October 2018   |   Volume 16   |   Issue 10

Fluid Therapy Overview

in this issue

in this issue

Fluid Therapy

Intercostal Blocks for Rib Fractures

Pruritus & Neuropathic Pain in a Dog

Top 5 Suggestions of Canine Hyperadrenocorticism

Differential Diagnosis: Increased or Decreased Total Thyroxine

Hemorrhagic Anterior Uveitis in a Labrador Retriever

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Hemorrhagic Anterior Uveitis in a Labrador Retriever

Alison Clode, DVM, DACVO, Port City Veterinary Referral Hospital, Portsmouth, New Hampshire

Ophthalmology

|Peer Reviewed

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Hemorrhagic Anterior Uveitis in a Labrador Retriever

Figure 1 The patient’s left eye on presentation. The generalized corneal edema, superficial and deep peripheral corneal vascularization, and intraocular hemorrhage, with a visible but difficult to visualize pupil, are evident.

THE CASE

Sammy, a 9-year-old neutered male Labrador retriever, is presented for evaluation of a red, cloudy, painful left eye. The abnormal appearance to the eye was noted by the owners after Sammy had been left to play unattended with the other dog in the household for approximately 2 hours. No treatment was administered by the owners, and Sammy was presented 45 minutes after the owners first noted the abnormality.

On examination, Sammy is bright, alert, and responsive. The left eye is blepharospastic, with mild swelling of the eyelids, conjunctival hyperemia, corneal edema, hyphema, and superficial and deep peripheral corneal vascularization (Figure 1). The pupil is difficult to visualize but appears miotic as compared with the right eye. Direct pupillary light reflex (PLR) is absent, and consensual PLR in the right eye is present but subjectively decreased. Dazzle reflex (ie, reflex reaction to stimulation of the eye by a bright light) is positive, but menace response is negative in the left eye. Menace response, direct PLR, and dazzle reflex are positive in the right eye, but consensual PLR in the left eye is difficult to visualize due to hyphema in the left eye. Schirmer tear test shows >15 mm wetting/min in both eyes, fluorescein stain is negative in both eyes, and intraocular pressure (IOP), estimated by applanation tonometry, is 14 mm Hg in the right eye and 6 mm Hg in the left. The remainder of the ocular examination in the right eye, including fundic examination, is normal.

What are the next steps?

THE CHOICE IS YOURS...

CASE ROUTE 1

Diagnose the patient with presumptive hemorrhagic anterior uveitis secondary to trauma in the left eye and treat for anterior uveitis.

CASE ROUTE 2

Diagnose the patient with hemorrhagic anterior uveitis of unknown etiology in the left eye and perform additional diagnostics.

IOP = intraocular pressure, PLR = pupillary light reflex

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Differential Diagnosis: Increased or Decreased Total Thyroxine

Shanna Hillsman, LVMT, University of Tennessee

M. Katherine Tolbert, DVM, PhD, DACVIM (SAIM), Texas A&M University

Endocrinology & Metabolic Diseases

|Peer Reviewed|Web-Exclusive

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Differential Diagnosis: Increased or Decreased Total Thyroxine

Following are differential diagnoses, listed in order of likeliness, for patients presented with increased or decreased total thyroxine (T4).

Increased Total Thyroxine

  • Hyperthyroidism
    • Functional benign adenomatous hyperplasia
    • Functional thyroid carcinoma
    • Thyroxine oversupplementation
    • Dietary causes
  • Analytical error (eg, false positive)

Decreased Total Thyroxine

  • Nonthyroidal illness (eg, euthyroid sick syndrome)
  • Hypothyroidism
    • Lymphocytic thyroiditis
    • Thyroid atrophy
    • Iatrogenic secondary to radioactive iodine therapy
    • Methimazole therapy
    • Thyroid neoplasia
    • Sulfonamides
    • Congenital
  • Hyperadrenocorticism
  • Drug effects
    • Phenobarbital
    • Potassium bromide
    • Carprofen
    • Clomipramine
    • Glucocorticoids
    • Propranolol
  • Analytical error

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Top 5 Suggestions of Canine Hyperadrenocorticism

Todd Archer, DVM, MS, DACVIM, Mississippi State University

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Top 5 Suggestions of Canine Hyperadrenocorticism

Canine hyperadrenocorticism is a clinical disorder characterized by several common clinical signs, including polyuria, polydipsia, polyphagia, alopecia, thin skin, a pot-bellied appearance, and panting.1 Hyperadrenocorticism results from excess cortisol production secondary to either an adrenal tumor or a pituitary tumor, causing excessive production of adrenocorticotropic hormone (and, subsequently, an excess production of cortisol).1

After a patient has been assessed through a detailed history and physical examination, preliminary testing should be performed prior to specific endocrine testing and should include CBC, serum chemistry profile, and urinalysis. Findings consistent with canine hyperadrenocorticism suggest that further endocrine testing is needed to arrive at a specific diagnosis of canine hyperadrenocorticism.

Following are the author’s 5 most common findings seen on CBC, serum chemistry profile, and urinalysis results in patients with confirmed canine hyperadrenocorticism.

1

Stress Leukogram & Thrombocytosis

A stress leukogram is a common but nonspecific finding in dogs with hyperadrenocorticism. It often consists of lymphopenia, eosinopenia, leukocytosis characterized by mature neutrophilia, and, occasionally, monocytosis.2 Multiple factors contribute to the development of mature neutrophilia, including an increased release of mature neutrophils from the bone marrow, a shift of marginated neutrophils from the periphery into circulation, and/or a decreased amount of neutrophils leaving the circulation into tissue.2 Lymphopenia occurs as a result of a redistribution of lymphocytes within the circulation, as well as possible lympholysis.2 Eosinopenia occurs through steroid-induced sequestration of eosinophils in bone marrow and in other tissues.2 If monocytosis is present, it is thought to result from a shift of marginated monocytes from the periphery into circulation.2

A high-normal–to–increased platelet count may also be found on CBC. As many as 75% to 80% of dogs may have thrombocytosis at the time of diagnosis.1

2

Elevated Liver Enzymes

Serum alkaline phosphatase (ALP) and alanine aminotransferase (ALT) are often elevated in dogs with hyperadrenocorticism. ALP tissue activity can be found in the intestine, kidney, liver, and bone.3 The liver is thought to contribute the majority of ALP measured on serum chemistry profile, with bone being a minor contributor.1 Little to no intestinal or renal ALP isoenzyme activity has been found in the serum of dogs because of the extremely short half-life.1 In the liver, the primary location of ALP is the bile canalicular membrane of hepatocytes.3 In dogs, steroids (exogenous or endogenous) cause an increase in ALP of hepatic origin (ie, the corticosteroid-induced isoenzyme of ALP). This steroid-induced increase in ALP is the most common abnormality found on serum chemistry profile in dogs with hyperadrenocorticism, with incidence at diagnosis often as high as 85% to 95%.4

ALT is a cellular leakage enzyme, and elevations are primarily thought to come from hepatocyte injury/damage. ALT also originates from skeletal muscle, and elevated ALT could come from muscle trauma or a myopathy. Measurement of creatinine kinase can help distinguish the source of increased ALT between liver and muscle. In dogs with hyperadrenocorticism, the increase in ALT is thought to occur secondary to hepatocyte damage from swollen hepatocytes, hepatocellular necrosis, accumulation of glycogen, and/or disturbances in hepatic blood flow.4

Whereas increases in ALT are typically mild, increases in ALP can range from mild to severe, with severe increases being as high as 10 times the upper limit of the normal reference interval. Liver enzyme elevations vary widely among affected individual dogs.4

3

Hyperglycemia

Dogs with hyperadrenocorticism often have mild hyperglycemia (30%-40% of affected patients).5 The ability of cortisol to increase hepatic gluconeogenesis—as well as its antagonistic effects on insulin in peripheral tissue, which decrease peripheral utilization of glucose—can cause blood glucose to increase.4 Hypercortisolism-induced hyperinsulinemia may subsequently develop as the pancreas continues to secrete insulin in an attempt to maintain normoglycemia; however, many dogs will have only mild hyperglycemia at diagnosis. A small subset of dogs will have overt diabetes (glucose, >250 mg/dL [>13.875 mmol/L] with glucosuria and consistent clinical signs) in addition to hyperadrenocorticism.4 Thus, the elevation in glucose must be critically evaluated to determine if diabetes is present.

4

Hypercholesterolemia

Elevated cholesterol is often noted on serum chemistry profile results in dogs with hyperadrenocorticism. Glucocorticoids can increase lipolysis in adipose tissue, generating both free fatty acids and glycerol, which serve as substrates for gluconeogenesis. This lipolysis in adipose tissue leads to an increase in blood cholesterol. Approximately 90% of dogs with hyperadrenocorticism will have hypercholesterolemia at diagnosis.1

5

Dilute Urine

Two of the most common clinical signs associated with canine hyperadrenocorticism are polyuria and polydipsia, which are observed in approximately 90% of patients with hyperadrenocorticism.4 Although the causes of polyuria and polydipsia can include several factors, polyuria has generally been thought to develop before polydipsia. The influence of cortisol at the level of the kidney causes an impaired tubule response to antidiuretic hormone,6 which prevents appropriate water reabsorption and causes urine to be less concentrated. Polydipsia subsequently develops to maintain hydration. This is considered a form of secondary nephrogenic diabetes insipidus in which there is a lack of kidney response to antidiuretic hormone. In most dogs, urine specific gravity is less than 1.0304; these dogs are also often found to be isosthenuric (ie, having a urine specific gravity of 1.007-1.015).7

Conclusion

A minority of patients with hyperadrenocorticism may be presented with polyuria, polydipsia, and dilute urine but have no other clinical abnormalities on CBC, serum chemistry profile, or urinalysis. Lack of a stress leukogram, liver enzyme elevation, hyperglycemia, or hypercholesterolemia should not prevent clinicians from performing specific endocrine testing for canine hyperadrenocorticism. Although most dogs with hyperadrenocorticism will have one or more abnormalities on CBC and serum chemistry profile, the condition should still be included on the differential list in any dog with polyuria and polydipsia, dilute urine, and normal CBC and serum chemistry profile results. 

ALP = alkaline phosphatase, ALT = alanine aminotransferase

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Pruritus & Neuropathic Pain in a Dog

Hélène L.M. Ruel, DMV, DÉS, MSc, DACVIM (Neurology), PhD Candidate, Université de Montréal, Quebec, Canada

Paulo V. Steagall, DVM, MS, PhD, DACVAA, Université de Montréal, Quebec, Canada

Neurology

|Peer Reviewed

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Pruritus & Neuropathic Pain in a Dog

History

A 4-year-old, 55-lb (25-kg), neutered male Portuguese water dog was presented for a 1-year history of intractable pruritus and excessive licking of the lateral aspect of the 5th digit of the left pelvic limb. BCS was 5/9. The pruritus began concomitantly with the growth of an erythematous cutaneous mass localized between the 4th and 5th digit on the same paw, which was later diagnosed as an abscess. The patient received an injectable course of antibiotics and corticosteroids followed by 2 oral antibiotic and corticosteroid courses over a 5-month period. There was no treatment response, so surgical excision of the mass was performed.

After the surgery, pruritus became almost continuous (10/10 using a canine pruritus severity scale1) and persisted even after the wound had healed. A second surgical procedure was performed 3 months after the first surgery to debride the wound, and the skin over the 4th and 5th digits was fused. The patient continued to exhibit compulsive licking and biting of the pelvic limb postoperatively, so the owners were instructed to use an Elizabethan collar or a sock over the affected paw to prevent self-mutilation.

Because pruritus persisted, radiography and ultrasonography of the distal limb were performed; no abnormalities were present. Prednisone (0.5 mg/kg PO q24h) and diphenhydramine (2.2 mg/kg PO q8h) were administered, and the degree of pruritus decreased to 3/10. The patient was referred to a dermatologist, who administered amoxicillin–clavulanic acid for treatment of suspected pyoderma. Pruritus was diminished but not resolved (2/10). Localized biting and licking in absence of an obvious local underlying cause was suggestive of a neurologic etiology, and the dog was referred to a board-certified neurologist for further diagnostic investigation. 

Physical Examination

Physical examination was unremarkable except for a 4-cm area of alopecia over the distal and dorsolateral aspect of the left pelvic limb and compulsive licking induced by a light touch and pin prick over the sensory distribution of the tibial nerve from the tibiofemoral joint to the extremity of the limb. The patient’s responses to the light touch and pin prick were thought to represent allodynia and hyperalgesia, respectively. Neurologic examination revealed the following changes:

  • Stiffness of the left pelvic limb characterized by weak flexion of the stifle and short strides
  • The patient favored a resting position in semi-sternal recumbency (ie, patient lying on his chest and left pelvic limb).
  • Decreased postural reactions on the left pelvic limb as compared with the ipsilateral side, which was normal
  • Normal spinal reflexes except for an incomplete left pelvic limb withdrawal reflex as compared with the ipsilateral side, which was normal
  • Pain elicited (ie, the patient flinched) on palpation of the lumbosacral junction 

Diagnosis

CBC and serum chemistry profile results were within normal limits. CT of the left pelvic limb and lumbosacral junction revealed a mild protrusion of the intervertebral disk at the lumbosacral junction, without evidence of compression of the cauda equina or L7 spinal root. Left iliac medial and popliteal lymphadenopathy were reported. MRI of the lumbosacral junction confirmed the protrusion at L7-S1 and showed another protrusive but apparently noncompressive disk at L6-L7. Bone remodeling of the cranial facet of S1 was noted protruding into the vertebral canal. Dynamic impingement could not be ruled out.

Concomitant allodynia and hyperalgesia localized over the area of the tibial nerve were suggestive of neuropathic pain. 

DIAGNOSIS:

INTERVERTEBRAL DISK DISEASE

In this case, spontaneous pruritus and excessive licking resulting in secondary abscess formation were thought to represent a sign of abnormal sensation in the affected limb (ie, dysesthesia). Neuropathic pain has no physiologic purpose and involves a lesion of the somatosensory system. Concomitant allodynia and hyperalgesia constitute a component of neuropathic pain. According to the International Association for the Study of Pain, allodynia refers to pain caused by a stimulus that does not normally provoke pain, whereas hyperalgesia corresponds to an increased sensitivity to noxious stimulation.2 Limb nerve entrapment and lumbosacral lesions have been described as potential causes for neuropathic pain in dogs.3,4 Diagnosis of neuropathic pain may be challenging due to the lack of validated tools for its assessment.

Treatment at a Glance

  • Gabapentinoids (eg, gabapentin) to block calcium currents involved in the maintenance of spinal cord central sensitization
  • N-methyl-D-aspartate antagonists (eg, amantadine, ketamine) to prevent or treat central sensitization
  • NSAIDs to reduce peripheral inflammation and hyperalgesia
  • Transcutaneous electrical nerve stimulation used as an adjuvant therapy and as part of a multimodal analgesic approach

Treatment & Long-Term Management

The owners declined surgery and opted for medical management. The patient was successfully treated with gabapentin (10 mg/kg PO q8h), meloxicam (0.1 mg/kg PO q24h), and amantadine (3 mg/kg PO q24h). Pruritus decreased with therapy (2/10). The patient itched occasionally. Gabapentinoids (eg, gabapentin) bind to α2δ-subunits of voltage-dependent calcium channels and block calcium currents involved in the maintenance of spinal cord central sensitization. Nerve injury causes increased glutamate activity. Glutamate binds to N-methyl-D-aspartate receptors, which contribute to spinal central sensitization.5

Transcutaneous electrical nerve stimulation—a technique used in physiotherapy to alleviate pain via inhibition of presynaptic transmission in the dorsal horn of the spinal cord and increased release of enkephalins, endorphins, and dynorphins—was used as an adjuvant therapy and as part of this patient’s multimodal analgesic approach. Transcutaneous electrical nerve stimulation has been used in humans with neuropathic pain as adjunct therapy.6,7

Prognosis & Outcome

After 2 months of treatment, meloxicam was decreased to 0.1 mg/kg q48h and amantadine was decreased to approximately 1-2 mg/kg q48h for 2 weeks, when treatment with both drugs was discontinued. Gabapentin (5 mg/kg PO q8h) was used as maintenance therapy, as the dog was mostly comfortable and only occasionally exhibited shaking of the left pelvic limb. Follow-up consultations every 3 months were suggested.

Take-Home Messages

Neuropathic pain is pain caused by a lesion or disease of the somatosensory system and should be suspected in the presence of central sensitization resulting in allodynia and hyperalgesia.2 Clinical signs of neuropathic pain are nonspecific and often require multidisciplinary collaboration to reach diagnosis. Surgery, primary neurologic disease, diabetes, and osteoarthritis are potential causes of neuropathic pain. The underlying mechanism of neuropathic pain is not fully understood but likely involves hyperexcitability of afferent neurons, peripheral and central sensitization, and activation of the microglia.3 Neuropathic pain is commonly refractory to conventional analgesia and requires a multimodal approach.4

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Lactate in Emergent Dogs & Cats

Selena L. Lane, DVM, DACVECC, University of Georgia

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Lactate in Emergent Dogs & Cats

In the Literature

Kohen CJ, Hopper K, Kass PH, Epstein SE. Retrospective evaluation of the prognostic utility of plasma lactate concentration, base deficit, pH, and anion gap in canine and feline emergency patients. J Vet Emerg Crit Care (San Antonio). 2018;28(1):54-61.


FROM THE PAGE …

Plasma lactate concentration and other acid-base parameters have been associated with patient clinical outcome and provide prognostic information in human ICU and emergency patients. Hyperlactatemia has been shown to provide information on veterinary patient outcomes and is associated with increased illness severity in dogs and cats. It is unknown whether these acid-base derangements are associated with survival in dogs and cats presented to the emergency room.

This retrospective study reviewed records of 566 dogs and 185 cats presented to a university teaching hospital emergency room over a 2-year period. Data collected on each patient included plasma lactate levels, electrolytes, acid-base status, clinical diagnosis, and in-hospital mortality.

Of the study patients, 53% of dogs and 30% of cats had plasma lactate levels >2.5 mmol/L on presentation. Dogs and cats with elevated lactate levels were more likely to have a concurrent metabolic acidosis than to have normal acid-base status. The most common underlying diagnostic categories of dogs with elevated lactate levels were traumatic injury and hemorrhage, neoplasia, and GI disease. In cats, urinary tract disease, traumatic injury and hemorrhage, and GI disease were the most common diagnostic categories associated with hyperlactatemia. Dogs with lactic acidosis had the highest mortality rate (59.8%) of all dogs in the study, which was similar to the high mortality rate (49%) seen in the study cats with lactic acidosis. Cats and dogs with normal blood lactate levels had the lowest mortality rate. Plasma lactate concentration was predictive of mortality in dogs and cats.

These findings are similar to studies performed in humans and support the importance of routine evaluation of lactate and acid-base status in dogs and cats presented on emergency. Evaluation of these parameters can guide owner expectations of outcome in emergent patients and may allow clinicians to recognize patients that may be at highest risk for poor outcome.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Plasma lactate concentration and acid-base parameters in small animal patients are clinically relevant diagnostic tools and should be used in the emergency room when possible.

 

2

Lactic acidosis is indicative of more severe underlying disease and should prompt the clinician to monitor patients for decompensation.

 

3

Lactate concentrations should be measured routinely in emergent patients to provide information about hemodynamic instability and lend insight to patient outcomes.

 

Suggested Reading

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Oral Melphalan for Refractory Relapsing Canine Lymphoma

Timothy M. Fan, DVM, PhD, DACVIM (Oncology, Internal Medicine), University of Illinois at Urbana–Champaign

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Oral Melphalan for Refractory Relapsing Canine Lymphoma

In the Literature

Mastromauro ML, Suter SE, Hauck ML, Hess PR. Oral melphalan for the treatment of relapsed canine lymphoma. Vet Comp Oncol. 2018;16(1):E123-E129.


FROM THE PAGE …

Canine lymphoma has been reported to be responsive to multiagent systemic chemotherapy, with durable and substantive clinical responses (partial and complete remission) achieved in >90% of patients.1,2 However, most dogs will ultimately experience disease relapse, and subsequent response rates and durations of remission with rescue therapies become progressively lower and shorter, respectively. Use of oral alkylating drugs as rescue agents can be appealing to pet owners wishing to minimize stress associated with intravenous therapies; however, some alkylating drugs, although modestly effective as rescue drugs, have potential to cause considerable toxicity and reduction of quality of life.3,4

This retrospective study examined tolerability and clinical activity of melphalan, an oral alkylating agent, for management of relapsing canine lymphoma. Although melphalan is commonly used for the treatment of multiple myeloma,5 its activity alone or in combination with prednisone has not been described as a rescue protocol for relapsing lymphoma. In this study, the tolerability and outcomes associated with oral melphalan and prednisone therapy were described in 19 heavily pretreated dogs with relapsing lymphoma. Oral melphalan exerted marginal activity, with an overall calculated clinical benefit of 31.6%. Although anticancer activity was limited, the tolerability profile of oral melphalan was favorable as determined by a low incidence of significant hematologic toxicity and rare GI toxicity.

These findings suggest that oral melphalan alone or in combination with prednisone can reduce lymphoma tumor burden for short durations in some dogs. Given the tolerability of oral melphalan, it might also be considered a palliative option for owners seeking to maintain quality of life without excessive risk for untoward side effects associated with more dose-intense protocols.

Dog with severe mandibular lymphadenopathy associated with relapsing lymphoma
Dog with severe mandibular lymphadenopathy associated with relapsing lymphoma

FIGURE 1 Dog with severe mandibular lymphadenopathy associated with relapsing lymphoma

FIGURE 1 Dog with severe mandibular lymphadenopathy associated with relapsing lymphoma

Cytology of aspirated enlarged lymph node confirming a diagnosis of relapsing, diffuse, large-cell lymphoma
Cytology of aspirated enlarged lymph node confirming a diagnosis of relapsing, diffuse, large-cell lymphoma

FIGURE 2 Cytology of aspirated enlarged lymph node confirming a diagnosis of relapsing, diffuse, large-cell lymphoma

FIGURE 2 Cytology of aspirated enlarged lymph node confirming a diagnosis of relapsing, diffuse, large-cell lymphoma


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Initial treatment of multicentric lymphoma in dogs is highly effective; however, most dogs will experience disease relapse and require reinstitution of rescue therapies to maintain quality of life and extend survival times.

2

Maintaining quality of life should become centrally important to pet owners of dogs with multicentric lymphoma that have been treated with a multitude of rescue therapies yet experience disease progression.

3

When combined with prednisone therapy, oral melphalan is extremely well tolerated in heavily pretreated dogs and can exert marginal anticancer activities.

 

4

Given its ease of administration, favorable tolerability, and marginal activity in heavily pretreated dogs with relapsing lymphoma, oral melphalan might be considered a palliative option for pet owners emphasizing quality of life during advanced stages of disease progression.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Dog Bites in Humans

Audrey Ruple, DVM, MS, PhD, MRCVS, DACVPM, Purdue University

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Dog Bites in Humans

In the Literature

Westgarth C, Brooke M, Christley RM. How many people have been bitten by dogs? A cross-sectional survey of prevalence, incidence and factors associated with dog bites in a UK community. J Epidemiol Community Health. 2018;72:331-336.


FROM THE PAGE …

A comprehensive understanding of how often humans are bitten by dogs is lacking, as most research into this topic has been based on hospital-admission records. Although not all dog bites are severe enough to warrant hospitalization, even minor dog bites can impact physical and psychologic health and can therefore be a burden on public health.

The authors of this study recognized the limitations of hospital-based data and aimed to survey the population of a semirural town in northwest England. Of the 694 participants representing 30.1% of households in the town, almost one quarter (24.78%) reported having been bitten by a dog at least once. Medical treatment was required in 33.1% of cases; only one bite resulted in hospitalization.

The authors further investigated human-related factors associated with dog bites and the relationships between humans and the dogs that bit them. It was determined that men were more likely than women to be bitten, and dog owners were more likely to be bitten than were non-dog owners, with further increased risk to owners of more than one dog. Personality indicators such as insecurity, fear, and instability were also associated with an increased risk for being bitten. More than half of the surveyed respondents were bitten by a dog they had never met before.

It is important to note that this survey was conducted in a limited geographic region and that these results may not be generalizable to a wider population. However, this study does provide the first investigation of dog bite incidence and risk factors at the community level rather than through hospital-admission records. The increased frequency of dog bites reported combined with the low proportion of bites requiring hospital admission lend credibility to the hypothesis that dog bites occur more commonly than reported.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Pet owners should be informed that although severe dog bites occur relatively infrequently, less severe bites may occur fairly commonly.

 

2

Owners should be educated about the risk for dog bites from unknown dogs, as owners may be likely to come in contact with unknown dogs while participating in activities with their dog or in public spaces frequented by other dogs (eg, dog parks).

 

3

Owners with multiple dogs in the household should be informed about the increased risk for being bitten, as owners of multiple dogs may be up to 27 times more likely to be bitten than non-dog owners.

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Central Venous Jugular Catheters

Jennifer Good, DVM, DACVECC, University of Georgia

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Central Venous Jugular Catheters

In the Literature

Reminga CL, Silverstein DC, Drobatz KJ, Clarke DL. Evaluation of the placement and maintenance of central venous jugular catheters in critically ill dogs and cats. J Vet Emerg Crit Care (San Antonio). 2018;28(3):232-243.


FROM THE PAGE …

Placement of central venous jugular catheters (CVJCs), which use the over-the-wire modified Seldinger technique, can be labor-intensive.1 CVJCs require sterile placement, daily cleaning and disinfecting, and radiography to confirm proper placement. Benefits of CVJCs include the ability to leave the catheters safely in place for several days, easier blood sampling, and the ability to deliver multiple fluid types or medications, including difficult-to-administer infusions (eg, high-percent dextrose). Catheters range from single to triple lumen and may be placed in a pelvic limb vessel if the length is sufficient to place the catheter tip into the caudal vena cava.

This prospective study of 27 dogs and 20 cats in a veterinary intensive care unit aimed to describe problems noted during CVJC placement, conditions associated with unsuccessful catheterization, and complications of CVJC maintenance. Daily assessment, inspection, and cleansing (with dilute chlorhexidine solution) of the insertion site were performed. The overall success rate for catheter placement was 91.5%, with most catheters successfully placed on the first attempt. Older patients and those with low BCS or weight were more likely to require more than one attempt. No complications were associated with catheter use in 67.4% of patients. Most complications were mechanical obstructions (eg, venous thrombosis, kinking, malposition) and irritation (eg, skin redness, local bruising, bandage-related cervical swelling). Inflammatory complications (eg, sterile phlebitis, catheter-related infections) were the least common. The majority of complications were minor and did not necessitate catheter removal. Level of staff experience and occupation of catheter placer (eg, veterinarian vs veterinary nurse) were not found to affect the number of complications.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

It is worthwhile to become trained in proper CVJC placement to prepare for patients hospitalized for prolonged periods. Use of multilumen catheters can help decrease the number of peripheral blood sticks and overall number of catheters needed.

2

Sterile placement of single-lumen intracatheters can be used in lieu of CVJCs. Single-lumen intracatheters are more common in general practice, come in a variety of lengths, do not require use of the modified Seldinger technique for placement, and can be placed in jugular veins or pelvic limb vessels to allow for repeated blood sampling and IV infusions. 

3

Daily unwrapping and cleansing of any catheter sites—peripheral or central—along with the use of gloves and hand-washing between patients can decrease catheter-related infections and should be an important part of hospital protocol.2

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Research Note: Rabies-Neutralizing Antibodies & Rabies Titers

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This study retrospectively reviewed serologic data for rabies-neutralizing antibodies in 662 young dogs to evaluate whether certain variables (eg, signalment, number of vaccinations, vaccine brand and multivalence, time interval between the most recent vaccination and blood sampling) affected dogs’ ability to achieve acceptable rabies titers. Dogs that had been vaccinated twice before 12 months of age were found to have significantly higher antibody titers than those vaccinated once; those vaccinated with monovalent vaccines were more likely to achieve an acceptable titer than those vaccinated with polyvalent vaccines. Dogs vaccinated after 3 to 6 months of age had higher antibody titers than those vaccinated earlier.

Source

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

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Maladaptive Pain in Cats

Tamara Grubb, DVM, PhD, DACVAA, Washington State University

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Maladaptive Pain in Cats

In the Literature

Adrian D, Papich M, Baynes R, Murrell J, Lascelles BDX. Chronic maladaptive pain in cats: a review of current and future drug treatment options. Vet J. 2017;230:52-61.


FROM THE PAGE …

Chronic pain should not be characterized by duration of pain but instead by changes that occur in the nociceptive components of the CNS in response to ongoing stimuli.1 These changes can lead to maladaptive pain, which has no protective purpose and can lead to a debilitating pain syndrome that is difficult to treat; this contrasts with acute pain, which protects the patient from further tissue damage by promoting limited movement of injured tissue.1 Although maladaptive pain is likely to occur in cats,2 there are few proven treatment options.

This review provides a comprehensive discussion of published literature on maladaptive pain and its treatment in cats, with supporting information from other species, including a clear and detailed explanation (with illustrations) of maladaptive pain and the importance of understanding that the disease and its treatment are multifactorial. The importance of pain assessment is discussed, as are potential therapies.

Aside from NSAIDs, few drugs have been proven to be effective in cats—or other veterinary species—for the treatment of chronic or maladaptive pain, and even those proven in humans are not always effective, primarily because of the complexity of the disease. In addition, the common use of acute pain models to test drugs for chronic pain therapy can skew interpretation of a drug’s utility.3,4

Because of the preservation of the mammalian pain pathway components across species,5 it is not considered to be anthropomorphization or malpractice to use drugs with proven efficacy in other mammalian species. However, adverse effects may not be the same across species, and safety studies are often more critical than are efficacy studies. Use of this evidence-based review in combination with treatment protocols from pain management experts6-9 to provide feline patients with evidence-guided pain relief may be beneficial. 


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Feline chronic pain should be treated early, and multimodal analgesia should be used, as chronic pain is often actually maladaptive pain, which can be complicated to treat.

 

2

When designing treatment protocols, clinicians should use evidence-based medicine while also embracing experience-based treatment recommendations from experts.

 

3

Assessment tools for owners to evaluate pets at home should be recommended. For example, having owners videotape their cat at home before and after treatment and sending the videos to the veterinarian to evaluate may be helpful. Clinicians should be cautious of placebo effects10 but also understand the ability of owners to detect quality-of-life changes in their pet.11

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Intercostal Blocks for Rib Fractures

Katherine Bennett, DVM, University of Tennessee

Christine Egger, DVM, MVSc, CVA, CVH, DACVAA, University of Tennessee

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Intercostal Blocks for Rib Fractures

Local analgesic techniques—including intercostal, epidural, and spinal blocks—are frequently used to treat pain related to thoracic surgery or trauma (eg, rib fractures).1

Pain associated with thoracic trauma, whether surgically induced or traumatic in origin, can lead to hypoventilation, delayed recovery, increased morbidity, and prolonged hospitalization.1,2 Local anesthesia at the level of the intercostal spaces provides benefits over thoracic epidural anesthesia by inducing less sympathetic blockade, addressing pain closer to the initiation of the pain pathway, and providing complete blockade of all pain fibers, with minimal effect on ventilation.3 Intercostal nerve blocks have been shown to improve pulmonary function in the postoperative period in human and veterinary patients undergoing thoracotomy4-6; in addition, in humans, intercostal nerve blocks used to treat multiple rib fractures have been shown to be effective and to decrease the amount of systemic opioid needed to control pain.5 Dogs and cats with multiple rib fractures are at risk for decreased pulmonary function and may require high rates of systemic analgesics to control pain.7

Relevant Anatomy

The paravertebral space involves the spinal nerve root, which is continuous with the intercostal nerve. This space is not completely segregated; drugs injected into one specific paravertebral space have the potential to spread cranially and caudally into additional paravertebral spaces, as well as medially and laterally into the epidural and intercostal spaces. The intercostal space is continuous with the paravertebral space and involves the nerve roots that branch from the paravertebral nerve and supply the ribs, intercostal muscles, and skin. In general, the neurovascular structures that line the thoracic cavity have both cranial and caudal branches, which divide and supply the skin and intercostal muscles of segments adjacent to that paravertebral space.

Due to this collateral circulation/innervation, blocking sites adjacent to rib fractures is recommended to ensure appropriate analgesia to the intended site. Risks associated with this procedure include iatrogenic pneumothorax, intraneural or intravascular injection, systemic toxicity of local anesthetics, and, rarely, introduction of bacteria into the intercostal or paravertebral space.

Agents for Intercostal Blocks

Drugs used in intercostal blocks can include local anesthetics, opioids, or α2 agonists; a combination of drugs is often recommended to increase effects on the pain pathway.1,2,5,8 Bupivacaine, a local anesthetic that provides long-term pain relief, is often recommended because it provides 6 to 8 hours of blockade.9 Mixing bupivacaine with either an opioid (eg, preservative-free morphine) or an α2 agonist (eg, dexmedetomidine) can provide additional analgesia by activating local opioid and α2 receptors and through systemic absorption.10 A study in humans noted that the risk for local anesthetic toxicity is highest when local anesthetics are administered at the paravertebral space, and another noted that local anesthetics are also rapidly absorbed from the intercostal space.9

TABLE

Local PERINEURAL Anesthetic Dosages1-3

Drug (Concentration)* Duration of Action** Dose (Dogs) Maximum Dose (Dogs) Dose (Cats) Maximum Dose (Cats)
Bupivacaine (0.5% or 0.25%) 4-12 hr (average, ≈6-8 hr) 0.5-1 mg/kg 2 mg/kg 0.25-0.50 mg/kg 1 mg/kg
Lidocaine (2%) 1-2 hr (average, ≈90 min) 1-2 mg/kg 5-6 mg/kg 0.5-1 mg/kg*** 1-2 mg/kg
Morphine (10 mg/mL or 25 mg/mL) 4-6 hr 0.1 mg/kg   0.1 mg/kg  
Methadone (10 mg/mL) 4-6 hr 0.1 mg/kg   0.1 mg/kg  
Dexmedetomidine (0.5 mg/mL) 4-6 hr 1-2 µg/kg   1-2 µg/kg  
* Onset of local analgesia can take up to 20 minutes but depends on the drug(s) used. Rapid-onset drugs (eg, lidocaine, α2 agonists) can be added to those with slower onset (eg, bupivacaine, opioids) to facilitate a faster onset of analgesia.
** The duration of the block itself is altered by the agents and dose selected for each patient.
*** Note: Systemic uptake should be avoided by ensuring the block does not go intravenously

Care should be taken when calculating drug dosages (Table), and the effects of systemic absorption of local anesthetics and adjunctive agents should be considered.9 If there are multiple rib fracture sites and more volume is needed to appropriately block all ribs, decreasing the dose of bupivacaine and adding lidocaine to increase the volume is ideal; however, this will decrease the overall duration of action. Adding sterile water (or saline) to the volume of local anesthetic may also be appropriate. After the number of fractured ribs is determined, the number of sites to block and the number of aliquots of local anesthetic to prepare should be calculated (see Calculating Intercostal Sites). If multiple ribs are broken on one side, many of these sites will overlap cranially and caudally.

Calculating Intercostal Sites

Fracture Site (rib #) = 7

Cranial Intercostal Spaces: 5-6, 6-7

Affected Space: 7-8

Caudal Intercostal Spaces: 8-9, 9-10

Total Spaces to Block: 5

 

Fracture Site (rib #) = 4, 6

Cranial Intercostal Spaces: 2-3, 3-4; 4-5, 5-6

Affected Spaces: 4-5, 6-7

Caudal Intercostal Spaces: 5-6, 6-7; 7-8, 8-9

Total Spaces to Block: 8 (Note: Several of these spaces overlap between the 2 fracture sites.)


STEP-BY-STEP

INTERCOSTAL BLOCKS FOR RIB FRACTURES


WHAT YOU WILL NEED

  • Clippers and preparation supplies (eg, chlorhexidine scrub, alcohol)
  • Gloves
  • Selected drugs divided into aliquots based on number of sites to block (see Calculating Intercostal Sites)
  • Aliquots of sterile saline
  • New spinal or hypodermic needle (22-25 g) for each site

STEP 1

Sedate (or anesthetize, if needed) the patient using an opioid and either a benzodiazepine or an α2 agonist, depending on the patient’s overall cardiovascular and systemic health status.11

Author Insight

If the patient has suffered fractures due to trauma, electrocardiography and close monitoring should be instituted to observe for evidence of cardiac contusions in the form of arrhythmias. The presence of arrhythmias may change the drug choice for sedation, general anesthesia, and/or paravertebral local blocks.


STEP 2

Obtain thoracic radiographs to confirm the location of the broken rib(s).


STEP 3

Block at least 2 intercostal spaces cranial to and caudal to the fracture on the ipsilateral side to deliver complete analgesia to the fracture site (see Calculating Intercostal Sites). Count sites multiple times to ensure the appropriate spaces are blocked. While wearing gloves, clip long hair at the injection site if needed for accurate palpation, and clear the site of debris and obvious contamination.

Clinician's Brief

STEP 4

Place the patient in lateral recumbency with the injured side up, and ensure supplemental oxygen is being provided. Insert a small (<22-gauge) spinal needle as dorsally as possible (near the intervertebral foramen) at the very caudal border of the rib cranial to the desired intercostal space.

Clinician's Brief
Clinician's Brief

Author Insight

Mask oxygen is considered adequate if the patient is not receiving additional support (eg, nasal cannulas). If the patient already has a nasal cannula, this is preferred over a mask but does not need to be placed solely for this procedure. 


STEP 5

Walk off the rib surface in a caudal direction, then aspirate with a syringe containing a small amount of sterile saline to confirm that the needle is not in a vessel or in the thoracic cavity. 

Clinician's Brief

Author Insight

Imaging (eg, ultrasonography, fluoroscopy) can help indicate the correct location.


STEP 6

Inject a small amount of sterile saline. If there is no resistance, disconnect this syringe and connect the syringe of local anesthetic; if resistance is encountered, carefully redirect the needle, using caution not to enter the thoracic cavity. Slowly inject the total volume for the site over 2 minutes. Repeat the process for each additional site. Monitor the patient for changes in respiratory rate/character or signs of respiratory distress that may be indicative of a pneumothorax. 


STEP 7

Continue with supplemental oxygen, and perform thoracocentesis if pneumothorax is suspected.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Fluid Therapy

Adesola Odunayo, DVM, MS, DACVECC, University of Tennessee

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Fluid Therapy

Fluid therapy is an essential therapeutic component in small animal practice. Normal cellular function can be impaired without water and potentially lead to patient death.1 Intravenous fluids may be prescribed to hospitalized patients to treat hypovolemia, dehydration, electrolyte imbalance, and acid-base abnormalities and to ensure that adequate cellular maintenance requirements are met.2

Fluid Compartments

Understanding the concept of fluid compartments can help the clinician determine the location of the fluid deficit and appropriate treatment. The body weight of nonobese cats and dogs is composed of approximately 60% water.2 Puppies and kittens have higher total body water amount (ie, up to 80% of body weight), as total body water decreases with age.3 In addition, fat has a lower water content; thus, the fluid prescription should be based on estimated lean body weight.4 In adult nonobese cats and dogs, approximately two-thirds of total body water (ie, 66% of total body water or ≈40% of body weight) is in the intracellular space. The remaining one-third (ie, 33% of total body water or ≈20% of body weight) is in the extracellular space; of this extracellular body water, 75% (≈15% of body weight) is in the interstitial space and 25% (≈5% of body weight) is in the intravascular space (Figure). Intracellular fluid loss is generally not appreciated on physical examination and typically manifests as hypernatremia. Treatment of intracellular fluid deficit is beyond the scope of this article. 

Distribution of total body water in an adult nonobese cat or dog
Distribution of total body water in an adult nonobese cat or dog

Figure Distribution of total body water in an adult nonobese cat or dog

Figure Distribution of total body water in an adult nonobese cat or dog

Intravascular fluid deficit (ie, hypovolemia) leads to inadequate oxygen delivery to the cells (ie, poor perfusion or shock). Untreated intravascular fluid deficit can be life-threatening, as oxygen is important for minute-to-minute cellular function maintenance. Inadequate oxygen delivery can lead to hyperlactatemia through anaerobic glycolysis, cell membrane disruption, cell death, and organ death.5 Physical examination findings of hypovolemia (Table 1) include tachycardia in dogs, bradycardia in cats (and in the terminal stages of shock in dogs), prolonged capillary refill time, pale mucous membranes, weak peripheral pulses, cold extremities, and altered mental state. Patients exhibiting these signs require emergent treatment to rapidly restore oxygen delivery. Common clinical conditions that lead to intravascular fluid loss include hemorrhage secondary to trauma, coagulopathy, neoplasia, gastroenteritis, pancreatitis, and peritonitis. 

TABLE 1

PHYSICAL & LABORATORY ABNORMALITIES IN PATIENTS WITH HYPOVOLEMIA & DEHYDRATION

Hypovolemia Dehydration

Tachycardia (bradycardia in terminal stages) in dogs

Pale mucous membranes

Weak peripheral pulses

Altered mentation

Prolonged capillary refill time

Cold extremities

Hypotension

Elevated lactate

Hypothermia, bradycardia (heart rate, <160 bpm), and hypotension*

Dry mucous membranes

Doughy abdomen

Sunken eyes

Skin tenting

Azotemia

Elevated hematocrit and total protein

* Cats tend to demonstrate this triad.

Interstitial fluid deficit (ie, dehydration) is commonly assessed based on a percentage of the estimated interstitial fluid lost (Table 2) and typically does not result in life-threatening abnormalities unless dehydration progresses to approximately 9% or greater. Signs of dehydration that may be identified on physical examination include skin tenting, dry mucous membranes, doughy abdomen, and sunken eyes. The different clinical approaches and urgency for treating poor perfusion and dehydration make differentiating between them vital (Table 1). 

TABLE 2

PHYSICAL EXAMINATION FINDINGS OF DEHYDRATION & ESTIMATE OF FLUID LOSS PERCENTAGE

Dehydration Percentage Physical Examination Findings
<5% Dehydration is not clinically detectable, but patient has history of fluid loss
5%-7%

Dry mucous membranes

Skin tenting

7%-9%

Dry mucous membranes

Skin tenting

Sunken eyes

Doughy abdomen

9%-12%

Dry mucous membranes

Skin tenting

Sunken eyes

Doughy abdomen

Evidence of hypovolemia may be present

12%-15%*

Dry mucous membranes

Skin tenting

Sunken eyes

Doughy abdomen

Evidence of hypovolemia is present

* Death is imminent. 

Fluid Types

A crystalloid is a water-based solution composed of osmotically active small molecules that are permeable to the capillary.6 A significant percentage of crystalloids move into the interstitial and intracellular space within approximately 45 minutes of intravenous administration. Isotonic crystalloids (eg, 0.9% NaCl, lactated Ringer’s solution), which are primarily used for fluid therapy in veterinary medicine, have osmolality similar to plasma and therefore do not cause cellular swelling or shrinkage when administered.6 Hypotonic and hypertonic crystalloids have lower and higher osmolality, respectively, as compared with plasma.

Synthetic colloids (eg, hydroxyethyl starch solutions) are crystalloid-based fluids composed of large molecules that do not cross the capillary membrane. Colloids can be used to treat hypovolemia and/or hypoproteinemia.7-9 Synthetic colloids should be used cautiously in veterinary patients10,11 because of concerns in human patients that acute kidney disease and coagulopathies may develop. 

Fluid Prescription

A quick stepwise approach that provides an individualized fluid plan for the patient is needed once it has been determined that fluid therapy may be beneficial. Using a fluid prescription consisting of 3 straightforward steps (vs arbitrarily putting a patient on a 2× maintenance fluid rate) ensures that the patient’s fluid deficit is identified and corrected in a timely manner (see Examples of Individualized Fluid Plans). Ongoing fluid losses are not included in this plan but should be replaced in patients with significant ongoing fluid loss (eg, a puppy with parvoviral enteritis with continued vomiting and diarrhea). 

Hypovolemia and dehydration can occur independently of each other; therefore, dehydrated patients may not be hypovolemic, and hypovolemic patients may not be dehydrated.

Step 1: Resuscitation (Identify & Treat Hypovolemia if Present)

Hypovolemia can lead to poor oxygen delivery and should be identified (Table 1) and treated quickly.12 If hypovolemia is suspected or identified, fluids should be administered intravenously or via the intraosseous route.

Fluids administered subcutaneously, in the peritoneal cavity, or through the oral route are not absorbed well because blood flow is diverted to the heart, lungs, and brain in a hypovolemic state. Cats with evidence of hypovolemia should be actively warmed to a body temperature of at least 97°F (36°C) before large volumes of fluids are given.

The shock dose is an estimate of the total blood volume (dogs, 90 mL/kg/hr; cats, 60 mL/kg/hr). It is unlikely that a hypovolemic patient will have lost its entire blood volume; thus, approximately 25% of the fluid prescription (dogs, 20 mL/kg/15 min; cats, 15 mL/kg/15 min13) should be administered using pressure bags, fluid pumps, or a 60-mL syringe. Fluid pumps run at 999 mL/hr and are best used for boluses when the total volume to be infused over 15 minutes is less than 250 mL.

The patient should be re-evaluated after the fluid bolus is given. Additional fluid boluses can be administered (dogs, ≤90 mL/kg/hr; cats, 60 mL/kg/hr) if clinical parameters of hypovolemia have improved but are not yet satisfactory (see Oxygen Delivery Restoration Parameters). Fluid administration can be discontinued when the patient has met the desired criteria, but, because isotonic crystalloids have a short lifespan in the intravascular space, the patient’s vital parameters should be monitored closely.

Synthetic colloids (eg, hydroxyethyl starch solutions; 1-5 mL/kg every 15 minutes) can be used to treat hypovolemia. The author prefers to use the low end of the dose range for cats, whereas dogs tend to tolerate the higher end.

OXYGEN DELIVERY RESTORATION PARAMETERS

  • Normal heart rate (dogs, 100-140 bpm; cats, >160 bpm)
  • Pink mucous membranes
  • Normal capillary refill time (<2 seconds)
  • Normal peripheral pulses
  • Improved mentation
  • Improved blood pressure (100-140 mm Hg systolic)
  • Improved serum lactate (1-2.5 mmol/L) 

Step 2: Rehydration (Identify & Treat Dehydration if Present)

After hypovolemia (if present) is treated, the patient should be evaluated (Table 1) and treated for dehydration as needed. The fluid deficit in the interstitial space can be determined by multiplying the patient’s body weight by the estimated dehydration percentage (Table 2)1:

Fluid deficit (liters) = weight in kg × % dehydration

The fluid deficit is then replaced over a period of 6 to 24 hours1 using any isotonic crystalloid. The author prefers to replenish the fluid deficit over 6 to 8 hours except in cats and in patients with underlying heart disease, in which the fluid deficit is replaced over 12 to 24 hours.

Step 3: Maintenance (Provide Cellular Maintenance Requirement)

Cells have a daily water requirement to maintain regular metabolism. Maintenance fluids (dogs, 60 mL/kg/q24h; cats, 45 mL/kg/q24h12) can be provided as part of the fluid plan when a patient is not eating or drinking, in addition to correcting dehydration and restoring perfusion. Multiple units of the maintenance dose (rates 2× or more above the maintenance rate) can be provided to patients that may benefit from diuresis (eg, after exposure to toxins). Isotonic crystalloids are typically used to provide maintenance requirements, but hypotonic crystalloids (eg, 0.45% NaCl) may also be used. 

Complications of Fluid Therapy

Like any drug used in clinical medicine, fluids are not benign, and their use can potentially lead to life-threatening complications, including respiratory distress secondary to volume overload, coagulopathies, electrolyte abnormalities, acid-base disturbances, and propagation of inflammation.14 Fluid prescriptions should be individualized and the patient monitored often to detect any adverse effects associated with fluid therapy.


EXAMPLES OF INDIVIDUALIZED FLUID PLANS

EXAMPLE 1

Gerald, a 4-year-old neutered male cat weighing 6.6 lb (3 kg), is presented for vomiting and diarrhea of 3 days’ duration. He was anorexic and lethargic prior to presentation.

On physical examination, Gerald is quiet and has a heart rate of 120 bpm, pale mucous membranes with a capillary refill time of about 2 seconds, weak peripheral pulses, initial blood pressure of 50 mm Hg (systolic), and a body temperature of 94°F (34°C). He is also estimated to be about 6% dehydrated based on skin tenting and dry mucous membranes.

Step 1: Resuscitation

Gerald has signs of hypovolemia (ie, bradycardia, hypotension, hypothermia, weak peripheral pulses, pale mucous membranes) and should be resuscitated immediately to restore oxygen delivery.

  • A peripheral catheter—or intraosseous catheter if a peripheral catheter is difficult to place—should be used. The medial saphenous veins may be easier to access in hypovolemic cats.
  • Exogenous heating (eg, forced air warming devices) should be used to raise body temperature to at least 97°F (36°C).
  • A 45-mL (15-mL/kg) balanced isotonic crystalloid (eg, lactated Ringer’s solution, 0.9% NaCl) should be administered over 15 minutes using a 60-mL syringe or a fluid pump.
  • Parameters should be reassessed and stopped if the patient has met the end goals (see Oxygen Delivery Restoration Parameters).
  • As the patient’s body temperature rises, additional fluid boluses can be given, if needed.

Step 2: Rehydration

Gerald responded well to the fluid given during resuscitation. His heart rate is now 200 bpm, blood pressure is 100 mm Hg, and mucous membranes are pink. He still has signs of dehydration based on skin tenting and dry mucous membranes and is estimated at 6% dehydration. This fluid deficit should be replaced using an isotonic crystalloid.

  • Fluid deficit calculation: 
    • Fluid deficit (liters) = weight in kg (3) × % dehydration (0.06) 
    • Fluid deficit = 3 × 0.06
    • Fluid deficit = 0.18 L (180 mL)
  • Timeframe needed to replace the fluid deficit (cats tend to be less fluid tolerant; Gerald’s deficit will be replaced over 12 hours):
    • 180 mL q12h = 15 mL/hr for 12 hours

Step 3: Maintenance

Hourly fluid requirements (ie, maintenance fluids) should be provided to maintain normal cellular activity. Because the patient is not eating or drinking, the maintenance requirement should be provided using an isotonic crystalloid; a hypotonic crystalloid can also be used to provide maintenance requirements.

  • The maintenance fluid requirement is:
    • 45 mL/kg q24h (45 × 3) = 135 mL/q24h or 6 mL/hr
  • Overall fluid prescription after treating hypovolemia is:
    • Fluid deficit (15 mL/hr) + maintenance (6 mL/hr) = 21 mL/hr for the first 12 hours; fluid rate is then reduced to 6 mL/hr (provided there are no ongoing fluid losses)

EXAMPLE 2

Sasha, a 4-year-old female Dachshund weighing 15.4 lb (7 kg), is presented for evaluation after being hit by a car. Physical examination findings reveal a heart rate of 160 bpm, pale mucous membranes, a capillary refill time of 3 seconds, and weak peripheral pulses. She has a broken left femur and some abrasions associated with the fracture. The remainder of the findings are within normal limits.

Step 1: Resuscitation

Sasha has signs of hypovolemia (ie, poor perfusion) based on tachycardia, prolonged capillary refill time, and weak peripheral pulses.

  • A large-bore intravenous catheter should be placed and fluid therapy initiated to restore oxygen delivery. An analgesic—ideally opioids—should be administered for fracture-associated pain that may also lead to tachycardia.
  • A 140-mL isotonic crystalloid bolus should be administered (20 mL/kg) rapidly over 15 minutes. A fluid pump may be used.
  • Physical examination parameters should be reassessed to ensure end goals (see Oxygen Delivery Restoration Parameters) have been met after providing a fluid bolus. The crystalloid dose may be repeated up to 90 mL/kg/hr.

Step 2: Rehydration

Physical examination findings consistent with dehydration are not found. This step can be skipped.

Step 3: Maintenance

Because Sasha is not likely to begin eating or drinking immediately, she will likely benefit from maintenance fluids.

  • Maintenance fluid requirement is:
    • 60 mL/kg q24h (60 × 7) = 420 mL q24h or 18 mL/hr
  • Overall fluid prescription after treating hypovolemia is:
    • Fluid deficit (0 mL/hr) + maintenance (18 mL/hr) = 18 mL/hr until she starts to eat and drink on her own (provided there are no ongoing fluid losses)

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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