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