Analgesia and anaesthesia of the GDV patient

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Analgesia and Analgesia of the GDV Patient
Claire Roberts RVN DipAVN(Surg) VNCertECC
Aetiology and Patient Presentation of the GDV Patient
GDV – gastric dilation volvulus
Gastric dilatation and volvulus is a common, life-threatening emergency in veterinary medicine. The
potential of a successful outcome will be dependent on the veterinary team being prepared,
anticipating the worst, and treating aggressively as soon as the patient presents
Gastric dilatation accounts for 0.8-2.8% of the animals presented to veterinary emergency clinics. In
animals with GDV, mortality rates range from 15-33%. While GDV can occur in any species dogs are
most commonly affected, although the syndrome has been reported in cats, guinea pigs and
primates.
Aetiology
Gastric dilatation and volvulus is an abnormal accumulation of gastric gas resulting in dilatation,
which can be further complicated by the rotation of the stomach (volvulus) of the stomach around
its mesenteric axis. This incorrect positioning and rotation of the stomach around its axis causes
obstruction to inflow and outflow, resulting in the rapid accumulation of intraluminal fluid and gas. It
is thought that the stomach rotates first, and then becomes distended with gas.
As the patient becomes uncomfortable, aerophagia can result in further gas accumulation within the
stomach. Gastric distension results in increased gastric pressure, and compression of the diaphragm
and great vessels, including the caudal vena cava. Inadequate venous return to the right heart
subsequently decreases cardiac preload (the volume of blood returning to the heart), with a
decrease in cardiac output. Decreased perfusion to the gastric mucosa and serosa also results in the
release of inflammatory cytokines. There are a variety of pathophysiological changes which take
place within the body and these changes are responsible for the high mortality rate which is
associated with gastric dilatation and torsion. The course of events which lead to a GDV as still not
fully understood.
Clinical Signs
Most owners will call the practice with concerns that their pet has increased salivation, has an
unproductive vomit and his/her abdomen looks distended, although recent episodes of self-limited
mild to moderate gastric distention, anorexia, or occasional vomiting can be noted prior to full
dilatation. Restlessness, retching, and excessive eructation or flatulence may also be reported.
On clinical examination the patient will have a distended painful abdomen which sounds ‘drum like’
on percussion. The patient may be tachycardic and tachypnoeic with pale mucous membranes and a
slow capillary refill time. As the condition develops the patient’s pulses will become increasingly
weak and thready.
Predisposing Factors
There are a range of factors (both environmental and individual patient) which have been suggested
or linked with GDV cases. These factors include breed, age, sex, chest confirmation, diet, stress and
exercise pattern.
Factors which are considered higher risk include:
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The patient breed
Giant and large breeds being most susceptible
Breeds which are deep and narrow chested.
Animals which have had a close relative which has had GDV.
Slightly older patients
Patients which are fed just once daily
have a tendency to rush their food therefore increasing the risk of aerophagia
Animals which are at risk of ‘stress’
Car journeys, dog shows or being kennelled.
Diagnosis
An initial diagnosis can be made using the clinical examination findings, blood samples can also be
taken as well as radiography of the abdomen carried out.
Blood sample results will give the status of the patient at that moment in time; therefore repeated
samples should be taken to monitor the condition of the patient. Lactate is the main blood
parameter which is extremely useful in the assessment of GDV patients as it gives a good predictor
of gastric necrosis and the prognosis for the patient.
Studies have shown in 99% of dogs with a plasma lactate concentration <6.0 mmol/L survived
compared with only 58% of dogs with a plasma lactate concentration >6.0 mmol/L. This test is
becoming widely more available with both dry chemistry analysers and hand-held blood gas analysis.
Radiography
Radiography can be useful in differentiating between GD and GDV patients but it needs to be carried
out carefully to prevent further stress to the patient. When taking radiographs of suspected GDV
patients a right lateral projection should be taken. If there is volvulus present the gas filled pylorus is
displaced cranially and dorsally to the fundus, and appears as an area of plication or
compartmentalisation between the two areas of the stomach.
Any abdominal radiographs taken should be carefully checked for the presence of free abdominal air
(stomach rupture), it should be remembered however that is gastrocentesis has been performed
that some air could have leaked as a result of this.
Changes which occur in the various body systems
Patients can present initially with very similar signs for both acutely occurring Gastric dilatation and
acute gastric dilatation and torsion. With both conditions cardiorespiratory dysfunction occurs due
to the increasing size of the gas filled stomach which puts an increased pressure on the diaphragm.
This increased pressure results in reduced expansion of the diaphragm and reduced capacity of the
lungs, resulting in hypoventilation which in turn will result in a ventilation-perfusion mismatch and
arterial hypoxia as the stomach increases in size and the degree of respiratory dysfunction worsens.
This in turn results in an increase in partial pressure of carbon dioxide will result in a respiratory
acidosis which further complicates the patient’s condition.
Within the cardiovascular system the venous vessels which are under relatively low pressure, e.g.
caudal vena cava, hepatic portal vein and splanchnic vessels located in the cranial abdomen become
easily compressed as the stomach begins to dilate. This compression results in causing several
negative effects on the patient, these include:
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A reduction in venous return
o will result in a reduction in cardiac output
o drop in systemic blood pressure
o Portal hypertension which leads to interstitial oedema and fluid leaking from the
vascular spaces
compromising circulating volume
reduction in tissue perfusion
myocardial injury
risk of reperfusion injury occurring when the circulation is re-established during treatment.
hypovolaemic shock.
Reducing cardiac contractility is myocardial depressant factor. This factor is thought to arise
due to reduced tissue perfusion in other organ systems, in particular the pancreas and
intestines.
The cardiovascular effects are further compromised by the release of catecholamines, which
increase peripheral resistance to compensate for the decrease in systemic blood pressure. This in
turn will result in a further reduction in tissue perfusion which can result in severe reduction in renal
perfusion and the loss of the intestinal mucosal barrier.
Gastric necrosis can develop as a result of torsion, occlusion and avulsion of the short gastric arteries
which supply the greater curvature and fundus of the stomach. This may lead to ischaemia which
can further develop to necrosis or large areas of the stomach that may well leak gastric contents.
During volvulus of the stomach, the spleen will also move with the greater curvature of the stomach.
This can lead to splenic necrosis due to compromise of the splenic vasculature during volvulus.
Initial stabilisation of GDV patients
The initial aim in the treatment of GDV patients is the restoration of the cardiovascular system, i.e.
the circulation. This will aid renal function and the respiratory system. In order to do this effectively
the effects of the dilated stomach on the abdominal veins and the respiratory system need to be
reduced. This is generally carried out by gastric decompression and the provision of intravenous
fluids. There are no definite rules as to whether the gastric decompression or fluid therapy should be
carried out first but gastric decompression should not be delayed for more than 10-15 minutes.
Initial Treatment Considerations
Treatment initially consists of rapid decompression of the stomach with a stomach tube. If this is
unsuccessful, then trocarisation of the stomach may be necessary.
Stomach tubing is carried out in order to decompress the stomach. With this technique a wide bore
stomach tube is measured from the patient’s nose to its 11th rib and marked. The tube should not
be placed any further than this length to prevent accidental rupture of the gastric wall.
The initial placement of the tube can be made with the patient in a sitting position. A temporary and
effective ‘gag’ can be made by placing a cohesive bandage end on between the patient’s teeth, and
mouth should then be held or taped shut over this gag and the stomach tube can then be passed
down the inner core of the roll. If it is not possible to access the stomach with the patient in this
position then the same technique should be attempted with the patient in right lateral recumbency.
Care must be taken when passing the stomach tube as over-vigorous placement may lead to
accidental rupture of the gastric wall. Once the stomach tube has been passed, gastric lavage should
be carried out using copious volumes of warmed normal saline or lactated Ringer’s solution.
If stomach tubing is unsuccessful trocarisation should be performed. Trocarisation is usually
performed by clipping an area over the right flank where the stomach is most distended and quickly
prepping the areas as for aseptic surgery. A large bore (>16 gauge) long intravenous catheter should
be placed through the skin and into the distended stomach. Correct placement of the catheter will
often be confirmed by the hissing sound as the gas escapes from the stomach. This technique will
cause temporary and minimal decompression of the stomach whilst further preparations can be
made for continued treatment. Once the pressure in the stomach has been reduced, stomach tubing
may be reattempted at this point.
Fluid therapy
The aim of fluid therapy should be to restore the circulation and to improve tissue and organ
perfusion. Fluids should be administered as quickly as possible by the placement of two wide bore
intravenous catheters into the cephalic or jugular veins. The saphenous veins should not be used for
intravenous fluids as they will be ineffective at restoring circulating volume due to the reduced
venous return caused by the gastric compression of the vena cava.
The choice of fluids is primarily crystalloids in combination with a colloid. This is the fluid
combination of choice as colloids have the advantage of prolonged effect within the circulation and
they also increase oncotic pressure, this has the effect of enhancing the effect of the crytalloids.
Another readily available and cheap fluid which has been used successfully in the treatment of GDV
patients is Hypertonic (7.2%) saline. Hypertonic saline should be given as a one off bolus at a rate of
5-10ml/kg over 15 minutes followed by crystalloids, e.g. Hartmann’s solution at 20ml/kg/hour.
Haemoglobin based oxygen carriers (HBOC) e.g. Oxyglobin® or synthetic blood substitutes may be
useful as an initial resuscitation fluid as it has the ability to help maintain intravascular colloid
oncotic pressure and perfuse tissues which whole blood cannot due to its small cell size, i.e.
ischaemic areas.
Colloids are not currently recommended for critical patients unless there has been acute
haemorrhage. However if the patient has a low PCV or haemoglobin level, then oxyglobin could be
considered to improve oxygen carrying ability and to provide some oncotic support.
Surgical Treatment
These patients will need to undergo a surgical procedure to decompress and return the stomach to
its normal position within the abdominal cavity. The surgeon will need to assess the stomach and
spleen for viability and in some cases a splenectomy will be indicated as may a partial gastrectomy id
irreversible tissue damage has occurred.
A gastropexy is usually performed to prevent any reoccurrence of the condition. Recurrence rates
are documented to be as high as 80% when a gastropexy is not performed.
It is paramount that the veterinary nurse is ready to go into theatre as soon as the triage phone call
has been taken.
Pre operative clipping is not normally recommended as it has shown to significantly increase
bacterial load on the skin resulting in increased risk of SSI rates. There is also some research that has
shown that the longer an area of skin has been clipped for directly correlates to the rate of skin
infection. In the GDV patient this is out weighed with the increased risks associated with anaesthesia
and pre operative clipping should be performed as much as possible.
Anaesthesia and Analgesia considerations
Common Complications
Anaesthesia of a patient with gastric dilation volvulus (GDV) can be very challenging. They often
have many problems with the cardiovascular system and respiratory system, as well as acid base
disorders and severe pain. As already discussed, early preparation is very important.
Likely complications include:
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Hypotension - hypovolaemia, shock, sepsis
Arrhythmias
Hypoventilation
Pain
Acid Base Disorders
Regurgitation
Oxygen should be provided by face mask if possible. If this is not tolerated, flow by techniques can
be used. Analgesia should be rapidly provided. Methadone is a licensed drug and easily available. In
critical patents it is wise to use lower doses and titrate up to effect as they may have a more
pronounced effect on collapsed animals. Methadone 0.2mg/kg very slow IV
The cardiovascular status should be assessed by ausculating the chest, feeling peripheral pulse
quality and taking a blood pressure reading. An ECG monitor should be attached to look for any
arrhythmias that might be present. Does the heart rate match the pulse rate? Are there any pulse
deficits?
Premedication
Premedication should be provided to calm the patient and should provide analgesia. Pure opioids
that are licensed for veterinary use are widely available now. They allow excellent analgesia to be
given to patients. They have minimal cardio-respiratory effects and can be easily reversed if
required.
Methadone has a short duration of action, 4-6 hours. It can be safely used intravenously (slowly) and
will provide a similar level of analgesia to morphine.
Morphine can be used in GDV patients. It does have a tendency to cause vomiting but this is most
often seen in patients that are not already in pain e.g. in pre-emptive analgesia. The dose and
duration of action is very similar to methadone.
Fentanyl can be used as a premedication, it has a short duration of action, 20-30 minutes and so is
best given shortly before induction.
ACP should not be used in any critical patient. It causes peripheral vasodilation and pooling of blood
in the periphery reducing blood pressure by causing a relative hypovolaemia.
Dexmedetomidine should also not be used in GDV patients; it has potent cardiovascular effects
including bradycardia and arrhythmias which may cause the patient to crash.
Induction
Propofol has negative cardiovascular effects which can be detrimental to a critical patient. It causes
a decrease in cardiac contractility and an increase peripheral vasodilation both of which result in
hypotension. Using a co-induction technique such as a benzodiazipine e.g midazolam alongside
propofol can reduce the required dose and minimise the side-effects.
If available a co-induction technique using midazolam and fentanyl is a good combination for
compromised patients, both drugs have minimal cardio respiratory depressant effects and are both
easily reversed.
Alfaxalone may be a better choice over Propofol due to its ability to maintain heart rate and blood
pressure better. Alfaxalone can also be used alongside a benzodiazipine as a co-induction.
The addition of Lidocaine to the induction protocol has many benefits. It is a well know antiarrhythmic drugs, but also adds to the analgesia.
During induction the patient should be provided with oxygen and the head held upwards in case of
regurgitation, this is especially important in gastric
Canine Induction doses
dilation cases. Suction should be set up and close by
Propofol
4mg/kg
so that any regurgitation can be quickly dealt with.
Alfaxan
2mg/kg
Ensure that the cuff of the endotracheal tube is
Midazolam
0.2mg/kg
properly inflated to prevent and stomach contents
Diazepam
0.5mg/kg
Fentanyl
5mcg/kg
from being inhaled.
Lidocaine
2mg/kg
All induction drugs should be given slowly and too
effect. Compromised patients will require much lower dosages to induce anaesthesia. All monitoring
should be attached to the patient before induction starts to allow close monitoring throughout.
Hypotension
Shock is very common in GDV patients, low blood pressure is caused by the dilated stomach
compressing the vena cava and reducing blood flow back to the heart, this reduces the subsequent
cardiac output. Patients can be hypovolaemic as well due to fluid sequestration. Septic shock can
develop later, especially if stomach necrosis has occurred.
Hypotension means that perfusion of vital organs is compromised and oxygen delivery is not
adequate. In this situation the tissues become hypoxic and revert to an anaerobic energy
production. A by-product of this energy production is lactic acid. This is lactic acidosis.
Measuring lactate can help to predict the outcome of GDV cases. 99% of GDV patients with a lactate
<6mmol/l are likely to survive compared to 58% who had a lactate >6mmol/l.
It is vital to reverse this chain of events and prevent lactate from building up.
This is achieved with fluid therapy and stomach decompression. Hartman's is the fluid of choice, it is
isotonic and contains precursors of bicarbonate to counteract acidosis whereas saline although
isotonic can be acidifying which is not helpful in an acidotic patient! Fluid boluses of 10-20ml/kg over
15 minutes can be given to improve blood pressure. Careful assessment of cardiovascular status
should take place after each bolus e.g. BP and HR. A continuous infusion of 10ml/kg/hr should be
provided throughout anaesthesia to compensate for vasodilation produced by anaesthetic drugs.
Colloids are not currently recommended for critical patients unless there has been acute
haemorrhage. However if the patient has a low PCV or haemoglobin level, then oxyglobin could be
considered to improve oxygen carrying ability and to provide some oncotic support.
Hypertonic saline can be considered for a severely hypotensive patient. 7.2% Saline can be given as a
bolus of 4ml/kg. Hypertonic saline draws fluid from the intracellular space into the intravascular
space increasing circulating volume. It must be followed by crystalloids to replace the fluid taken
from the intracellular space.
Once the stomach has been untwisted there is a risk that endotoxins and cytokines will be released
due to the restoration of perfusion to compromised areas of tissue. These can cause a reduction in
myocardial contractility and vasodilation. This is a particular risk if the stomach wall has become
necrotic. The release of cytokines can induce systemic inflammatory response (SIRS).
Positive inotropes can be used to improve blood pressure (once any fluid deficits have been
corrected). They can either improve contractility or improve systemic vascular resistance
(vasodilation).
The two most common positive inotropes are Dobutamine and Dopamine. Dobutamine increase
myocardial contractility which will increase cardiac output and blood pressure. Dopamine increase
contractility but at high doses it will also increase systemic vascular resistance. Both drugs can cause
hypertension, tachycardia and arrhythmias so there must be blood pressure and continuous ECG
monitoring available to detect these problems.
Arrhythmias
Arrhythmias are commonly seen in the GDV patient. They can be caused by hypotension (cardiac
ischaemia), endotoxins, hypoxia, and splenic involvement. Pain can also be a factor in creating
arrhythmias.
Ventricular arrhythmias are the most commonly seen arrhythmia, either runs of ventricular
premature contractions or ventricular tachycardia. They should be treated if they are causing a
negative effect on cardiac output.
An ECG is the best way to diagnose the presence of an arrhythmia, but it is important to also assess
blood pressure and pulse quality to identify its effect on cardiac output.
If an arrhythmia is detected, the patient should first be provided
with oxygen and analgesia. Electrolyte abnormalities should be
identified and treated e.g. hypokalemia. If the patient does not
respond to these therapies or the patient is deteriorating then
anti-arrhythmic drugs should be administered. The most
common drug used is Lidocaine, this can be given as a bolus
followed by a CRI.
Lidocaine
3mg/kg IV (can be
repeated)
CRI – 50mcg/kg/min
Be aware those large breed dogs that are susceptible to GDV are also known to have cardiac
problems such as dilated cardiomyopathy. Listen to the heart - is there a history of heart problems?
Hypoventilation
Hypoventilation is a reduced tidal volume, this is likely to be a complication of GDV’s due to the
enlarged stomach restricting the diaphragm and the pain involved in this disease.
A reduced tidal volume prevents the excretion of carbon dioxide, this builds up in the body resulting
in respiratory acidosis. This can be corrected by providing ventilatory support. This can be either
manual IPPV or mechanical ventilation if available. This should aim to provide a normal tidal volume
which will normalise carbon dioxide levels and correct respiratory acidosis.
Pain
Gastric torsion is a very painful experience! Opioid CRI provides the best means for managing that
pain.
Fentanyl CRI provides excellent analgesia with minimal effects on the cardiovascular system, it is
short acting and so is rapidly removed from the system within 30 minutes after it is stopped. The
dose can be quickly titrated to effect. It can cause some respiratory depression so be prepared to
provide ventilatory support.
Morphine CRI can be used during anaesthesia, it will provide very good analgesia with minimal
cardiovascular effects although some respiratory depression may be seen.
Ketamine CRI could be considered if opioid and lidocaine CRI does not provide enough analgesia.
Sub-anaesthetic doses are used for analgesia purposes so the sympathetic stimulation see at
induction doses may not be a problem.
Epidural morphine can provide up to 24hours analgesia, and would be a good choice for a GDV
patient assuming their coagulation factors are normal. It may be best to provide an epidural post
surgery before recovery due to the need to get these patients into surgery quickly.
Lidocaine in GDV’s
Lidocaine has many useful properties besides its anti-arrhythmic abilities. It can scavenge free
radicals and prevent re-perfusion injury seen
Canine CRI Dose
with restoration of blood flow to compromised
Fentanyl
2 - 20mcg/kg/hr
tissue. It may help to prevent ilieus following
Morphine
0.2mg/kg/hr
gut surgery.
Lidocaine
25 – 50mcg/kg/min
It is useful as part of an analgesia protocol for
Katamine
10-20mcg/kg/min
severe/intractable pain. It has a synergistic
(1-3mcg/kg/min if
effect with other analgesics providing a better
conscious)
pain control. It also provides a MAC sparing effect (minimum alveolar concentration) on inhalant
anaesthetics, allowing the reduction of isoflurane/sevoflurane used and minimising their negative
effects.
Acid Base Disorders
Metabolic acidosis caused by high levels of lactic acid can severely impair cardiovascular function
and be a barrier to successful resuscitation.
Venous blood gas analysis will provide you with information on pH, bicarbonate levels, PCO2, and
venous oxygen saturation. Taking repeated samples will allow you to monitor the progression of the
acidosis and assess the effectiveness of your therapy.
Metabolic acidosis can be complicated by poor ventilation which prevents carbon dioxide excretion
and causes respiratory acidosis so the respiratory system cannot compensate for the metabolic
element. Resolving perfusion is the key to correcting the acidosis.
Regurgitation
This is a very serious risk especially once the stomach has been untwisted. Regurgitation can cause
oesophagitis which is a very painful condition or even oesophageal stricture which can prove to be
life threatening.
Aspiration of stomach contents causes pneumonia which again can be a life threatening
complication.
It is very important to make sure that the cuff on the endotracheal tube is properly inflated so that
no gas can be heard escaping around it. Before recovery the patient’s pharynx and oesophagus
should be examined and if fluid is present suctioned clear then flushed with saline to remove the
highly acidic material and prevent injury to the oesophagus.
Placing a stomach tube during surgery to empty the stomach can help to remove the stomach
contents safely. But the oesophagus and pharynx should still be thoroughly checked at the end of
the procedure.
Recovery
Before ending the anaesthetic you should:
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Ensure the pharynx and mouth are clear of stomach contents
Check if the patient can maintain a normal saturation on room air.
Check the patient’s temperature
Repeat blood work - lactate, PCV/TP, glucose, BUN/crea.
In the recovery area they should have oxygen available, nasal oxygen prongs or nasal catheters are a
good way of providing oxygen. These patients are at risk of hypoventilation and so hypoxaemia, due
to their generally large size, they will have been in dorsal recumbency for a long time, and they may
be on respiratory depressant drugs.
Active warming should be used to increase and maintain the patients’ core temperature.
Closely monitoring the patient post surgery is crucial in the first few hours. Monitoring heart rate,
rhythm, pulse rate and quality will indicate if there is an arrhythmia.
Ideally the patient should be connected to an ECG machine in recovery and have blood pressure
monitored regularly. If this equipment isn’t available then cardiac auscultation and monitoring heart
rate, pulse rate, rhythm will still indicate abnormalities.
If the patient is poorly perfused or has suffered periods of hypoxia sinus tachycardia or Ventricular
premature complexes can be present in recovery. These should subside when the patient is more
stable in recovery.
Aggressive fluid therapy may be necessary in these cases. As GDVs are common in large breed dogs
large amounts of crystalloids may be required to improve perfusion.
Monitoring the patient’s hydration status is very important. Are the mucous membranes tachy (dry)
dehydrated? Are they moist? Is the patient feeling nauseous post surgery? Are they pink, pale, grey
and in need of oxygen supplementation, blood transfusion? Is the CRT prolonged or normal? (1-2
seconds)
Analgesia must continue in recovery, adding anti emetics may be of advantage to the patient. If the
patient is tachycardic in recovery assess pain first of all to rule out the cause of the tachycardia.
If the patient is tachycardic and having VPCs then therapy for this may be indicated. If you do not
have an ECG machine to confirm this but you have weak pulses or deficits then VPCs are very likely.
Giving low doses of lidocaine (1mg/kg slow iv) and auscultating the heart and checking pulse quality
to see if this make the heart and pulse rhythm regular can confirm if the lidocaine is helping the
arrhythmia. Maximum dose is 8mg/kg total. Setting up a CRI maybe indicated (see above)
High lactate levels can indicate poor tissue perfusion and hypoxia.
The surgeon may place a gastrotomy tube at the time of surgery, not only can the tube be used to
feed the patient, but can also relieve bloating post surgery which is a possible post operative
complication.
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