila za rutinsko nadomeščanje kalija pri hipokalemičnih živalih. Vrednosti so le orientacijske in jih je potrebno prilagoditi glede na patofiziološke potrebe vsakega pacienta posebej!

Serumska koncentracija ml KCl/500 ml Največja dovoljena hitrost K (mmol/L) 0.9% NaCl aplikacije infuzije (ml/kg/h)

< 2 40 6

2.1 - 2.5 30 8

2.6 - 3 20 12

3.1 - 3.5 15 18

3.6 - 4.5 10 25

HIPERKALCEMIJA (kritična vrednost Ca >3.75 mmol/L) (2)

Kako jo prepoznamo? Tipični klinični znaki so huda po-liurija in polidipsija (psi, ne mačke), anoreksija, zaprtje, os-labelost in letargija. Hudo prizadete živali lahko postanejo ataksične, pojavi se trzanje mišic, epileptiformni napadi in koma. Na EKGju se pojavi bradikardija, podaljšan PR interval,

Doc. dr. Darja Pavlin, dr. vet. med., Univerza v Ljubljani, Veterinarska fakulteta, Klinika za kirurgijo in male živali, Gerbičeva 60, 1000 Ljubljana



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razširjen QRS kompleks, razpirjen T zobec. Bradiaritmije lahko napredujejo v popoln srčni blok, asistolo in srčni zastoj.

Možni vzroki: paraneoplastični sindrom (limfom, mul-tipli mielom, različni karcinomi: paranalke, ščitnica, pros-tata, mlečna žleza), primarni hiperparatiroidizem (tumor na obščitnici), akutna in kronična ledvična bolezen, hipervitami-noza D (iatrogena, zastrupitev z določenimi rastlinami, roden-ticidi s holekalciferolom), hipervitaminoza A, lezije na skeletu (osteomielitis, novotvorbe - primarne ali metastaze, hiper-trofna osteodistrofija, infarkt kosti, osteoporoza), zastrupitev z rozinami/grozdjem.

Princip zdravljenja: Najprej moramo vzpostavi normalno hidracijo oz. normalni intravenski volumen, saj hipovolemija zmanjša glomerularno filtracijo in s tem izločanje Ca iz or-ganizma. Nato lahko uporabimo zdravila s kalciuretičnim učinkom (furosemid) in kortikosteroide.

HIPOKALCEMIJA (kritična vrednost Ca < 2 mmol/L) (2)

Kako jo prepoznamo? Najpogosteje se pojavijo mišični tremorji in fascikulacije, praskanje obraza, mišični krči, trda hoja, nemir, agresija, dezorientiranost. Redko pride do epilep-tiformnih napadov, sopenja, povišane telesne temperature, pri mačkah pa prolapsa tretje veke.

Možni vzroki: primarni hipoparatiroidizem, kronična ali akutna odpoved ledvic, hipoalbuminemija, akutni pankrea-titis, eklampsija, intestinalna malabsorbcija, - zastrupitev z etilenglikolom, transfuzija citratne kravi, pomanjkanje vitam-ina D, sindrom lize tumorja, masivna travma tkiv, hiperfos-fatemija

Princip zdravljenja: Intravenska aplikacija kalcijevih pre-paratov, ki jih je zaradi možnih kardiotoksičnih učinkov potrebno aplicirati počasi in pod kontrolo EKG-ja.

HIPOGLIKEMIJA (kritična vrednost glu < 3 mmol/L) (3)

Kako jo prepoznamo?V normalnih razmerah je glukoza glavni vir energije za možganske celice, zato so možgani pri-marni organ, na katerega ima hipoglikemija negativni učinek. Znaki variirajo od blage depresije do stuporja, kome ali kon-vulzij. Pri kritično bolnih živalih je že blaga hipoglikemija lahko pokazatelj sepse.

Možni vzroki: neonatalna oz. juvenilna hipoglikemija (zlasti majhne pasme), kombinacije stradanja, povečane telesne aktivnosti, stresa, predoziranje inzulina oz. drugih hipoglikemičnih zdravil, funkcionalni tumor β celic pankreasa (inzulinom), sepsa, malabsorpcija, obolenja jeter, hipoadre-nokorticizem

Princip zdravljenja: Konvulzije zdravimo najprej z aplikacijo glukoze in če je potrebno tudi z antiepileptiki oz. pomirjevali. Nadaljnja terapija mora biti usmerjena k primarnemu vzroku hipoglikemije.

Glukozo apliciramo v naslednjem odmerku:

50% raztopina glukoze 20% raztopina glukoze

Mladiči 0.2 ml/100 g t.t. 0.8 ml/100 g t.t

Majhni psi 3-5 ml 6-12 ml

Veliki psi 10-15 ml 20-35 ml

Pri alikaciji glukoze se izogibamo i.v. aplikacije zelo visokih koncentracij (50%), uporabljamo do največ 25% glukozo(pri odraslih živalih) oziroma naveč 10% glukozo pri mladičih do 4mesecev. Priporočljivo je, da glukozo v koncentraciji nad 5% apliciramo skozicentralno veno zaradi hiperosmotskega učinka raztopine. Glukozo nadomeščamo intravensko, dokler se živali ne povrne apetit, takrat ji ponudimo hrano.

Reference

1. Riordan LL, Schaer M. Potassium disorders. In: Silverstein DC, Hopper K., eds. Small animal critical care medicine. St.Lous: Saunders Elsevier, 2009: 229-233.

2. Green Todd, Chew DJ. Calcium disorders. In:Silverstein DC, Hopper K., eds. Small animal critical care medicine. St.Lous: Saunders Elsevier, 2009: 233-239.

3. Reusch CE, Robben JH, Kooistra HS. Endocrine pancreas. In: Rijnberk A, Kooistra HS, eds. Hannover: Schlütersche Verlagsgesellschaft, 2010: 155-187.



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ROJSTVO S CARSKIM REZOM – ELEKTIVNI ALI URGENTNI CARSKI REZ

Maja Zakošek Pipan, Tanja Plavec Univerza v Ljubljani, Veterinarska fakulteta, Gerbičeva 60, 1000 Ljubljana [email protected], [email protected]

V zadnjem desetletju se veterinarji vse pogosteje srečujejo z željo rejcev, ki želijo pri psicah opraviti elektiven carski rez. Elektiven carski rez sicer priporočamo pri psicah, pri katerih je v preteklosti že prišlo do distocije in urgentnega carskega reza, pri psicah z manj kot tremi plodovi ter pri pasmah kjer imajo plodovi velike glave oziroma medenica matere ni do-volj široka (bokserji, buldogi, mopsi, boston terierji, škotski terierji). Nekateri specialisti priporočajo preventivni carski rez tudi pri tistih psicah, ki imajo več kot 8 plodov, zaradi more-bitne pretirane izčrpanosti matere. Na ta način se izognemo urgentnemu carskemu rezu, s tem pa povečamo verjetnost preživetja mladičev in omogočimo hitrejše okrevanje psice. Ker lahko carski rez varno opravimo šele 63 dan po LH valu, je v primeru elektivnega carskega reza nujno potrebno natančno določiti čas poroda.

Urgenten carski rez je indiciran v primeru distocije, ki lahko nastane kot posledica zgoraj navedenih vzrokov; v pri-meru neustreznega krčenja maternice, ki ga zaznamo z UZ; nezadostnega krčenja maternice, ki ga z uporabo zdravil ne uspemo povečati, neustreznega položaja mladiča v porodnem kanalu; strukturnih motenj porodnega kanala in kadar z UZ zaznamo, da so plodovi v stresu.

V kratkem predavanju bova predstavili prednosti in sla-bosti elektivnega oziroma urgentnega carskega reza, povedali v katerih primerih je smotrno opraviti elektiven carski rez in se osredotočili na kaj je potrebno biti pozoren pri urgentnem car-skem rezu. Kljub temu, da je carski rez varen poseg, je lahko namreč povezan s številnimi komplikacijami. Najpogostejše med njimi so hude krvavitve, infekcije in manjša verjetnost preživetja matere in mladičev.

EPIDURALNA ANALGEZIJA PRI KRITIČNO BOLNIH PSIH

Bojan Edvard Frantar, Matej Zupanc Veterinarska bolnica Šentjur, Ambulanta VET-Med, Glonarjeva ulica 2, 1000 Ljubljana, [email protected]

V prispevku predstavljamo tehnike enkratne aplikacije epi-duralne analgezije in kontinuirane – z epiduralnim katetrom. Predstavljamo vrste in indikacije uporabe epiduralne anestezi-je in analgezije pri kritično bolnih psih, v pre, med in poopera-tivnem obdobju. V prispevku prikazujemo tudi naše izkušnje in rezultate z uporabo epiduralne analgezije.

NAČRTOVANJE IN IZVEDBA RESEKCIJ TUMORJEV

Janoš Butinar1, Ana Rejec1, Tommaso Pilla1, Jani Pečar2 1 Bolnica za živali Postojna, Cesta v Staro vas 20, 6230 Postojna, [email protected] 2 Hraše 31c, 1216 Smlednik, [email protected]

V humani onkologiji se pri tumorskih boleznih za ozdrav-itev smatra preživetje vsaj 5 let. K temu še vedno največ prispeva kirurško zdravljenje, tesno mu sledi radioterapija. V veterinarski onkologiji je kirurško zdravljenje, posebej kot monoterapija še pogostejše kot v humani onkologiji. V hum-ani in veterinarski onkologiji je dokazano, da so rezultati preživetja boljši, če pacienta operirajo kirurški onkologi s po-globljenim znanjem biologije tumorjev in kirurške onkologije.

Resekcija tumorja je sestavljena iz dveh praviloma ločenih, a hkrati neločljivo povezanih sestavin – pravilne odstranitve tumorja in rekonstrukcije defekta. Pravilna odstranitev tu-morja je usmerjena v čim boljšo dolgoročno prognozo, re-konstrukcija defekta pa v funkcionalno in kozmetično spre-jemljivost. Določanje razširjenosti tumorske bolezni in stanja pacienta (angl. staging) je nujen del celotnega postopka, ki mora biti opravljen pred operacijo. Metode za uspešno oprav-ljen staging so skrben onkološki klinični pregled, RTG, UZ, MR, scintigrafija, CT in laboratorijske preiskave. V onkologiji je CT najpomembnejša slikovna diagnostika, ki omogoča do-ber staging in načrtovanje operacij po načelih kompartmentov (anatomskih razdelkov, omejenih z jasnimi barierami) in upo-rabe tkiv, odpornih na širjenje tumorjev kot varnostnih robov. Biologija tumorjev nalaga načrtovanje obsežnosti resekcij, kar običajno prevedemo v izraz doseganje »zdravih robov«. Bi-ologijo tumorjev spoznamo s citopatološko, histopatološko, imunohistokemijskimi metodami, pretočno citometrijo, z znanjem onkologije in uporabo ustrezne literature.

Med rekonstrukcijskimi tehnikami vedno najprej izbi-ramo enostavne in postopoma prehajamo na naprednejše in zahtevnejše. Prispevek bo na lastnih primerih prikazal post-opke diagnostike, staginga, načrtovanje in izvedbo resekcij in rezultate.

PERFORATIVNE POŠKODBE OČESA

Tadej Zemljič Veterinarske storitve, Tadej Zemljič s.p., Milčinskega ulica 62, 1000 Ljubljana, [email protected]

Perforacija očesa (roženice ali beločnice) je največkrat pos-ledica ostre travme.

Natančen očesni pregled je kritičnega pomena, saj lahko obseg in specifika intraokularnih lezij bistveno spremeni tera-pevtski pristop, prognozo in rezultat zdravljenja.

Pri manjših perforacijah, ki tesnijo, šivanje ni vedno potrebno. Obsežnejše perforativne rane je potrebno san-irati operativno, saj v nasprotnem primeru pogosto pride do pojava kroničnega uveitisa, nastanka katarakte in glavkoma ter izgube vida ali celo očesa. V primeru izpada šarenice je potrebna repozicija ali amputacija izpadlega tkiva. Če je prisotna tudi laceracija lečne kapsule, je pogosto indicirana ekstrakcija leče, lahko celo istočasno s sanacijo perforacije roženice. Rane brez izgube tkiva (primarnega ali kot posled-ica debridmenta) zašijemo direktno, zato je ključna kirurška obdelava z minimalno možnim debridmentom v čim krajšem času od nastanka poškodbe. V kolikor rane ni mogoče zašiti direktno, je potrebna rekonstrukcija z uporabo bodisi last-nega tkiva (npr. roženično-veznična transpozicija ali veznični



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reženj) oziroma nativnega ali predelanega donorskega tkiva (npr. roženica, beločnica; intestinalna submukoza).

Za kirurško sanacijo perforativnih očesnih poškodb je potrebna ustrezna povečava, inštrumentarij, kirurški mate-rial in poznavanje načel mikrokirurgije. Prav tako je kritičnega pomena tudi ustrezna fiksacija pacijenta med pregledom, previdna manipulacija očesa med pripravo na kirurški poseg ter uporaba ustrezne anestezije, v izogib povečanja očesnega pritiska in s tem morebitne posledične ekspulzije intraoku-larnih tkiv. Poleg morebitnega kirurškega posega je za san-acijo očesnih perforacij potrebna tudi topikalna in sistemska medikamentozna terapija, ki obsega antibiotike, protivnetna in protibolečinska zdravila, ter midriatike/cikloplegike.

TRANSSFENOIDNA HIPOFIZEKTOMIJA KOT MOŽNOST ZDRAVLJENJA CUSHINGOVE BOLEZNI

Darja Pavlin Univerza v Ljubljani, Veterinarska fakulteta, Klinika za kirurgijo in male živali, Gerbičeva 60, 1000 Ljubljana, [email protected]

Zdravljenje hipofizne oblike Cushingovega sindroma je lahko bodisi medikamentozno (adrenokortkostatik trilostan, ki je najprimernejša oblika zdravljenja za mikrotumorje hipofize, ki tipično rastejo počasi in je tveganje za razvoj nevroloških znakov majhno), druga možnost je radioterapija (predvsem primerna za zdravljenje makrotumorjev, vendar se učinek pokaže šele čez več mesecev po obsevanju, poleg tega živali pogosto potrebujejo še dodatno medikamentozno terapijo), tretja možnost pa je kirurško zdravljenje (hipofizektomija, ki je najprimernejša oblika zdravljenja za srednje velike tumorje pri mlajših psih v dobri kondiciji). Ker je slednja možnost iz-vedljiva samo v visoko specializiranih ustanovah z izkušeno kirurško ekipo v tujini in je povezana tudi z nezanemarljivimi stroški, se lastniki psov s Cushingovim sindromom v Sloveniji le redko odločajo zanjo. Zato želimo v prispevku predstaviti diagnostiko, kirurško zdravljenjein doživljenjsko postopera-tivno oskrbo šestletne psičke pasme Boston terier z mak-roadenomom hipofize, z namenom, da bi olajšali odločitev za tovrstno zdravljenje še za kakšnega drugega primernega pacienta iz Slovenije.Transsfenoidna hipofizektomija je bila opravljena na Veterinarski fakulteti Univerze v Utrechtu, Nizozemska. Kljub nekaj resnejšim postoperativnim zapletom (povišan intrakranialni tlak, edem mehkega neba, zaradi kat-erega je potrebovala začasno traheostomo) je psička odlično okrevala. Klinični znaki Cushingove bolezni so izzveneli zelo hitro, zaradi česar se je po besedah lastnikov kvaliteta njen-ega življenja izrazito izboljšala kljub temu da bo doživljenjsko potrebovala nadomestno hormonsko terapijo s hidrokortizo-nom, tiroksinom in antidiuretičnim hormonom. Najlepša hva-la doc. dr. Sari Galac za veliko pomoč pri organizaciji celotne kirurške obravnave in prof. dr. Bjornu Meiju ter preostali ekipi Veterinarske fakultete Univerze v Utrechtu za kirurški in post-operativni del posega, ki je bil izveden na resnično vrhunskem nivoju.

TRAVMATSKA POŠKODBA MOŽGAN: STREL V GLAVO

Petra Jelovčan 1, Nina Mlakar 2 1 Univerza v Ljubljani, Veterinarska fakulteta, Klinika za kirurgijo in male živali, Gerbičeva 60, 1000 Ljubljana, [email protected] 2 Univerza v Ljubljani, Veterinarska fakulteta, Ambulanta za ptice, male sesalce in plazilce, Inštitut za zdravstveno varstvo perutnine, Gerbičeva 60, 1000 Ljubljana, [email protected]

Hude poškodbe glave so pri živalih in ljudeh pogosto pov-ezane s smrtnim izzidom. Zaradi kompleksnosti in specifičnosti posameznega primera ostaja ustrezno zdravljenje tovrstnih poškodb v veterinarski medicini nedorečeno in predstavlja izziv mnogim veterinarjem. Poškodba glave je dokaj pogos-ta poškodba psov in mačk, ki je največkrat posledica avto-mobilske nesreče, padca iz višine, napada druge živali, tope travme ali strelnega orožja. Travmatska poškodba možgan je sestavljena iz primarne poškodbe, ki nastane ob travmatskem dogodku in zakasnele sekundarne poškodbe. Ta je posledica krvavitve, ishemije in edema možgan. Zdravljenje tovrstnih poškodb je usmerjeno v stabilizacijo pacienta, preprečevanje nastanka oz. progresije sekundarnih poškodb in vzdrževanje primerne perfuzije možgan. S predstavitvijo kliničnega prime-ra psa s poškodbo možgan, kot posledico strela v glavo, želiva predstaviti problematiko zdravljenja hudih poškodb glave pri mačkah in psih ter primerjava našo terapijo z literaturnimi priporočili.

ULTRASONOGRAFSKA DIAGNOSTIKA URGENTNIH ABDOMINALNIH IN TORAKALNIH STANJ

Nina Mlakar1, Aleksandra Domanjko Petrič2 1 Univerza v Ljubljani, Veterinarska fakulteta, Ambulanta za ptice, male sesalce in plazilce, Inštitut za zdravstveno varstvo perutnine, Gerbičeva 60, 1000 Ljubljana, [email protected] 2 Univerza v Ljubljani,Veterinarska fakulteta, Klinika za kirurgijo in male živali, Gerbičeva 60, 1000 Ljubljana, [email protected]

Pri obravnavi kritičnega pacienta so glavni cilji veterinarja zgodnje odkritje in zdravljenje primarnega vzroka ter odprav-ljanje sekundarnih posledic, ki bi lahko povzročile nepoprav-ljive poškodbe organov, organskih sistemov ali celo smrt živali. Pogosto s samim kliničnim pregledom, hematološko in biokemijsko preiskavo krvi ali urinogramom ne moremo postaviti dokončne diagnoze in se zato poslužimo dodatnih slikovnih diagnostičnih metod. Med njimi v diagnostiki t.i. akutnega abdomna ali suma druge abdominalne ali torakalne patologije po naših izkušnjah prvo mesto zaseda ultrasono-grafija. Metoda je zelo uporabna pri odkrivanju in lociranju tujkov v prebavilih, obstrukcij votlih organov, odkrivanju ileu-sa, proste tekočine v telesnih votlinah, ruptur votlih organov in tumorjev, zasuka vranice, odkrivanju tumorjev v trebušni ali prsni votlini, diafragmatske hernije, pankreatitisa, idr.... Rezultati ultrasonografske preiskave so pogosto ključni za pravilno in hitro odločitev zdravljenja kritičnega pacienta. Na-men raziskave je predstaviti ultrasonografske karakteristike najpogostejših urgentnih abdominalnih in torakalnih stanj.



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ZAGOTAVLJANJE KAKOVOSTI LABORATORIJSKIH REZULTATOV »IN HOUSE« VETERINARSKIH LABORATORIJEV

Erika Furman Labor InVitro GmbH, Rennweg 95 1030 Wien, Avstrija, [email protected]

Veliko veterinarskih organizacij vodi lastni klinično-patološki laboratorij, t.i. »in-house« laboratorij. Le redke pa imajo izdelan sistem zagotavljanja kakovosti laboratorijskih rezultatov (Quality assessement, QA). Vsak laboratorijski iz-vid/rezultat je toliko zanesljiv, kolikšen je poudarek na kontroli kvalitete meritve.

V humanih laboratorijih QA urejajo različni regulatorni in akreditacijski organi.

V veterinarski medicini ni obvezujoče regulacije za izvajan-je testiranja v »in-house« veterinarskih laboratorijih. Ameriško združenje veterinarske klinične patologije (American Society for Veterinary Clinical Pathology) je izdalo priporočila za izva-janje QA v »in-house« laboratorijih.

Namen QA je, da se uspešno in pravočasno odkrijejo ter odpravijo napake v predanalitični (odvzem vzorca, transport), analitični (meritev) in postanalitični (poročanje/interpretacija izvida) fazi/procesu pridobivanja izvidov. Predanalitično in postanalitično fazo se lahko nadzoruje z ustreznim znanjem in upoštevajem določenih pravil. Nadzor analitične faze lahko poteka z uporabo primernih metod za merjenje določenih analitov, ustreznim skladiščenjem in uporabo reagentov, prim-ernim vzdrževanjem analizatorjev, ustreznim šolanjem kadra ter doslednim izvajanjem QA programa. Takšen program je možno izvajati na več načinov oz. s kombinacijo le-teh.

Eden od načinov je kontrola kakovosti (quality control, QC) analitične faze z merjenjem kontrolnega materiala. Z re-zultati meritve kontrolnega materiala izračunamo natačnost, oz. koeficient variacije (coeficient of variation, CV) in pravil-nost (bias, sistematično napako meritve) meritve določenega analita. CV in bias skupaj predstavljata skupno opazovano napako meritve (total observer error, TEobs). Če je TEobs < TEa (total analytical error, največja dovoljena skupna napaka določena v literaturi), to pomeni, da meritev določenega ana-lita dosega standarde zahtevane kvalitete.

Za vsakodnevni nadzor analitične faze se uporablja 13s pravilo (rezultat mora biti znotraj treh standardnih deviacij od ciljne vrednosti). Če temu ni tako, pomeni, da se je zgodila napaka, rezultat se zavrže. Po odpravi napake se meritev ponovi in če je rezultat v skladu z 13s pravilom, se meritev lahko sprejme. Meritev na vzorcih pacientov pred sprejemom rezultatov kontrole, se ne opravlja.

DISGERMINOM JAJČNIKA PRI PSICI

Maja Brložnik1, Mujagić Emir1, Siniša Faraguna2, Tanja Švara3, Mitja Gombač3 1 PRVA-K, Klinika za male živali, Gorkičeva 6, 1000 Ljubljana, [email protected]

2 študent Veterinarske fakultete, Gerbičeva 60, 1000 Ljubljana, [email protected] 3 Univerza v Ljubljani, Veterinarska fakulteta, Inštitut za patologijo, sodno in upravno veterinarstvo, Gerbičeva 60, 1000 Ljubljana, [email protected], [email protected]

Novotvorbe jajčnikov so pri psicah relativno redko obolen-je. Tumorji zarodnih celic, kamor uvrščamo maligni disgermi-nom, so med novotvorbami jajčnika najredkejši. V prispevku predstavljamo disgerminom jajčnika z metastazami po peči pri psici.

Petletno psičko pasme bordojska dogasmo na kliniko sprejeli zaradi izostajanja gonitev. Z ultrazvočno preiskavo trebuha smo ugotovili tumor na desnem jajčniku, ki je meril 6 x 4 cm, zato smo opravili ovarihisterektomijo. Pri posegu smo na peči ob jajčniku opazili multifokalne okrogle spre-membe, zato smo odstranili tudi del peče. S citološko preiska-vo odtisov tumorja jajčnika smo ugotovili posamezne celice in skupine močno anizocitotičnih in pleomorfnih – okroglih do poligonalnih novotvorbnih celic, z zmerno količino svetlo sive citoplazme in močno anizokariotičnimi jedri in velikim jedrcem. Posamezne celice so bile dvojedrne in v delitvi. S citološko preiskavo smo novotvorbo diagnosticirali kot disger-minom jajčnika, t. j. maligni tumor jajčnikovih zarodnih celic. S patohistološko preiskavo smo potrdili citološko diagnozo in spremembe v peči diagnosticirali kot zasevke tumorja. Last-niki so odklonili nadaljnjo diagnostiko in zdravljenje.

ORTOTIČNA OSKRBA PSA PO OBSEŽNI POŠKODBI TARZALNEGA SKLEPA

Anita Čurin1, Jurij Žel2, Mojca Divjak3 1 Univerza v Ljubljani, Zdravstvena fakulteta, Študentka ortotike in protetike, Zdravstvena pot 5, 1000 Ljubljana, [email protected] 2 Univerza v Ljubljani, Veterinarska fakulteta, Klinika za kirurgijo in male živali, Gerbičeva 60, 1000 Ljubljana, [email protected] 3 Univerza v Ljubljani, Zdravstvena fakulteta, predstojnica oddelka za ortotiko in protetiko, Zdravstvena pot 5, 1000 Ljubljana, [email protected]

Travmatske poškodbe ligamentov v tarzalnem sklepu, so dokaj pogoste. Če so le te tako hude, da pes ne more vz-postaviti normalnega vzorca hoje, se naredi artrodeza. Lahko pa se odločimo za alternativno rešitev, to je oskrba tace z opornico- ortozo.

Namen raziskovalnega dela je izdelati ortozo po mavčnem odlitku, za psa po poškodbi medialnega kolateralnega liga-menta, ter ugotoviti njeno učinkovitost. Pes tace, zaradi bolečin in nestabilnosti sklepa, ne uporablja. Z aplikacijo or-toze, bi psu omogočili varnejšo, bolj stabilno in učinkovito hojo, predvsem pa preprečili nadaljnje poškodbe in artrodezo.

Ortozo smo izdelali po standardnem postopku, ki ga nav-aja pregledana strokovna literatura na področju ortotike in protetike. Vsi postopki so v prispevku tudi opisani. Uspešnost ortoze smo ocenjevali na podlagi obremenitve zadnjih okončin po metodi dveh tehtnic, klinične ocene šepanja, napredovan-jem mišične atrofije prizadete okončine in ocene lastnika z kratkim vprašalnikom o učinkovitosti in uporabnosti ortoze. Po postopnem uvajanju ortoze smo začeli opažati izboljšave.



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Po enem mesecu uporabe je pes začel hoditi tekoče, celo tekati in skakati. Metoda dveh tehtnic je pokazala zanemar-ljive razlike v obremenjevanju teže na zadnjih okončinah. Sto-pnja šepanja pa se je iz ocene 4, izboljšala na oceno 1.

Na področju veterine v Sloveniji, je aplikacij ortoz zelo malo. Glede na pozitivne rezultate, učinkovitosti takšne ap-likacije, lahko določene poškodbe in nestabilnosti sklepov os-krbimo z takšnimi pripomočki.

PIOTORAKS PRI MAČKI – KAJ STORITI, DA BO ZDRAVLJENJE USPEŠNO?

Elvira Jagodič1, Jurij Žel2, Tanja Plavec2, Martin Kovše3, Mitja Gombač4, Tanja Švara4, Irena Zdovc5, Majda Golob5 1 študentka Veterinarske fakultete, Gerbičeva 60, 1000 Ljubljana, [email protected] 2 Univerza v Ljubljani, Veterinarska fakulteta, Klinika za kirurgijo in male živali, Gerbičeva 60, 1000 Ljubljana, [email protected], [email protected] 3 Veterinarska postaja Slovenj Gradec, Celjska cesta 126, 2380 Slovenj Gradec 4 Univerza v Ljubljani, Veterinarska fakulteta, Inštitut za patologijo, sodno in upravno veterinarstvo, Gerbičeva 60, 1000 Ljubljana, [email protected], [email protected] 5 Univerza v Ljubljani, Veterinarska fakulteta, Inštitut za mikrobiologijo in parazitologijo, Gerbičeva 60, 1000 Ljubljana, [email protected]

Piotoraks pri mačkah predstavlja svojevrsten izziv tako za natančno laboratorijsko diagnostiko kot za uspešno zdrav-ljenje. Običajno je posledica ugriza ali bakterijske pljučnice. Torakocenteza in citološka analiza punktata sta prvi korak v smislu hitrega diagnostičnega ter (začasnega) terapevtskega ukrepa, vendar predstavljata komaj začetek intenzivne obrav-nave pacienta. Pri zdravljenju piotoraksa je ključna natančna mikrobiološka determinacija povzročitelja, ki je pomembna za dolgoročno ciljano antibiotično terapijo. Običajno sta nu-jna agresivno nemedikamentozno zdravljenje, ki vključuje vstavitev torakalnih drenaž, redno lavažo prsne votline ter hospitalizacijo,in pravilna izbira ustreznega antibiotika.

V prispevku opisujemo klinična primera piotoraksa pri mački, povzročena z bakterijami iz rodu Actinomyces. Prvi primer piotoraksa smo diagnosticirali pri triletni evropski kratkodlaki mački, drugi primer pa pri osemletnem mačku pasme Maine Coon. Obe mački sta bili zaradi dihalne stiske, neješčnosti in shiranosti hospitalizirani v veterinarski am-bulanti. Pri obeh smo s punkcijo odvzeli vzorec tekočine iz prsne votline za citopatološko in bakteriološko preiskavo. S citopatološko preiskavo smo v razmazu tekočine ugotovili ve-like bakterijske kolonije, ki so jih sestavljale nitaste bakterije, številne nevtrofilce in posamezne makrofage s fagocitiranimi bakterijami. Bakterije so se po Gramu obarvale pozitivno, kar je skladno z rezultati gojiščne preiskave, kjer smo na krvnem agarju po večdnevni inkubaciji v anaerobnih pogojih izolirali bakterije iz rodu Actinomyces. Z antibiogramom po disk-di-fuzijski metodi smo pri izolatu mačke ugotovili občutljivost za amoksicilin, eritromicin, metronidazol in trimetoprim-sulfametoksazol. Po antibiotični terapiji in drenaži je maček ozdravel, mačka pa je po dalj časa trajajoči antibiotični terapiji in vstavitvi drena poginila.

Zaključimo lahko, da je uspešnost zdravljenja piotoraksa odvisna predvsem od hitre torakalne drenažein ustrezne antibiotične terapije.

EPITELIOTROPNI LIMFOM PRI PRITLIKAVEM ŠNAVCERJU

Urša Luštrek Klinika Loka, Klinika za male živali, Kidričeva cesta 33b, 4220 Škofja Loka, [email protected]

Epiteliotropni limfom je pri psih redka neoplastična bolezen neznanega vzroka. Za obolenje je značilna infiltracija neoplastičnih limfocitov T v epidermisu. Prognoza je slaba in sicer zaradi slabega odziva na terapijo. Literatura navaja dobo preživetja od nekaj mesecev do 2 let. S peroralno uporabo Lomustina (60 -70 mg/m² na vsake 3 tedne s 4x ponovitvijo), bi bila lahko prognoza nekoliko boljša.

Psa pasme pritlikavi šnavcer, starega 13 let so na kliniko pripeljali zaradi neješčnosti, letargije, bruhanja in kožnih sprememb. Ob pregledu kože smo ugotovili pomanjkljivo pigmentacijo na smrčku in ustnicah. Po hrbtu je bila prisotna rdečina ter suha seboreja, na trebuhu pa je bilo najdeno večje število makul, plak in vozličev.

Psu smo odvzeli odtise in biopte sprememb na koži tre-buha za patohistološko preiskavo.

S citološko preiskavo odtisov sprememb na koži trebuha smo ugotovili večje število okroglih celic z bazofilno citoplaz-mo in okroglo - ovalnimi jedri.

Na osnovi kliničnega pregleda in citopatološkega izvida smo posumili na limfom, za dokončno potrditev diagnoze pa je bil potreben še izvid poslanih bioptov kože. Dokončna di-agnoza primera je bila epiteliotropni limfom.

Na epiteliotropni limfom moramo posumiti pri vsakem starejšem psu s kroničnimi kožnimi težavami (generalizirano rdečino, seborejo, pomanjkljivo pigmentacijo in ulceracijami), ki ne odreagirajo na protimikrobno in imunosupresivno tera-pijo. Prognoza je slaba, saj zaenkrat še ni ustrezne terapije, ki bi imela dolgoročen uspeh.

POLICITEMIA RUBRA VERA (PRIMARNA ERITROCITOZA) PRI MAČKI: PREDSTAVITEV KLINIČNEGA PRIMERA IN SPREMLJANJE ZDRAVLJENJA S CITOSTATIKOM HIDROKSIUREA

Maja Ostrouška, Marco Goruppi Ambulatorio Veterinario Goruppi Dr. Marco, Via dei Lantieri 29, 34170 Gori-zia, Italia, [email protected], [email protected]

Do danes je v svetovni literaturi opisanih le nekaj primerov primarne eritrocitoze pri mačkah.V naši ambulanti smo spre-jeli pet let staro mačko in sicer zaradi znakov, kot so: motnje v delovanju centralnega živčnega sistema,nenaden pojav tre-



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senja, krčev, slinjenja in bruhanja. Omenjeni nevrološki znaki so se pri mački prvič pojavili v noči pred sprejemom v ambu-lanto. Zabeležili smo pomembno povečanje števila eritrocitov (Er = 21,1 x 106/μl) in z metodo izključevanja diagnosticirali primarno eritrocitozo.

Vzroki za nastanek eritrocitoze pri živalih so lahko različni.Pri ljudeh je primarna eritocitoza posledica avtonomne čezmerne tvorbe eritrocitov zaradi napake v krvotvornih matičnih celicah ali pa posledica različnih obolenj. Težave in simptomi so posledica večje mase eritrocitov, povečanja vo-lumna in viskoznosti krvi.

Poleg splošnega kliničnega in natančnega nevrološkega pregleda je diagnostični protokol vključeval še podroben pregled očesnega fundusa, odvzem krvi za hematološke in biokemijske preiskave, kemijsko-fizikalni pregled urina, ul-trazvok srca in abdomna, rentgensko slikanje prsnega koša ter pretočno citometrijo (za izključitev morebitne levkemije).

Terapevtski protokol je obsegal takojšnjo venopunkcijo, ki smo jo izvedli večkrat zapored (povprečen odvzem krvi je bil 21ml/kg), ter nadaljevanje zdravljenja z ustreznim antibio-tikom, diazepamom, acetilsalicilno kislino in citostatikom hi-droksiurea.

Zdravstveno stanje mačke in njen epileptični status spremljamo periodičnoŠe vedno jo zdravimo s hidroksiureo, acetilsalicino kislino in diazepamom oz. fenobarbitalom – in-dividualni protokol zdravljenja.Mačka zdravljenje s hidrok-siureo dobro prenaša, sajpo šestih (6) letih terapije ne kaže neželenih učinkov in je trenutno brez težav.

KRONIČNO VNETJE ČREVESJA (ZA ANTIBIOTIKE DOVZETNA ENTEROPATIJA) PRI ŠARPEJU

Gašper Trojner MZ Vet d.o.o., Pesnica pri Mariboru 21a, 2211 Pesnica pri Mariboru, [email protected]

Za antibiotike dovzetna enteropatija (antibiotic-responsive enteropathy - ARE) je sindrom pri katerem pride do nenor-malne reakcije tankega črevesja na bakterije, ki ga kolonizira-jo. Eden od vzrokov je lahko anatomska anomalija z motnjo prehoda hrane.

Naš pacient je bil 5 let star šarpej, z anamnezo da je 14 dni dnevno bruhal, občasno driskal in izgubljal telesno težo ter zadnja 2 dni ni bil več živahen. Zaradi pogostih težav z gastro-enteritisi ter okužbami z Giardio sp., so ga hranili s komer-cialno dieto, ki pa jo je v zadnjem času zavračal. Ob kliničnem pregledu nismo opazili odstopanj od normalnih vrednosti, le abdomen je bil na dotik rahlo boleč. Od zadnjega obiska je izgubil 2 kg. Z analizo krvi in krvnega seruma, smo ugotovili le hipokalemijo – 3,3 mmol/l (referenčna vrednost (RV) 3,8-5,6 mmol/l). Z ultrazvokom smo postavili sum delne obstrukcije tankega črevesja, ki pa ga s kontrastno rentgensko preiskavo nismo uspeli potrditi, ker je kontrast ostal v želodcu. Z gas-troskopijo smo ugotovili spazem pilorusa ter odvzeli vzorce sluznice želodca in duodenuma (na slepo) za patohistološko preiskavo. Z laparotomijo smo našli mesto invaginacije jeju-

numa skozi ileum do kolona dolgo 30 cm. Invaginiran del črevesja smo resecirali ter izvedli anastomozo med jejunu-mom in ileumom. Terapija po posegu je bila amoksicilin s klavulansko kislino (10mg/kg/12 ur) ter metronidazol (30 mg/kg/12 ur) 2 tedna ter hiposenzibilna dieta. Pacient je po op-eraciji dobro okreval, ko pa je prenehal dobivati antibiotike, se je driska ponovno pojavila. Test insuficience trebušne sli-navke (TLI) je bil negativen, koncentracija vitamina B12 je bila znižana - 61,64 pg/ml (RV: 300-800 pg/ml), vitamin B6 20 ng/ml (RV: 3-10 ng/ml) pa je bil povišan, kar je patognomonično za ARE. Parazitološka preiskava blata je bila negativna, ob ponovni terapiji z metronidazolom (10 dni) pa so simptomi izginili.

Trenutno je pes na hiposenzibilni komercialni dieti in tedensko mu apliciramo vitamin B12 (0,5 µg s/c).Pridobil je 3 kilograme v enem mesecu, blati trikrat dnevno, blato je formirano.

ASSESMENT OF CARDIAC TROPONIN I CONCENTRATIONS ASSOCIATED WITH MEDETOMIDINE SEDATION IN HEALTHY DOGS

Maja Vasiljević1, Sanja Stanković2, Petra Zrimšek3, Alenka Nemec Svete4, Vanja Krstić1, Alenka Seliškar4 1 University of Belgrade, Veterinary Faculty, Clinic for Small Animal Medicine, 11000 Belgrade, Serbia, [email protected], [email protected] 2 Center for Medical Biochemistry, Clinical Center of Serbia, 11000 Belgrade, Serbia, [email protected] 3 University of Ljubljana, Veterinary Faculty, Clinic for Reproduction and Horses, 1000 Ljubljana, [email protected] 4 University of Ljubljana, Veterinary Faculty, Clinic for Small Animal Medicine and Surgery, 1000 Ljubljana, [email protected], [email protected]

The aim of this study was to establish whether medeto-midine (0.04 mg/kg IM) would cause myocardial hypoxic in-jury, as indicated by increased serum cardiac troponin I (cTnI) concentration in 15 healthy client owned dogs presented for ultrasonographic or orthopaedic examination. Sedation last-ed 30 minutes, after which the dogs were given atipamezole (0.15 mg/kg IM). Venous blood samples were withdrawn be-fore and at 6 h, 12 h and 4 days after the administration of medetomidine. Serum cTnI concentrations were measured using the Architect STAT Troponin-I assay with a detection limit of 0.006 ng/ml. A significant increase of serum cTnI, relative to pre-sedation and to 6 hours after medetomidine administration, was observed at 12 hours after administra-tion of medetomidine. An increase was evident in 11 out of 15 dogs (73%). Four days after sedation, cTnI did not differ from pre-sedation values. This study shows that myocardial hypoxemic injury due to medetomidine was not severe and was well tolerated in healthy dogs.



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ZNAKI ESTRUSA PRI STERILIZIRANI MALTEŽANKI

Maja Zakošek Pipan Univerza v Ljubljani, Veterinarska fakulteta, Gerbičeva 60, 1000 Ljubljana, [email protected]

Prispevek opisuje klinični primer vpliva lastničinega zdravi-la na njeno psičko.

Pri štiri leta stari maltežanki, sterilizirani pred prvo go-nitvijo, se je pred šestimi meseci pojavil vaginalni izcedek in nabreklost vulve. V zadnjem mesecu so opazili tudi povečano zanimanje samcev za psičko. Lečeči veterinar je pred 5 meseci postavil diagnozo sindroma ostanka jajčnika (ovarian remnant syndrome) in opravil diagnostično laparotomijo, pri kateri je bil po navedbah veterinarja, zaostali del jajčnika odstranjen. Kljub temu, da je bila psička po posegu brez vaginalnega izcedka, se je ta pozneje povrnil. Psička razen antiparazitikov ni prejemala drugih zdravil.

Pri kliničnem pregledu smo ugotovili nabreklost vagine, vaginalni izcedek in rahlo nabreklost mlečne žleze. Citologija vaginalnega brisa je pokazala 80% superficialnih celic, veliko število eritrocitov in nekaj bakterij brez prisotnih nevtrofilcev, kar je potrjevalo fazo estrusa. Hemogram in biokemija sta bila v mejah normale, prav tako UZ abdomna. Izmerjena kon-centracija serumskega progesterona je bila nizka (0,5 ng/ml), vrednost serumskega estrogena pa visoka (70 pg/ml). Z ap-likacijo GnRH (2,2 µg/kg) smo poskusili sprožiti ovulacijo. Po 10 dneh sta hormona ostala na podobnih vrednostih in sicer: estrogen (55 pg/ml), progesteron (pod 0,5 ng/ml). Na podlagi teh rezultatov smo izključili sindrom ostanka jajčnika in iskali drugi izvor estrogena. Temeljit pogovor z lastnico je razkril, da se zaradi hudih menopavzalnih težav gospa hormonsko zdravi z uporabo topikalnega zdravila v obliki kreme, ki vs-ebuje estradiol. Lastnici smo predlagali, da si mazilo namaže z uporabo rokavic, namazano področje pa dobro prekrije, da psička ne bo prišla v stik z njim. Na kontrolnem pregledu po enem mesecu psička ni več kazala znakov estrusa.

Opisani primer je odličen prikaz vpliva lastnikovih zdravil na zdravstveno stanje naših pacientov. Poleg tega razkriva pomembnost podrobne anamneze in temeljitega pogovora z lastnikom v primerih, ko obstaja možnost, da so dejavniki iz okolja vzrok za prisotno klinično sliko.

DILATACIJA IN ZASUK ŽELODCA - NAŠI IZSLEDKI PRI KIRURŠKO OSKRBLJENIH PSIH

Barbara Lukanc, Jurij Žel, Vladimira Erjavec Univerza v Ljubljani, Veterinarska fakulteta, Klinika za kirurgijo in male živali, Gerbičeva 60, 1000 Ljubljana, [email protected], [email protected], [email protected]

V obdobju treh let smo na Kliniki za kirurgijo in male živali Veterinarske fakultete kirurško oskrbeli 22 psov s klinično sliko dilatacije in zasuka želodca. Predstavljamo podatke o pasmi, starosti, spolu, času hospitalizacije in pooperativnem preživetju. Pri vseh psih smo naredili ventralno mediano lapa-

rotomijo, opravili repozicijo želodca in incizijsko gastropeksi-jo. Navajamo zaplete po operaciji, kot so aritmije, ledvična odpoved, sistemski vnetni odgovor in druge potrebne kirurške postopke med posegom, kot je resekcija dela želodca in odstranitev vranice. Pacientov, ki so bili oskrbljeni samo z dekompresijo želodca ali so bili evtanazirani, nismo vključili.



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zbornik referatov xxviii. simpozija · 2018-01-03 · zbornik referatov xxviii. simpozij o...

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