Case advisors: Dr Sarah Boston, Dr Alexa Bersenas

Program advisor: Dr Karol Mathews

History and signalment5 y.o NM Boxer ‘Lennox’Collapsed with profuse rectal hemorrhageHypotensive + tachycardic @ rDVMCBC, chemistry, abdominal radiographs performedTransferred to OVCArrived 2 ½ hours after initial collapse

Physical exam findingsRecumbent, poorly responsiveT=36.4, HR=220 bpm, RR=42, MAP<60mmHgWhite m.membsAbdominal pain+ free fluid, profuse rectal hemorrhageQUATS

PCV=32%, TS=38g/l lactate=7.6 mmol/l, AG=16Stress hyperglycemia 11.1 mmol/lHypokalemia 2.7mmol/lMixed metabolic+ respiratory acidosis pH=7.22, BE=-7.6

PCO2=45mmHg

TreatmentOver the next 60 min

Fluids3 litres PLA (100ml/kg)300 ml pentastarch (10ml/kg)472ml FFP (17ml/kg)405mls whole blood300mls PRBCs

AnalgesiaPotassium CRI

ResponseCentrally responsive, in sternal, PCO2 ↓ 35mmHgHR=136, membs pink, MAP=98mmHgProfuse rectal hemorrhage continuing...

02468

101214

admission after 30 min after 60 min

glucose

K

iCa

TS

lactate

What did we do?Improved perfusion

Perfused brain now CO2 responsive- PCO2 ↓by 10mmHgM.membs pinkLactate decreasedNormalised bp, established urine production

Unmasked anemia + hypoproteinemiaPCV 15%, TS=2.2BE = +5.2Hypoproteinemia raises BENarrows the anion gap- hides lactate

The bigger picture....

60 min afteradmission

So that....

At surgery....before

And after....

Intestinal torsion Surgical emergencyHigh mortality rateGSD, Great Danes,

Neapolitan Mastiff, English Pointers

Diagnosis on clinical signsShockAbdominal painAbdominal distension+/- Hematochezia

Plain radiographs

Review of veterinary literatureAetiology and incidence

unknownMortality rate reported as

100% 6/6 cases 1984(Harvey, Rendano, Vet Surg)

89% 8/9 cases 1992(Shealey, Henderson, Vet Surg)

100% 4/4 cases 1999(Cairo, Font , JSAP)

58% 7/12 cases 2004(Junius, Appeldorn, JSAP)

Surgery within 60 minutes of presentation

Comparative aspectsReported in dogs, cats, pigs, cows, horses, humans and

whalesExtensively investigated in humans

Most commonly presents in infancyCan occur in children/ adultsPresentation- GI malrotation

Many asymptomaticBilious vomitingAbdominal pain, chronic waxing/waning GI signs,

weight loss, refluxAcute intestinal volvulus and shock

AetiologyFailure of normal

embryological intestinal development

Shortened distance between dorsal attachments of cecum and duodenojejunal junctions

Variable dorsal attachment of duodenal jejunal junction

Narrowed mesenteric root predisposed to twist

Introducing the...Ligament of TreitzNot well known in

clinical vet medWell characterised in

canine applied comparative physiology

Regulates outflow from duodenum to jejunum

Physiologic sphincterRole in embryologic

GI rotation

Treatment- Ladd procedureCounterclockwise

derotation of the intestinal twist

Careful dissection between caecum and ligament of Treitz to mobilise dorsal attachments and widen mesenteric root

Positioning of duodenum on right and large bowel on left

Prophylactic appendectomy

Key questions....Does the syndrome of intestinal malrotation exist in

dogs?Is there the same variation in distance between the

attachment of the ligament of Treitz and the base of the caecum in dogs?

Does this alteration in the base of the mesenteric root predispose to intestinal volvulus?

Intestinal torsion pathophysiology Mesenteric vein obstructed > arteryIntestine congests- mucosa sloughs +

blood leaks into lumenVilli rapidly compromised-

↑susceptibility -countercurrent mechanism

Tissue hypoxia and ischemia→generalised ileus and pain

Abdominal fluid transudate from venous and lymphatic

congestion exudate with rupture

Ischemia and re-perfusion injury

Relevance?

Post-op concernsHypotensiveArrhythmiasOngoing massive GI losses

3.5l in first 24 hrs NG tube

Comatose, bilateral miosisRespiratory acidosis Coagulopathic

Platelets= 46,000 PT=15.1 (5.5-9.8) aPTT=25.6 (9.8-19.6)

Hypoproteinemic Alb=12g/l COP=9.6mmHg

But...Responsive to pressors and

fluid supportNorepinephrine8l fluids

Oxygenating wellUrine output>2ml/kg/hrPCV=37%

CNS dysfunction in the critically illComa

Global hemispheric dysfunction

Brainstem RASDisruption to BBB

Cytokine mediated Vasogenic+ cytotoxic edema

DDx Sepsis encephalopathy Narcotics Electrolyte/ acid base

derangement Shock Thrombosis

Interventions- supportiveNaloxone trialIntubation and ventilation

PaCO2↓ to 30mmHg Airway protected

Colloidal supportCefoxitinGI protectantsTrickle feeding

VS

Response...Regained consciousness/ extubated 35 hours post-opContinued hemorrhagic diarrhoea- ↓volumeNormotensiveIleus resolvingContinued hypoalbuminemia/ low COP

2 units platelet rich FFP Pentastarch CRI 1ml/kg/hr Eating spontaneously on day 4 post-op

Sudden decline in PCV @ day 4 29%→14%Marked facial edema

Diffuse facial edemaHypersensitivity reaction

FFP Recipient Abs vs donor plasma

proteins Within 48 hours of administration

Drugs Antibiotics Opiates

Artificial colloidsLocal venous/ lymphatic obstruction

Jugular thrombosis associated with central line

Acute decline in PCVDelayed transfusion

reactionAcute GI bleed

No clinical signsImmune mediated

Delayed transfusion reactionsInciting antigen

DEA 3,5,7 natural alloantibodies in 5 to 30% dogsOnly primary transfusion needed

Any other antigen ‘Priming’ transfusion sensitises 3 to 5d priorReaction with any subsequent transfusionAcute hemolytic with DEA 1.1, 1.2 ‘Delayed’ type with other antigens

Delayed transfusion reactionsDelayed

NOT PREVENTABLE with type/ crossmatch3-14d post transfusionMultiple manifestations

Extravascular hemolysis- PCV dropFeverThrombocytopeniaPost transfusion immunosuppression

Back to Lennox....Treatment supportiveFurther PRBC transfusion

givenImmunosuppression not

indicatedDischarged 8 days after

admissionRe-admitted for further

transfusion support 7d later- icteric

2 weeks later PCV=38%

And thanks to:Dr Ainsley BoudreasDr Judy BrownDr Sylvan BichotICU techniciansThe blood bank