Download Anesthetic Challenges in the Blocked Cat Chantal

Anesthetic Challenges in the Blocked Cat
Chantal Faraudo, CVT, CVPP
DoveLewis Annual Conference Speaker Notes
As we all know urethral obstruction in young male cats is all too common and is a lifethreatening emergency. We will discuss the pathophysiology of feline urethral obstruction,
emergency stabilization, and how we treat the hyperkalemia that can develop as a result of the
obstruction. We will also discuss how to deal with anesthetic challenges and how the
sacrococcygeal block in these cats can mitigate anesthetic risks.
The most commonly seen patient we see with a urethral obstruction is the young, neutered
male cat with a long, narrow, small urethral opening between the ages of 1-10 years of age.
These patients can present with signs and symptoms that can vary from mild to severe. Initially,
these cats may show signs of urinary tract inflammation and discomfort, including straining to
urinate, frequent urination, blood in the urine, painful urination, and inappropriate urination
(urinating outside of a litter box). Inflammation plays a major role in a cat becoming obstructed.
The cause of the inflammatory materials and stone formation it not well understood, though
viral infections and diet may contribute to the problem.
There are risk factors that have been identified in cats prone to lower urinary tract disease.
Increased risk was found in cats that eat dry food and are kept indoors and cats that have
nervous, fearful, or aggressive behaviors. Also, cats that live in a stressful environment, are
overweight, get little exercise and live in a multi-cat household are considered higher risk. Cats
can experience stress for many reasons, the most common being environmental changes,
changes in food schedule, and changes in the number of animals in the household.
Interestingly, the incidence of urinary obstructions is reportedly higher in the winter months.
There are many theories as to why this occurs but none that have evidenced based studies to
back them up. Some cats develop bladder inflammation leading to mucous plugs; which is more
common in male cats. Congenital outpouchings of the bladder (vesicourachal diverticula) can
increase the risk of bladder infection, but may also be a result of chronic inflammation.
Studies done recently show that urethral obstruction is caused by plugs about 18% of the time.
Plugs are made up of protein, cells and crystals. Uroliths make up about a third of the cases and
idiopathic causes make up the rest, which is the majority. The urethra can become obstructed
with things like plugs or calculi or in the case of idiopathic obstructions many experts feel these
cats become blocked due to urethral spasm and/or edema. When you combine the idiopathic
causes with plugs this makes up the majority of the cases that veterinarians diagnose as
idiopathic cystitis. A very small percentage will have a coexisiting infection that can lead to
obstruction and even rarer are the cases that we will actually see a bacterial infection. It is
actually less than 8%.
Urolithiasis (Urinary Stones)
Another possible cause of FLUTD is urinary stones—or uroliths—which are rock-hard collections
of minerals that form in the urinary tract of cats. Cats with urinary stones will exhibit many of
the common signs of FLUTD. X-rays or ultrasound are usually needed to make a diagnosis of
urinary stones. The treatment of a cat with urinary stones depends on what the stones are
composed of; however, surgical removal of stones is often required. The two most common
stone types in cats are struvite and calcium oxalate.
For cats with struvite stones, a special stone-dissolving diet may be prescribed to eliminate the
stones. If the diet fails to dissolve the stone, then surgical removal may be necessary. Struvite
stones are becoming less common in cats because most commercial feline diets are now
formulated to reduce the likelihood of struvite formation by limiting the amount of dietary
magnesium and by promoting the production of urine that is more acidic. Unfortunately, the
percentage of stones composed of calcium oxalate has increased. The role that diet may play is
currently being studied.
Urethral Obstruction, why is it an emergency?
This is because the kidney is the primary regulator of potassium. In urethral obstruction, it leads
to increasing bladder, ureteral, and renal pressures, and this eventually results in a decrease in
the glomerular filtration rate (GFR) and that results in a reduction of urine production and leads
to a decrease in the excretion of potassium. Potassium excretion is dependent on the flow rate
of urine through the tubules in the kidneys, and then can actively be excreted in the distal
tubule by the effects of aldosterone. You may remember that aldosterone helps the reabsorption
of sodium and water and exchanges potassium and hydrogen for sodium within the kidney. In
the case of urethral obstruction, when there is a decrease in GFR, there is a decrease in the rate
of urine flow and therefore, a decrease in the excretion of potassium. As urethral obstruction
progresses, this leads to decreases in renal blood flow that can result in renal ischemia and
nephron loss.
Urethral obstruction is a true medical emergency, and any cat suspected of suffering from
this condition must receive immediate veterinary attention.
When the urethra is completely blocked, the kidneys are no longer able to remove toxins from
the blood and maintain a proper balance of fluids and electrolytes in the body. If the obstruction
is not relieved, the cat will eventually lose consciousness and die. Death usually occurs as a
result of electrolyte imbalances, which ultimately cause heart failure. The time from complete
obstruction until death may be less than twenty-four to forty-eight hours, so immediate
treatment is essential.
What are the effects of hyperkalemia and why does it pose such a problem for us?
As the potassium concentration increases in excitable tissues, the resting cell membrane
potential becomes less negative. When this happens, the sodium channels and the sodiumpotassium ATPase pumps become inactivated and that leads to difficulty in cell
depolarization. This can affect atrial cardiac cells as well. When the cardiac cells are affected,
the automaticity of the heart is affected, and we start to see cardiac arrhythmias. Depolarization
means the loss of the difference in charge between the inside and outside of the plasma
membrane of a muscle or nerve cell due to a change in permeability and migration of sodium
ions to the interior. More simply put, it means when nerves/cells are not firing they are
polarized; negative charge on the inside, positive charge on the outside.
When the ATPase pump is working and enough positive ions cross the membrane it makes the
cell/nerve depolarize. It changes its negative/positive charge at the membrane of the cell/nerve.
This depolarization of the cell/nerve continues along the entire length until it reaches its
terminal end where it causes an Action Potential to occur. The cells get excited and ion
channels are opened to let charged ions in and out of cell or nerve causing it to be depolarized,
ultimately causing an action potential to stimulate the muscles of the atria to contract. To recap:
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Intracellular levels of potassium rise and the resting cell membrane potential becomes
less negative
Sodium channels and the sodium potassium ATPase pump becomes inactivated and cells
then have difficulty depolarizing
When cardiac cells are affected the automaticity of the heart is affected and arrhythmias
develop
The table on the next page shows the ECG abnormalities that we might encounter in animals
that develop hyperkalemia. When Potassium is just slightly high at 5.5-6.5 (remember normal K+
levels are around 3.7-5.2) the first thing we might see is a tented T wave or normal sinus
rhythm. In the 6-7 range, we start to see prolongation of the QRS and the P-R intervals. The 7-8
range is when we really start to see changes where there is a decrease in P-wave amplitude and
an increase in the length of the P-wave, as well as prolongation of the QT interval. Then when
we get into the 8-10 range we begin to see atrial standstill and the fusing of the QRS and the T
wave. This pattern is called a sinoventricular rhythm. Once we have K+ over 10 then there is a
high probability of severe signs and patients can arrest and die from rhythms like ventricular
flutter or fibrillation and asystole.
One thing to keep in mind is that cats don’t always follow the rules, because, well, they are
cats! Often times the clinical signs don’t always follow this pattern and there are often other
electrolyte abnormalities that can cloud the issue. In urethral obstruction, many cats often have
an ionized hypocalcemia and an ionized hypermagnesemia, so between the two, we do not
always see nice textbook progression of ECG changes, although, as the potassium gets into the
8 range, we often do see the expected ECG abnormalities, based on what we know from studies
that have been done.
Triage of the cat with urethral obstruction
Similar to any patient presenting on an emergency basis, the first thing we always do is assess
the ABCs. Is the airway clear? How are they breathing? Are they breathing? What is their
effort? What is their respiratory rate? Do you auscult any abnormalities like wheezes, crackles,
stridor, etc.?
The next thing is to assess the circulation. What is the color of the mucous membranes? In
urethral obstruction, we are particularly focusing on heart rate as well as pulse quality and
assessment for murmurs or a gallop rhythm.
When any cat, particularly a male cat, that presents on an emergency basis, bladder palpation is
essential as part of the primary survey. The bladder doesn’t have to be huge and the size of a
grapefruit either. Sometimes the bladder will be small. The firmness of the bladder is key to
diagnosis and the inability to express urine determines whether the cat is obstructed or not. Be
very careful when palpating the bladder that you do not squeeze to hard and rupture the
bladder, it does happen. DO NOT perform a cystocentesis on a blocked cat. If a veterinarian
wants to do a cystocentesis, have them do it. It is very easy to rupture a bladder doing this.
At this point you should be thinking about how you are going to unblock this cat if he is
obstructed. Think about what his labs may look like? What might his EKG reveal? If you have to
unblock him how will you go about it? Can he tolerate general anesthesia? Can he not?
When we are stabilizing one of these poor, unfortunate, obstructed fellows, what do we do
first?
1. Give analgesics!!! (Pain medication: Pure Mu Opioid +/- a benzodiazepine, then a physical
exam and vital signs including a Doppler BP. These guys are painful!!!
2. Place an IV catheter 20 (best) or 22 gauge. Get IV fluid orders from DVM.
3. Draw blood (preferably from the catheter when it is placed).
4. At a minimum check electrolytes, PCV Total solids and renal values.
5. If you can run a venous blood gas, that is helpful. A CBC and Chemistry is also ideal.
These patients tend to be young cats without chronic disease, so the majority of the time
the CBC tends to be pretty boring and liver values are often normal. So, if you have to
omit something due to client cost constraints this is one thing to consider.
6. Get an ECG and look for arrhythmias. The ECG may alert us to the presence of cardiac
arrhythmias, as well as the physical exam may also. We can do an ECG while the blood
work is running.
A study out of JVECC 2006 by Dr. Lee and Dobratz found that patients with hypothermia, rectal
temps between 95-96, heart rate less than 120, weak pulses, an increased respiratory rate and
cardiac arrhythmias were all associated with hyperkalemia. They also found that cats that were
obstructed for the first time were more likely to be hyperkalemic, as well as cats that had a
history of vomiting. In their study they combined heart rate of less than 120, rectal temp of less
than 95 and found it was 98% sensitive and specific for predicting hyperkalemia.
What is the FIRST line of treatment for a cat with cardiac arrhythmias due to hyperkalemia?
As we talked about earlier, hyperkalemia can cause cells to be unable to depolarize and can lead
to life threatening cardiac arrhythmias. The way to protect the heart is to give Calcium
gluconate with ECG monitoring. The Calcium Gluconate will protect the heart, but it will NOT
reduce potassium levels in the blood.
How do we treat the hyperkalemia?
1. Give IV fluids. The goal of IV fluid administration is to dilute the potassium. After
protecting the heart with Calcium gluconate and stabilizing cardiac arrhythmias we
would want to drive the potassium into the cells. This is a temporary fix but can stabilize
your kitty before you unblock him.
2. One way to drive potassium into the cells is to give 25% Dextrose 0.7-1g/kg IV over 3 to 5
minutes and see if this will cause the pancreas to release insulin and drive the potassium
into the cell. This method can take about an hour to see a result, if it is going to work.
This is less than ideal due to the length of time it takes to see a result.
3. A faster more effective option is to give 25% Dextrose with Regular insulin at 0.5U/kg
IV with dextrose at 2g/U of insulin administered. This will allow for the translocation
of potassium into the cell and usually we see a result in about 15 minutes.
4. Administering Terbutaline, a Beta 2 Agonist, commonly used as a tocolytic (anticontraction medication) and a relief inhaler for the management of asthma in humans,
0.01mg/kg IV slowly can stimulate the Na+/K+ -ATPase pump to drive potassium into the
cell. Nebulized albuterol is also used by some in human medicine for this purpose.
5. If all else fails, sodium bicarbonate can be given, but it often does not work and actually
can cause metabolic alkalosis, which is the opposite problem blocked cats generally have,
which is metabolic acidosis. Usually IV fluids, calcium gluconate, and insulin will stabilize
patients. When bicarbonate is given, hydrogen moves out of the cell in exchange for
potassium, so the hydrogen is going to combine with the bicarbonate to make carbonic
anhydrase, and that is going to be converted into water and carbon dioxide, which the
cat will then breathe off. The drawback to bicarb is that it takes 30 or more minutes to
work, if it does work, so it is slow to take effect.
6. Finally the ultimate solution is to go ahead and establish urine flow by unblocking the
cat, so enhancing excretion of potassium via the kidneys. What we don’t want to do is
anesthetize an unstable patient, so stabilization is critical.
Which IV fluids are best?
With IV fluids, generally we start them on a rate of 5-10mL/kg per hour. If the cat is hypotensive,
which is rare (most cats are normotensive or hypertensive) but could happen, we start with a
bolus, usually in the range of 10-20 mL/kg, over 20-30 minutes. Any isotonic crystalloid is
appropriate for these cats. Potassium-containing fluids are okay. The amount of potassium in
Plasmalyte or Norm-R is negligible. It used to be that all of the textbooks recommended only
giving normal saline because it was potassium-free, but actually, Dr. Drobatz and Dr. Cole in
JVECC in 2008 published a study and found that there was no difference in outcome in cats that
got saline vs. cats that got Normosol –R and the rate of potassium change was no different
either. They also found that the improvement in metabolic acidosis was slower to resolve with
the saline only treated cats. The cats treated with Norm-R resolved their metabolic acidosis
faster. It is not surprising since normal saline is very acidic. It really doesn’t matter what
crystalloid is used since the hyperkalemia is going to resolve quickly once the cat is unblocked.
Calcium gluconate deserves a little more discussion and why it is so beneficial for treating
hyperkalemia. We do not want to anesthetize a cat having cardiac arrhythmias. Any way we can
help mitigate the need for general anesthesia will make it safer for the kitty to be unblocked.
Calcium gluconate basically increases the cell membrane threshold potential, reestablishing the
difference between resting membrane potential and threshold potential. Remember, the
threshold potential is less negative (more +) with hyperkalemia and when we give calcium, that
increases the resting membrane potential (making it more -) reestablishing the difference. The
dose is about 3 mL per cat IV, 50-100 mg/kg, and we are usually giving it over about 5 minutes
while continually monitoring the ECG. We are only going to be giving this medication in a cat
that is experiencing cardiac arrhythmias. If a cat is hyperkalemic without cardiac arrhythmias,
there is no reason to give calcium gluconate, you can just proceed with the unblocking
procedure. The effects are immediate and you can watch the ECG and immediately start to see
improvements in the cardiac arrhythmias.
Calcium gluconate precautions
Contraindicated in V-fib or hypercalcemia. You must NOT give IV too rapidly. If given too fast it
can cause hypotension, cardiac arrhythmias and cardiac arrest. It can also cause sloughing and
tissue necrosis if given perivascularly (outside of the vein.)
Sedation protocols for the blocked cat
The goal of the unblocking procedure is to heavily sedate or place the cat under general
anesthesia to minimize struggling; we do not want our patient struggling while we are trying to
place the urinary catheter. We want to provide analgesia because it is uncomfortable when we
place the urinary catheter, and many of these cats are really painful from their cystitis. We also
want the urethra to be relaxed to limit the chance of trauma to the urethra that could result in
strictures or tears. Also, there are those patients that are not stable enough for general
anesthesia and a protocol that doesn’t require full anesthesia is beneficial for these patients.
When choosing a drug protocol for unblocking a cat you want it to be multimodal and have a
good analgesic included. I will list a few potential protocols, of course each patient presents
with unique issues and lab values so sedation protocols must be adapted to each patient.
1. Combination sedation protocol using a pure mu opioid (oxymorphone, hydromorphone,
methadone (my personal favorite in blocked cats) and a benzodiazepine (midazolam or
diazepam). This is works well to sedate these painful cats.
2. Combination sedation protocol using low doses of ketamine (30mg) and benzodiazepine
(1.5mg). These are cats with no cardiac arrhythmias. Titrate to effect starting with 0.1 ml
of each to start.
3. Propofol only. There is no analgesia in this protocol so a pre-med should be given that
includes a pure mu opioid. Propofol does cause myocardial depression and vasodilation
and apnea if given too fast, so every patient will be unique in their anesthetic needs. My
personal favorite drug combination in this situation is methadone which is a pure mu
opioid with NMDA antagonist and midazolam.
4. Combination sedation protocol (pure mu opioid + benzodiazepine) and a sacrococcygeal
epidural. This is an ideal protocol that can be used to unblock a cat without having to use
general anesthesia.
5. Pre-medication with general anesthesia with inhalant. Make sure your pre-med contains
a pure mu opioid for good analgesia.
Sacrococcygeal Epidural
A sacrococcygeal epidural (in addition to sedation) with 2% lidocaine works well in cats with
urethral obstruction. This works great in cats that have significant urethral spasm, ones that are
especially difficult to unblock, or in very sick cats.
Why would we do a sacrococcygeal block? It will provide regional anesthesia to the perineum,
the penis, the urethra, the colon and the anus. It does this by blocking the pudendal, pelvic, and
the caudal nerves while still allowing motor function in the hind limbs.
Where do we administer it and what are we giving? Preservative-free lidocaine is
recommended, however regular 2% lidocaine can be used if it is a new unopened bottle.
Bupivacaine can be used but the onset can take longer so lidocaine tends to be a better choice.
Onset is about 3 minutes or less. The lidocaine lasts up to 60 minutes and the bupivacaine lasts
about 3-5 hours. It is not intended to be a long lasting epidural. It is intended to get you through
the unblocking procedure.
The injection is going to be done between the sacrum and the 1st coccygeal vertebra, or the 1st
and 2nd coccygeal vertebrae. It is really an epidural done caudally. There is less risk when
performing this type of epidural because the spinal cord ends at about L7, so when you are
doing this epidural, we are very caudal to this area. The landmark is right where the tail bends.
You will feel a space or divot right on the bend.
Getting set-up for a sacrococcygeal block:
• Gather all materials and draw up your 2% lidocaine (0.1-0.2ml/ kg) with a maximum dose
of 0.5ml per cat.
• Make sure that your patient has already received generalized analgesia and potentially
other sedative medications. The goal of this local block is to avoid the need for general
anesthesia in many cases but lidocaine is only one facet of a complete multimodal
analgesia protocol.
• Palpate the space between the sacrum and first caudal vertebra by lifting the tail
dorsally.
• Palpate the space between the sacrum and first caudal vertebra by lifting the tail dorsally
• Clip the hair around this space and surgically scrub the area.
• Don sterile gloves and have an assistant lift the tail dorsally to allow you to again palpate
the space between the sacrum and first caudal vertebra. Make sure that your assistant
then drops the tail as the intervertebral space will be much more challenging to enter
when “pinched” closed in this fashion.
• Direct a 25g needle through the skin at midline at an approximately 45 degree angle from
horizontal and advance it through the interarcuate ligament. When appropriately placed
you will commonly (but not always) feel a pop and the needle will be seated much more
securely than if it were placed simply into the subcutis. If you hit bone while you are
trying to find the intervertebral space, you can gently walk your needle forwards or
backwards until you fall into the space and, hopefully, get into the epidural space.
• Attach the syringe to your needle and aspirate to ensure that there is no blood. If no
blood is noted inject the lidocaine and remove the needle and syringe. If blood is noted
then remove the needle and start again. It should be fairly easy to inject. There isn’t an
easy way to check that you are in the epidural space because it is so small, so you can not
do the hanging drop technique.
• Monitor for decreasing tail and anal tone which usually occur within less than one
minute. If this is not noted within five minutes then the procedure should be repeated
but do not attempt to administer more than two injections before attempting another
means of intervention to prevent lidocaine toxicity. You will also notice a flaccid tail when
the block is working and the anus is often wide open.
• Proceed with urethral deobstruction, tail amputation, or other procedures as indicated.
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Sacrococcygeal blocks reduce the amount of additional sedation that is needed during
the unblocking of the cat and if the block is successful usually nothing more is
needed. They are pretty much awake during the catheterization, but they don’t really
care what is happening, and we get maximal urethral relaxation. The block is also useful
for those cats that have stones because the urethra relaxes and allows the stones to be
retropulsed back into the bladder so the urinary catheter can be passed.
Sacrococcygeal blocks are not difficult and CVT’s can learn to do them and administer them as
well as veterinarians. These blocks are a very valuable tool to help mitigate the risks of
anesthesia and provide excellent pain management in the cat with a urethral obstruction.