Leptospirosis - Hope Advanced Veterinary Center

January 2012
Focus on Hope
Newsletter for The Hope Center for Advanced Veterinar y Medicine
Leptospirosis:
A Life-Threatening,
Zoonotic Disease
Hepatobiliary Disease:
Making the Diagnosis
Cataracts:
An Overview of Care
Coming Up...
The Hope Center for Advanced Veterinary Medicine | 140 Park Street SE | Vienna, VA 22180 | 703-281-5121 | HopeCenter.com
Leptospirosis
Diagnosis via Clinical Signs
By Amy Cordner, DVM, DACVIM
Leptospirosis is a life-threatening, zoonotic, multi-organ infection caused
by motile spirochete bacteria, also called leptospires. Leptospirosis affects
more than 150 species of mammals, and there are over 250 serovars. The
most noted pathogenic species in dogs include
Leptospira interrogans (Icterohaemorrhagiae,
Canicola, Pomona, Bratislava, and Autumnalis)
and Leptospira kirschneri (Grippotyphosa). This
organism and the potential for disease has a worldwide distribution. In the United States, the highest
concentration of disease exists in the mid-Atlantic
coastal regions (including Northern Virginia and
the greater DC metro area), the upper Midwest, the
Northeast, Texas, Colorado, and Hawaii.
Dr. Amy Cordner
Natural Life Cycle and Transmission
Leptospirosis has a relatively simple life cycle. Live organisms are shed in
the urine of wildlife and domestic livestock reservoirs (cows, horses, pigs,
raccoons, rodents, skunks), and organisms can survive in contaminated
soil and bodies of water for weeks to months. New infections can be acquired through direct contact with infected urine into recipient mucous
membranes, via bite wounds, and via venereal and transplacental transmission. Indirect transmission occurs through exposure to contaminant
areas and moist environments. Very few organisms are needed to induce
a new infection in a naïve animal.
Signalment and Risk Factors
Given the transmission of Leptospirosis and the reservoir population,
rural and hunting dogs and intact males are at an increased risk for
acquiring infection. Furthermore, outbreaks are more common in
warmer climates and following rainy periods. Infection can occur
year-round, but in the United States, the incidence of infection is greatest in the Fall. Despite higher infection rates in rural and hunting dogs,
Leptospirosis is also increasingly identified in urban and suburban
dogs. There are urbanized wild animal populations, including raccoons and rodents, and backyard and park environments for soil
reservoirs. Given these risk factors, it is always important to question
families about their pet’s travel history and environment.
Pathophysiology
Leptospires invade a new host by invading through mucous membranes or through skin wounds. Bacteria begin to replicate as early as
1 day after entering the blood supply; the bacteremic phase of disease
is short, only a few days time. Organisms then colonize tissues, including the kidneys, spleen, liver, eyes, central nervous system, genital
tract, and endothelium. Incubation time is about 7 days until organisms are once again shed into the urine.
Organ damage develops secondary to cytokine production and inflammation in host tissues. The extent of organ damage depends upon both
the virulence of the infecting serovar and the host’s innate susceptibility.
Additionally, recovery from infection depends upon the host immune
response. In general, animals that develop a high antibody titer are more
likely to eliminate the infection; individuals that develop a poor antibody
response are more likely to acquire severe clinical disease. A proportion
of animals with a moderate antibody response become persistently infected with Leptospires and continue to shed them in urine. Without
appropriate treatment, shedding of organism from the kidneys may
occur for weeks to months after clinical recovery.
Fortunately, cats are known to be resistant to Leptospirosis.
Leptospirosis patients can present with a variety of clinical signs, including fever, polyuria/polydypsia, oliguria or anuria, inappetence,
vomiting, abdominal/renal pain, conjunctivitis, uveitis, dyspnea,
muscle pain, jaundice, edema/vasculitis, and petechiations.
Occasionally, dogs can present only with polyuria and polydipsia.
Veterinarians should suspect Leptospirosis in cases of acute renal or
hepatic failure (especially concurrently), PU/PD of unknown origin,
uveitis, DIC, thrombocytopenia, acute febrile illness, and myalgia.
Leptospirosis Pulmonary Hemorrhage Syndrome (LPHS) was originally reported to have an immune-mediated mechanism in people
and is also recognized in infected dogs. There is no correlation between infecting serovar and the development of LPHS.
Diagnosis via Laboratory Findings
Laboratory diagnosis is made with routine biochemical and hemological tests and specific Leptospirosis tests. Typical CBC changes
include a neutrophilia with left shift, mild non-regenerative anemia,
and thrombocytopenia in just over 50% of cases. Serum chemistry
reveals azotemia (mild to severe) in up to 90% of cases. Liver value
changes also occur frequently, with increased ALP and hyperbilirubinemia more notable than elevated ALT. Hepatic changes are often
less severe than renal changes, though evidence of true dysfunction
(hypoalbuminemia and hypoglyceIn the United States, mia) can be present. Urinalysis
the highest concentra- reveals evidence of tubular dysfunction of disease exists tion, with isosthenuria, glucosuria,
in the mid-Atlantic bilirubinuria, proteinuria, and/or
coastal regions includ- hematuria. Leptospiral organisms
ing Northern Virginia cannot be seen on routine urinalysis.
and the greater DC Approximately 15% of cases have
metro area
laboratory evidence of DIC with coagulation testing.
Imaging changes can include nodular or interstitial to alveolar pulmonary infiltrates (LPHS). Abdominal ultrasound can reveal a variety
of renal abnormalities and changes consistent with inflammation and
antigenic stimulation (lymphadenopathy, splenomegaly, and peritoneal effusion).
Several laboratory tests are available to diagnose Leptospirosis. The
microscopic agglutination test (MAT) is the most commonly used
test, which is a visible reaction of patient sera with live, Leptospiral
organisms using dark field microscopy. Because acutely infected animals can have negative MAT titers in the first week, convalescent
titers within 10-14 days are strongly recommended. A 4-fold increase
in convalescent titers is supportive of infection, and is the strongest
diagnostic support for clinical Leptospirosis.
However, the MAT is not perfect. The subjective nature of MAT
means that it is difficult to standardize results between laboratories
(make sure to use the same laboratory for acute and convalescent
titers). Additionally, there is cross-reactivity between serogroups.
Contrary to previous belief, the highest MAT titer cannot be used to
predict the infecting serovar. It is known that vaccination can influence MAT results (vaccine titers decline by 4 months after vaccination).
Titers from natural infection usually persist for a year, and antimicrobial therapy can blunt the antibody response.
PCR is a complimentary diagnostic test with its own pros and cons. It
can be used to detect Leptospires in the blood or urine (before development of antibodies), but the test should be performed prior to
antibiotic use. Importantly, vaccination will not cause a false positive
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PCR result, but it does not accurately distinguish the infecting serovar. At this time, there is limited evidence regarding PCR validation.
Other, less common diagnostic tests include histopathology and silver
staining and culture and isolation (difficult and dangerous). Because
no diagnostic test is perfect, make a clinical diagnosis combining
available information, convalescent titers, and response to treatment.
Treatment
At this time, the recommended treatment for Leptospirosis is doxycycline at a dose of 5 mg/kg IV or PO twice daily for 14 days. This
therapy is thought to clear bacteria both from the blood stream and
from the kidneys. Previously, treatment with penicillins prior to treatment with doxycycline was advocated; this strategy can still be used
but is no longer considered necessary.
Further supportive care is indicated based on the severity of disease
and particular syndrome involved. IV fluid therapy is often needed to
supply required fluids for typically very polyuric patients (can exceed
200 mg/kg/day). Renal dialysis or continual renal replacement therapy can be life saving in severely azotemic or oliguric/anuric patients.
Closed urinary collection systems assist in quantification of ins/outs
and also in containment of infectious biomaterial.
Prognosis
In general, the prognosis for dogs with Leptospirosis good, with survival rates of up to 80%. However, extensive and expensive inpatient
supportive care may be needed. The prognosis with LPHS is unfortunately worse, with only about 30% survival and possible death within
3 days. In general, it takes about 10-14 days for significant clinical improvement; however, regeneration of renal tissue and tubular function
can take a month or longer. Patients may be left with chronic renal
disease or chronic hepatitis.
Vaccination and Preventative Medicine
Current vaccines against Leptospirosis appear to be effective in preventing
disease caused by the included serovars (Lepto4 includes serovars Canicola,
Icterohemorrhagia, Pomona, and Grippotyphosa), and immunity can last
up to 12 months. Newer evidence suggests that Leptospirosis vaccines do
not induce any more allergic reactions than other vaccines. Because
Leptospirosis can be a fatal and zoonotic disease, annual 4-way vaccination is recommended for all dogs with an exposure risk.
Preventive measures are indicated at home and in the clinic. In the
clinic, all dogs with acute kidney or liver failure should be treated as a
suspect Leptospirosis case until an alternate diagnosis is confirmed.
Gloves, protective eyewear, and gowns should be worn when interacting with patients and changing urinary catheters or collection systems.
Isolation is not necessary; however, patients should be housed on
floor-level cages in low traffic areas where possible. If a urinary collection system is not used, patients should be walked frequently to prevent
indoor accidents, and voiding should occur on a non-permeable, easily
cleaned surface (subsequent cleaning with a 10% bleach solution).
Normal laundering of bedding will inactivate the organism.
At home, treated dogs represent a low risk to household members;
however basic hand washing and avoidance of urine is still important.
Human family members should be directed to seek the guidance of
their own doctor in the event of illness. All dogs in the household
should be tested for Leptospirosis, due to presumed shared environmental exposure, and all should likely be treated with two weeks of
doxycycline therapy.
The information in this article comes primarily from the 2010 ACVIM consensus
statement on Leptospirosis. Other references are also available upon request.
Hepatobiliary Disease
Making the Diagnosis
By Kelly Gisselman, DVM, MS, DACVIM
Diagnosing hepatobiliary disease in small animals can be challenging.
Due to the dual blood supply of the organ (systemic and portal) it is susceptible to insult from systemic disorders as well as primary organ
disease making clinical signs of liver disease often very non-specific (inappetance, lethargy, weakness, vomiting). More specific hepatobiliary
signs often occur with severe or end-stage disease such as icterus, hypoglycemia, bleeding tendencies, hepatic encephalopathy and ascites.
History
A good history is important for patients that
present with a suspicion of hepatobiliary disease.
Be sure to ask about medications (prescribed or
over-the-counter (e.g. non-steroidal anti-inflammatory drugs, Tylenol, phenobarbital,
ketoconazole, lomustine, potentiated sulfonamindes) or supplements and nutraceuticals (e.g.
pennyroyal oil)), exposure to toxins (e.g. xylitol)
Dr. Kelly Gisselman
and infectious agents (e.g. Leptospirosis), recent
anesthetic events (poor recovery from anesthesia
can be suspicious for portosystemic vascular anomaly (PSVA)), historical events (overweight felines with inappetance and weight loss can
suggest hepatic lipidosis), environment (e.g. aflatoxin exposure), travel
and vaccine status (e.g. Leptospirosis, Canine Adenovirus) as well as
noting breed specific hepatobiliary diseases (e.g. copper-associated hepatopathy in Bedlington Terriers).
Clinicopathology
It is important to note on physical exam size of liver, jaundice, abdominal
pain, fluid wave, fundic abnormalities (chorioretinitis) and pyrexia.
Clinicopathologic evaluation can help to identify hepatobiliary disease as
well as other organ systems that are affected. Complete blood count can
reveal microcytosis without anemia (seen with PSVA), target cells, poikilocytes and Heinz bodies (cats). Anemia can develop due to a coagulopathy,
anemia of chronic disease or bleeding gastric ulcers. Thrombocytopenia
can develop due to decreased hepatic thrombopoietin production.
Biochemistry profile can revealed increased alanine aminotransferase
(ALT) and/or aspartate aminotransferase (AST), secondary to leakage
from damaged hepatocytes which is seen with primary hepatocellular disease, and/or elevations in alkaline phosphatase (ALP) and/or
gamma-glutamyl transferase (GGT), indicating elution from damaged
membranes or increased synthesis (ALP) which can be seen with cholestatic disease. There are three types of ALP that can be released – the bone
isoenzyme (released with bone growth and destruction), the liver isoenzyme and the steroid isoenzyme (with exogenous steroid use this enzyme
will resolved 2-3 months off medication). The magnitude of hepatobiliary
enzyme elevation can be proportional to the severity of active hepatobiliary damage but not predictive of hepatobiliary functional capacity.
Biochemical parameters that indicate hepatobiliary function are the bilirubin, glucose, cholesterol, blood urea nitrogen (BUN) and albumin. Besides
decreased hepatic update, bilirubin is also affected by posthepatic disease
interfering with excretion of bilirubin and cholestasis of sepsis (seen in cats
and can occur in the absence of hepatobiliary damage).
Other tests to consider for hepatobiliary disease include urine analysis
to look for bilirubin and ammonium biurate crystals (can be seen with
PSVA), coagulation profile, bile acids (serum and urine), ammonium
blood level, thoracic and abdominal radiographs, abdominal ultrasound, fluid analysis (if ascites is present) +/- hepatic cytology,
Page 3
infectious disease screening, endocrine disease testing, scintigraphy,
CT and MRI. Hepatic biopsy is considered if there are persistent serial
increases in liver enzymes, abnormal hepatic function tests, hepatomegaly of unknown cause, ultrasonographic abnormalities of the
hepatic parenchyma and to evaluate for breed-specific hepatopathies.
Treatment
The aim of treatment for hepatic disease is to address underlying
cause (if known), reduce/prevent inflammation, copper accumulation, oxidative damage and fibrosis, provide adequate nutrition and
treat complications of disease (HE, coagulopathy, gastric ulceration,
fluid/electrolyte disturbances, ascites, infectious disease). Antioxidants
used to treat hepatobiliary disease include vitamin E, Milk Thistle
(Silymarin) and S-Adenosylmethionine. Antifibrotics and anti-inflammatories include cholchicine, gamma-interferon, milk thistle,
penicillamine, prednisone, ursodeoxycholic acid and zinc.
Coagulopathies can be treated with Vitamin K +/- plasma therapy.
Ascites can be treated with diuretics (spironolactone).
Common Hepatopbiliary Diseases
Feline Inflammatory Liver Disease has recently been reclassified by the
World Small Animal Veterinary Association (WASVA) Liver
Standardization Group. This group prefers the term cholangitis to cholangiohepatitis because the primary inflammation in felines surrounds the
bile ducts. The four categories are most commonly neutrophilic cholangitis – acute and chronic form, lymphocytic cholangitis, cholangitis
associated with liver flukes and lymphocytic portal hepatitis. The acute
neutrophilic form is seen mostly in young to middle age male cats, causes
vomiting, diarrhea, anorexia and lethargy with fever, dehydration, icterus
and abdominal pain +/- hepatomegaly. A neutrophilic leukocytosis can
be seen in cats with a fever as well as ALP, GGT, ALT, bilirubin and bile
acids can be elevated. Most commonly Escherichia coli is cultured from
the bile or liver in this disease and the mainstay of treatment is with antibiotic therapy (cephalosporins, amoxicillin or amoxicillin-clavulanic acid
+/- fluroquinolones). Chronic neutrophilic cholangitis (also known as
lymphoplasmacytic cholangitis) is typically seen in older cats and is many
times associated with inflammatory bowel disease and pancreatitis, 83%
and 50% respectively (Gagne et al., 1996). Etiology of this condition is unknown, so the role of bacteria is unclear; however, antibiotics and
corticosteroids are typically used to treat this condition. The other categories are further discussed in the WSAVA standards for clinical and
histological diagnosis of canine and feline liver disease (Elsevier, 2005).
Feline Hepatic Lipidosis is typically seen in overweight cats that experience a period of anorexia and is often secondary to another primary
condition that triggered that anorexia (such as pancreatitis, inflammatory bowel disease and/or cholangitis). ALP, bilirubin, ALT and AST are
commonly elevated with a normal GGT. These patients can be coagulopathic, so a coagulation panel (at least prothrombin time (PT)) should
be evaluated. Treatment is nutritional support as well as other supportive medications, vitamin K therapy +/- plasma therapy if PT is prolonged,
H2 blockers and treatment of hepatic encephalopathy if present as well
as treating any underlying conditions that lead to the hepatic lipidosis.
Congenital PSVA can be classified as intrahepatic shunt (seen in large
dogs), extrahepatic shunt (seen in small dogs and cats) and microvascular dysplasia (recently renamed as hypoplasia of the portal vein).
These patients can have normal hepatic enzymes, but abnormal liver
function parameters (high bile acids, hypoglycemia, hypoalbuminemia, low BUN). Ultrasound, portograms and nuclear scintigraphy
can help to diagnose this condition. Protein C activity has been used
to help distinguish between portosystemic shunts (<70% protein C
activity) and microvascular dysplasia (>70% protein C activity)
(Oliver et al., 2006). These patients can be medically (with lactulose,
low protein diet and neomycin, metronidazole or amoxicillin to help
reduce ammonia production/absorption) and surgically managed.
Most patients with microvascular dysplasia don’t require therapy.
Gallbladder mucoceles seem to be an emerging cholestatic disease (it
was rarely reported prior to 1990). Mucoceles are an accumulation of
the mucus component of bile in the gallbladder with hyperplasia of
mucus-secreting cells seen on histopathology. Shetland sheepdogs
seem to be over-represented for this disease (Aguirre et al., 2007).
The odds of a mucocele formation were also 29 times higher in dogs
with hyperadrenocorticism as compared to those without (Mesich et
al., 2009). Mucoceles have primary cholestatic enzyme elevations and
can be diagnosed on ultrasound – most patients with clinical signs
from mucocele disease have abdominal pain, are lethargic and anorexic and are at risk for gallbladder rupture and subsequent bile
peritonitis. Medical management has been described to attempt to
resolve mucoceles (Walter et al., 2008) but surgery is the recommendation for mucoceles causing clinicopathologic disease.
Canine chronic hepatitis can be familial (e.g. Doberman Pinchers,
Bedlington Terriers), infectious (e.g. leptospirosis), drug-induced (e.g.
anticonvulsants) or idiopathic. It is more of a primary hepatocellular
disease, so ALT and AST will be higher than the cholestatic liver enzymes and these patients have elevated serum bile acids. Imaging may
reveal a normal to small size liver. Liver biopsy is needed to confirm the
diagnosis (wedge biopsy is preferred to needle biopsy (Cole et al, 2002)).
It is recommended to also submit aerobic/anaerobic cultures (bile cultures yields higher positive culture results than liver (Wagner et al, 2007))
and to stain for and quantify copper levels. Treatment is immunosuppressive agents (if not an infectious etiology), choleretics, antioxidants,
low protein diet and supportive care; if copper-associated hepatitis use
copper chelators (zinc, penicillamine) and copper-restricted diet.
References
1.Aguirre AL, et al. Gallbladder disease in Shetland Sheepdogs: 38 cases (1995-2005).
JAVMA, 231, p79. 2007.
2.Balkman CE, et al. Evaluation of urine sulfated and nonsulfated bile acids as a diagnostic
test for liver disease in dogs. JAVMA, 222, p1368. 2003.
3.Bonagura JD and DC Twedt. CVT XIV: Gastrointestinal Disease. p476. 2009.
4.Carlisle CH, et al. Anatomy of the portal and hepatic veins of the dog. Vet Rad & Ult,
36(3), p227. 1995.
5.Center SA. Diseases of the gallbladder and biliary tree. Stombeck’s Small Animal
Gastroenterology, 3rd Edition. p860. 1996
6.Center SA, et al. Evaluation of the influence of S-adenosylmethionine on systemic and
hepatic effects of prednisolone in dogs. AJVR, 66, p330. 2005.
7.Center SA, Warner KL, Erb HN. Liver glutathione concentrations in dogs and cat with
naturally occurring liver disease. AJVR, 63, p1187. 2002
8.Cole TL et al. Diagnostic comparison of needle and wedge biopsy specimens of the liver
in dogs and cats. JAVMA, 220 (10), p1483. 2002.
9.D’Anjou MA, et al. Ultrasonographic diagnosis of portosystemic shunting in dogs and
cats. Vet Rad Ultr, 45, p424. 2004.
10. Elsevier publisher. WSAVA standards for clinical and histological diagnosis of canine
and feline liver disease. 2005.
11.Gagne JM et al. Clinical features of inflammatory liver disease in cats: 41 cases (19831993). JAVMA 214:513, 1999.
12. Gerritzen-Bruning MJ, et al. Diagnostic value of fasting plasma ammonia and bile acid
concentrations in the identification of portosystemic shunting in dogs. JVIM, 20, p13. 2006.
13. Mesich, et al. Gallbladder mucoceles and their association with endocrinopathies in
dogs: a retrospective case-control study. JSAP. 50(12): 630-5, December 2009.
14.Meyer D, Thompson MD, Senior D. Use of ursodeoxycholic acid in a dog with chronic
hepatitis: effects on serum hepatic tests and endogenous bile acid composition. JVIM,
11, p195. 1997.
15. Olivier T et al. Evaluation of plasma protein C activity for detection of hepatobiliary
disease and portosystemic shunting in dogs. JAVMA, 229, p1761. 2006.
16. Trainor D, et al. Urine sulfated and nonsulfated bile acids as a diagnostic test for liver
disease in cats. JVIM, 17, p145. 2003.
17.Wagner et al. Bacterial culture results from liver, gallbladder, or bile in 248 dogs and cats
evaluated for hepatobiliary disease: 1988-2003. JVIM, 21(3) 417-24, May-Jun 2007.
18.Walter R. et al. Nonsurgical resolution of gallbladder mucocele in two dogs. JAVMA,
232 (11). 2008.
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Cataracts
By Elizabeth Adkins, DVM, MS, DACVO
The term “cataract” refers to any opacity in the lens of the eye that has
the potential to block vision. Cataracts can be incomplete and occupy
only a small portion of the lens, or can be complete, involve the entire
lens, and be blinding. Most cataracts are breed or age-related or secondary to diabetes mellitus or inflammation. Common breeds
affected by cataracts include Boston Terriers, Cocker Spaniels, Bichon
frises, and Labrador retrievers among others.
How are cataracts treated?
The only currently available effective treatment
of cataracts is surgical removal of the abnormal
lens. Most cataracts are removed surgically when
vision impairment can be detected at home.
Once cataracts are affecting vision, surgery
should be performed as soon as possible to avoid
greater risk of complications. Cataracts that have
been present for a significant period of time that
have become “hypermature” are associated with
greater postoperative complications including
retinal detachment, inflammation, secondary
glaucoma, and longer surgical times.
Dr. Elizabeth Adkins
Why should the client pursue cataract surgery?
Some post-operative complications may include, but are not limited
to, postoperative glaucoma, retinal detachment, inflammation, infection, corneal ulceration and intraocular scar formation (e.g., capsular
fibrosis). These complications, although rare, may require additional
examinations, long-term medication, or even additional surgery and
could result in blindness or loss of the eye. However, your patient will
be monitored carefully after surgery for all of these complications so
that the eye can be treated as needed.
What is involved in the post-operative care?
Your patient will most likely go home the day of or the day after surgery.
The intraocular pressures must be critically monitored for the first 24
hours. Dr. Adkins will check for signs of inflammation or corneal ulceration and treat as needed. The patient will go home in an Elizabethan
collar for 3 weeks to prevent him or her from traumatizing the eyes.
It will be necessary for your client to give the patient topical medications
four times a day for the first week, and then with decreasing frequency
after the first recheck. The patient will also go home on systemic antibiotics and anti-inflammatory medications. A typical recheck schedule
will involve appointments the week after surgery, then 2 weeks after, 1
month after, 2 months after, 4 months after then every 6 months.
Medications and recheck regimen will vary if complications occur.
While the post-operative medications can be time-consuming, the success of cataract surgery depends heavily on owner compliance and
administration of medications after surgery is complete.
Early removal of cataracts and restoration of vision can provide a dramatic improvement in the quality of your patient’s life. Careful screening
of patients for health issues that would increase the risk of complications
of anesthesia or ocular surgery is crucial to selecting ideal patients, since
surgery is not indicated in every patient. The referring veterinarian and
the Hope Center Ophthalmology department can help the client make
this decision if the patient’s vision is impaired by cataracts.
Is my patient a candidate for surgery?
If you diagnose cataracts in one of your patients the next step is referral to
the Hope Center Ophthalmology Department for further evaluation. We
will then examine the lenses to determine whether the patient is a good
candidate for surgery and perform two pre-operative tests to ensure that
the eye is healthy and that the patient is a candidate for surgery.
The first test is an electroretinogram (ERG), which determines whether
the retina is functioning adequately. The second test is an ocular ultrasound to examine the structure of the eye and rule out abnormalities such
as a retinal detachment. As cataract surgery requires general anesthesia, a
normal physical exam and laboratory tests including a chemistry panel, a
complete blood count, and a urinalysis will be needed prior to surgery and
these test can be done in your practice or at the Hope Center.
What is involved in the surgical procedure?
After passing the pre-operative tests, your patient will be placed under
general anesthesia and carefully monitored with state-of-the-art
equipment. During the surgical procedure, a small incision is made in
the cornea and a circular opening is created in the outer capsule of the
lens to provide access to the cataract. The cataract then undergoes a
process called phacoemulsification, during which an ultrasonic probe
breaks the cataract into small pieces that can then be aspirated from
the eye. If the lens capsule that remains in the eye appears healthy, an
artificial intraocular lens (IOL) can be placed within the capsule. Most
of the lenses implanted at the Hope Center are foldable, injectable
lenses similar to those used in human cataract patients. The incision
is then closed with fine suture.
How successful is cataract surgery?
Cataract surgery is successful in 90-95% of patients. Vision is typically
restored as soon as the patient has fully recovered from anesthesia.
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Coming Up...
Client Service Manager
We would like to formally introduce our
new Client Service Manager, Mrs. Lisa
Daley, LVT. This position was created with
the sole purpose of examining the entirety
of the client experience and discovering
avenues for continued improvement. If you
ever have questions, concerns, or compliments
about a client’s feedback regarding our
hospital, please contact her at 703-281-5121.
Lisa Daley, LVT
The Hope Center and Veterinary Surgical Centers invite you to
join us for Facets: A Veterinary Continuing Education
Symposium to be held on March 11, 2012. The event will take
place at The Mason Inn at George Mason University, 4352
Mason Pond Drive, Fairfax , VA 22030
• 6 Hours of CE Credit for Veterinarians and Technicians
• Free to Attend Thanks to Support from our Sponsors
• Multitract Experience with Choice of 20 Veterinarian Courses
• Beginner and Intermediate Ultrasound Wet-Labs
• Technician Tract with 6 Hours of Credit
• Post-Event Social Hour in Hotel Lounge
• More Information and RSVP at www.HopeCenter.com/CE
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