Gastric(dilata+on(and(volvulus( Gastric(dilata+on(and(volvulus(

(GDV) (GDV)

Gastric(Dilata+on(and(Volvulus(
Aidan B. McAlinden MVB, CertSAS, Dip ECVS, MRCVS!
European Specialist in SA Surgery
Occurs when gas and fluids accumulate in the stomach Occurs when gas and fluids accumulate in the stomach
and the normal means of removing it (eructation, and the normal means of removing it (eructation,
vomiting, pyloric emptying) are dysfunctional vomiting, pyloric emptying) are dysfunctional

Bucharest, Romania 2015 Which occurs first: bloat vs. volvulus? 3

Predisposing(factors((EBM) Diet(related Predisposed(breeds

• Purebred(large(/(giant(breed( • Great(Danes(
• Ea+ng(fewer(meals(per(day(
• Deep(and(narrow(chest(conforma+on( • Gordon(seKers(
• Being(fed(a(food(with(small(par+cle(size(
• Long(hepatogastric(ligament( • Irish(seKers(
• Exercising(aJer(a(meal(
• Previous(history(of(bloat( • Weimaraners(
• Ea+ng(rapidly
• History(of(bloat(or(GDV(in(1st(degree(rela+ve( • St.(Bernard’s(
• Increasing(age( • Standard(poodles(
• Aggressive(or(fearful(temperament • BasseK(hounds
 Clinical(signs
• Unproduc+ve(vomi+ng(retching( Stomach
Pylorus moves
• Abdominal(distension( ventrally and
progressively
toward left body
distends as rotation
continues
Notice Greater!
• Restlessness(or(agita+on( wall Omentum
• Hypersaliva+on(
• Progression(to(weakness,(shock,(collapse...

180 degree rotation:

Typically finish
Pylorus to left of
with 270-360
midline and cranial
degree rotation
to body of stomach

8 9

Distended stomach compresses Ischaemic injury to Ischaemic injury to Reduced venous return and
CVC and portal vein Sympathetic response sympathetic stimulation
intestinal mucosa gastric mucosa further
compounded by stretching
Splanchnic pooling Bacterial endotoxin of gastric vessels
Reduced cardiac cycle and reduced
release diastolic filling pressures
Reduced venous
return to right atrium Reduced hepatic Myocardial hypoxia and
clearance due to venous ischaemia
congestion
Reduced cardiac output
Further reduction in cardiac
Endotoxaemia contractility and output
Compromised Hypovolaemia
diaphragmatic function
Vasculitis Dysrhythmmias
Stimulates sympathetic Loss of circulating fluids
response to preserve vital DIC
from vascular space
If sustained leads to blood flow Interstitial and Exacerbated by hypoxia,
hypoxia & metabolic pulmonary oedema catecholamines, hypokalaemia
acidosis

Shock Shock Shock

 Shock has three stages… Continued loss or untreated… Prolonged tissue hypoxia and acidosis…

De-compensatory
Compensatory Clinical signs Early de-compensatory Clinical signs Clinical signs
(terminal)
Mild loss intravascular Redistribution of blood
Mild increase in HR / RR Tachycardia / tachypnoea Auto-regulatory escape Bradycardia
volume flow to priority organs
Stimulates sympathetic Corresponding decrease Massive vasodilation all Pale/cyanotic MM,
Brick red MM Pale MM, CRT > 2 sec
response to other organs organs No CR
Increase intravascular Severe hypotension /
CRT < 1 sec Tissue hypoxia Hypotension / weak pulse Circulatory collapse
volume and CO No pulse
Hypermetabolic
Normal mentation Lactic acidosis Poor mentation Blood pools in periphery Comatose
hyperdynamic state

Normal B.P Hypothermia Vital organs not perfused Profound hypothermia

Signs often overlooked, but reversible stage! Agressive fluid therapy critical! Resuscitation usually impossible

Treatment Stabilisation: 1st priorities IntraXvenous(fluid(therapy

• Secure(two(large(bore(peripheral(IV(access(
• Target(main(things(driving(shock(response( • Cephalic(veins!(
• Hypovolaemia( • Consider(jugular(catheter
• Hypoxia(
• Endotoxaemia
 IVFT • But(~80%(into(inters++al(space(within(one(hr( Hypertonic saline
of(administra+on
• Crystalloids(appropriate(ini+ally(
• ‘Shock’(doses:(
• 7%(NaCl(
• (90mls/kg/hr((dog)(55mls/kg/hr((cat)( • 2X6(ml/kg(
• Give(in(increments(and(reassess(q.(15(min • Administered(at(1(ml/kg/min(
• Useful(for(small(volume(resuscita+on(in(
1/4 3/4 large(dogs(
LRS = fluid of
choice
• 23%(saline(with(colloid((1:2(ra+o)(has(longer(
las+ng(effect(
In practical terms this is equivalent
to vascular volume
• Follow(up(with(isotonic(fluids 21

Synthe+c(colloids Oxygen(supplementa+on An+biosis

• Ven+la+on(impaired(in(GDV(
• E.g.(Hetastarch(or(Voluven( • Interference(with(diaphragm(movement(by(gas(filled(viscus( • Endotoxaemia(is(a(clear(indica+on(for(
• Retained(in(the(vascular(space(for(12X48(hrs(
• Small(increase(in(FiO2(significantly(improves(haemoglobin( therapeu+c(an+bio+cs(
oxygen(satura+on
• Draws(fluid(into(vascular(space(from(inters++um( • Bacterial(transloca+on(
• 10X20(mls/kg/24(hours((dog)( • Broad(spectrum((
• May(be(given(as(boluses(( • Intravenous(
• Dose(can(be(exceeded(if(indicated

24
 Gastric(decompression
VS.
Orogastric intubation Gastrocentesis

First step If intubation fails

Rapid deflation Uncooperative patient

Non traumatic Less effective

Copyright T. Clarke, vetCPDonline
May need sedation Local anaesthesia
Pre-measure tube from nares to last rib and mark
Airway protection Point max. distension May require gentle rotation to get through cardia
26

Analgesia Monitoring(response(to(treatment

• Opioid(analgesia(impera+ve( • Haemodynamic(parameters(
• Don’t(overlook(analgesia(in(shocked(pa+ent( • ECG(
• Methadone(/(morphine(appropriate( • Non(invasive(blood(pressure(
• Will(facilitate(gastric(decompression • Pulse(oximeter(
• +/X(bloods(for(electrolytes(and(acidXbase(
status

Insert cannula at point of maximal tympany!

and consider an ‘angiocatheter’ 28
 Compartmentalised stomach or inverted ‘C’
Diagnosis
• What(is(the(purpose(if(an(abdominal(
radiograph?(
!
• Where(do(radiographs(fit(into(your(
management(of(a(suspected(case(of(GDV?(

32 33
Right lateral abdominal radiograph Right lateral abdominal radiograph

Association between outcome and changes Association between outcome and changes
Other(diagnos+c(inves+ga+ons in plasma lactate concentration during presurgical in plasma lactate concentration during presurgical
SMALL ANIMALS

SMALL ANIMALS
treatment in dogs with gastric dilatation-volvulus: treatment in dogs with gastric dilatation-volvulus:
64 cases (2002–2008) 64 cases (2002–2008)
Laurie A. Zacher, DVM, DACVS; John Berg, DVM, DACVS; Scott P. Shaw, DVM, DACVECC; Raymond K. Kudej, DVM, PhD, DACVS Laurie A. Zacher, DVM, DACVS; John Berg, DVM, DACVS; Scott P. Shaw, DVM, DACVECC; Raymond K. Kudej, DVM, PhD, DACVS

• Bloods( Objective—To determine whether changes in presurgical plasma lactate concentration (be- Objective—To determine whether changes in presurgical plasma lactate concentration (be-
fore and after initial fluid resuscitation and gastric decompression) were associated with fore and after initial fluid resuscitation and gastric decompression) were associated with
• TP(/(PCV( short-term outcome for dogs with gastric dilatation-volvulus (GDV).
Design—Retrospective case series.
short-term outcome for dogs with gastric dilatation-volvulus (GDV).
Design—Retrospective case series.
Animals—64 dogs. Animals—64 dogs.
• Electrolytes( Procedures—Medical records were reviewed, and signalment, history, resuscitative treat-
ments, serial presurgical lactate concentrations, surgical findings, and short-term outcome
Procedures—Medical records were reviewed, and signalment, history, resuscitative treat-
ments, serial presurgical lactate concentrations, surgical findings, and short-term outcome
were obtained for dogs with confirmed GDV. were obtained for dogs with confirmed GDV.

• AcidXbase(balance(
• Urea(X(Crea+nine(
• Lactate?(
Cut offs for Results—36 of 40 (90%) dogs with an initial lactate concentration ≤ 9.0 mmol/L survived,
compared with only 13 of 24 (54%) dogs with a high initial lactate (HIL) concentration (> 9.0
mmol/L). Within HIL dogs, there was no difference in mean ± SD initial lactate concentra-
improved survival:
!
tion between survivors and nonsurvivors (10.6 ± 2.3 mmol/L vs 11.2 ± 2.3 mmol/L, respec-
tively); however, there were significant differences in post-treatment lactate concentration,
absolute change in lactate concentration, and percentage change in lactate concentration
Initial: < 9.0 following resuscitative treatment. By use of optimal cutoff values within HIL dogs, survival
Post: < 6.4
rates for dogs with final lactate concentration > 6.4 mmol/L (23%), absolute change in
lactate concentration ≤ 4 mmol/L (10%), or percentage change in lactate concentration ≤
42.5% (15%) were significantly lower than survival rates for dogs with a final lactate con-
Change: > 4.0 centration ≤ 6.4 mmol/L (91%), absolute change in lactate concentration > 4 mmol/L (86%),
% change > 42.5% or percentage change in lactate concentration > 42.5% (100%).
Conclusions and Clinical Relevance—Calculating changes in plasma lactate concentration
following initial treatment in dogs with GDV may assist in determining prognosis and identifying
patients that require more aggressive treatment. (J Am Vet Med Assoc 2010;236:892–897)
Care with
Results—36 of 40 (90%) dogs with an initial lactate concentration ≤ 9.0 mmol/L survived,
compared with only 13 of 24 (54%) dogs with a high initial lactate (HIL) concentration (> 9.0
mmol/L). Within HIL dogs, there was no difference in mean ± SD initial lactate concentra-
cut off values.
Significant
tion between survivors and nonsurvivors (10.6 ± 2.3 mmol/L vs 11.2 ± 2.3 mmol/L, respec-
tively); however, there were significant differences in post-treatment lactate concentration,
absolute change in lactate concentration, and percentage change in lactate concentration
overlap following resuscitative treatment. By use of optimal cutoff values within HIL dogs, survival
between
rates for dogs with final lactate concentration > 6.4 mmol/L (23%), absolute change in
lactate concentration ≤ 4 mmol/L (10%), or percentage change in lactate concentration ≤
42.5% (15%) were significantly lower than survival rates for dogs with a final lactate con-
groups. centration ≤ 6.4 mmol/L (91%), absolute change in lactate concentration > 4 mmol/L (86%),
Practicality? or percentage change in lactate concentration > 42.5% (100%).
Conclusions and Clinical Relevance—Calculating changes in plasma lactate concentration
following initial treatment in dogs with GDV may assist in determining prognosis and identifying
patients that require more aggressive treatment. (J Am Vet Med Assoc 2010;236:892–897)

G astric dilatation-volvulus is an acute life-threatening

condition that primarily affects large-breed dogs. By
definition, the initiating event of the syndrome involves an
abnormal entrapment and accumulation of fluid and air
within the gastric lumen that results in extreme, traumatic
distention of the stomach (dilatation) and variable rotation
of the stomach on its long axis (volvulus). Early clinical
signs (discomfort, pacing, panting, drooling, retching, and
abdominal distention) are indicative of the initial events.
However, the pathogenesis of GDV involves a more
complex progression of physiologic disturbances that can
rapidly (within hours) culminate in death unless immedi-
ate medical and surgical treatment is provided. Increased
intragastric pressure obstructs blood flow in the caudal
vena cava and portal vein, which results in decreased ve-
nous return and cardiac output (ie, obstructive shock). Al-
though compensatory mechanisms are activated initially
to maintain arterial pressure, corrective measures must
be taken, or inadequate tissue perfusion will progress and
compromise organ function. Eventually, the shock will be-
come refractory, multiple organs will fail, and death will be
imminent.1 Even with intensive treatment, including pre-
From the Department of Clinical Sciences, Cummings School of Vet-
erinary Medicine, Tufts University, North Grafton, MA 01536. Dr.
Zacher’s present address is Central Texas Veterinary Specialty Hos-
pital, 4434 Frontier Trail, Austin, TX 78745.
Address correspondence to Dr. Zacher (laurie.zacher@ctvsh.com).
CI
ABBREVIATIONS
Confidence interval
GDV Gastric dilatation-volvulus
HIL High initial lactate
OR Odds ratio
ROC Receiver operating characteristic
surgical stabilization, surgery, and postsurgical care, mor-
tality rates for dogs with GDV range from 13% to 43%.2–6
To lower morbidity and mortality rates, a clear under-
standing of the progression of a disease is required, and the
ability to accurately assess and address factors most criti-
cal to survival is needed. Ideally, prognostic factors can be
identified to assess critical components in the progression
of disease, which can then be used to guide alternative or
aggressive treatment strategies when appropriate. In nu-
merous studies,3,4,7–9 investigators have identified prog-
nostic indicators with regard to death of dogs with GDV.
However, many of these indicators are of limited utility
with regard to improving morbidity and mortality rates
because they do not have alternative treatment strategies
(eg, gastric necrosis,4 partial gastrectomy,9 and combined
splenectomy and partial gastrectomy8) or are complica-
tions that develop later in the course of the disease and
alternative treatment strategies are limited (eg, peritonitis,
sepsis, and disseminated intravascular coagulation).8
G astric dilatation-volvulus is an acute life-threatening
condition that primarily affects large-breed dogs. By
definition, the initiating event of the syndrome involves an
abnormal entrapment and accumulation of fluid and air
within the gastric lumen that results in extreme, traumatic
distention of the stomach (dilatation) and variable rotation
of the stomach on its long axis (volvulus). Early clinical
signs (discomfort, pacing, panting, drooling, retching, and
abdominal distention) are indicative of the initial events.
However, the pathogenesis of GDV involves a more
complex progression of physiologic disturbances that can
rapidly (within hours) culminate in death unless immedi-
ate medical and surgical treatment is provided. Increased
intragastric pressure obstructs blood flow in the caudal
vena cava and portal vein, which results in decreased ve-
nous return and cardiac output (ie, obstructive shock). Al-
though compensatory mechanisms are activated initially
to maintain arterial pressure, corrective measures must
be taken, or inadequate tissue perfusion will progress and
compromise organ function. Eventually, the shock will be-
come refractory, multiple organs will fail, and death will be
imminent.1 Even with intensive treatment, including pre-
From the Department of Clinical Sciences, Cummings School of Vet-
erinary Medicine, Tufts University, North Grafton, MA 01536. Dr.
Zacher’s present address is Central Texas Veterinary Specialty Hos-
pital, 4434 Frontier Trail, Austin, TX 78745.
Address correspondence to Dr. Zacher (laurie.zacher@ctvsh.com).
CI
ABBREVIATIONS
Confidence interval
GDV Gastric dilatation-volvulus
HIL High initial lactate
OR Odds ratio
ROC Receiver operating characteristic
surgical stabilization, surgery, and postsurgical care, mor-
tality rates for dogs with GDV range from 13% to 43%.2–6
To lower morbidity and mortality rates, a clear under-
standing of the progression of a disease is required, and the
ability to accurately assess and address factors most criti-
cal to survival is needed. Ideally, prognostic factors can be
identified to assess critical components in the progression
of disease, which can then be used to guide alternative or
aggressive treatment strategies when appropriate. In nu-
merous studies,3,4,7–9 investigators have identified prog-
nostic indicators with regard to death of dogs with GDV.
However, many of these indicators are of limited utility
with regard to improving morbidity and mortality rates
because they do not have alternative treatment strategies
(eg, gastric necrosis,4 partial gastrectomy,9 and combined
splenectomy and partial gastrectomy8) or are complica-
tions that develop later in the course of the disease and
alternative treatment strategies are limited (eg, peritonitis,
sepsis, and disseminated intravascular coagulation).8

892 Scientific Reports JAVMA, Vol 236, No. 8, April 15, 2010 892 Scientific Reports JAVMA, Vol 236, No. 8, April 15, 2010

Surgery:(Pa+ents(with(bloat(alone
• Need(gastropexy!(
! • DeXrotate(and(reposi+on(stomach(
• In(series(of(68(dogs(presen+ng(with(bloat(
• All(survived(ini+al(medical(management(
• 81%(of(those(that(did(not(have(a(gastropexy(
died(due(to(GDV(within(1(yr
General(approach:(technical(
Surgery:(Pa+ents(with(GDV
considera+ons
• Technical(considera+ons
• Goals(
• Assess(gastric(viability(
• Resect(any(deXvitalised(+ssue(
• Create(permanent(adhesion(between(
pylorus(and(right(body(wall

Stomach de-rotation manoeuvre

1.(Gastric(reposi+oning 2.(Gastric(assessment

• Ideally(decompress(fully(first( • Palpate(cardia(to(ensure(complete(deXrota+on(
! • Explore(remainder(of(abdomen(
• Orogas+c(intuba+on*( • Allows(+me(to(gastric(and(splenic(reXperfusion(
• Cuffed(ET(tube(in(place!( • Monitor(ECG,(BP(for(reXperfusion(injury(
! !
• Needle(decompression • Greater(curvature(in(area(of(fundus(/(body(
• Assess(spleen(for(necrosis(/(thrombosis

41
 • Gastric(wall(resec+on(
Determinants(of(viability Dealing(with(necro+c(wall
• Excise(back(to(healthy(bleeding(+ssue(
• Use(stay(sutures(and(pack(abdomen(to(
• Visual(( • Gastric(invagina+on minimise(spillage(
• Serosal(colour,(peristal+c(waves,(bleeding(( • Two(layer(closure:(apposi+onal(plus(Cushing(
• Tac+le( • 2(metric(synthe+c(monofilament(absorbable(
• Thickness((
• 85%(accurate(at(determining(viability(

Incisional Completed incisional gastropexy

3.(Gastropexy gastropexy
• Essen+al(
• Between(pylorus(and(right(bodywall(
• Key:(Ensure(incision(through(serosal(layers(
• Aim(to(place(stomach(in(anatomical(posi+on(
• Avoid(tempta+on(of(ventral(placement(
• Lateral(to(the(rectus(muscle(
• Posi+on(caudal(to(last(rib

48
Belt-loop Circumcostal
gastropexy gastropexy PostXopera+ve(care

• Ongoing(fluid(therapy(
Costochondral junction • Intensive(monitoring(of(ECG,(BP,(urine(output(
11th or 12th rib
• Analgesia(
• Encourage(to(eat(aJer(12X24(hours

Complica+ons(/(management Prognosis Recurrence(rates

Complication Cause Management • Survival(rates(73X90%( • Circumcostal:(0%(X(6.9%((mean(4.9%)(
ileus GIT Inflammation Feeding, prokinetics
(metaclopramide, lidocaine) • Nega+ve(prognos+c(indicators( • BeltXloop:(0%(
Vomiting Ischaemic Gastritis Anti-emetics • Dura+on(clinical(signs(>(6(hours( • Incisional:(No(data(X(anecdotal(support(of(
Invagination / gastric • Concurrent(gastrectomy(or(splenectomy( technique(
Gastric ulcers Antacid, sucralfate
necrosis • Hypotension( !
Dehiscence / • Gastric(necrosis,(peritoni+s(or(sepsis(
Peritonitis Revision surgery
perforation • All(three((and(laparoscopic)(produce(small(
• PreXop(arrhythmias(
Haemorrhage DIC Plasma, heparin differences(in(strength(when(tested(
• DIC mechanically(but(not(deemed(sta+s+cally(
Arrhythmias (VPCs,? Myocardial ischaemia,
IVFT, O2, Lidocaine
VTac reperfusion injury significant