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Macadamia Nut Toxicosis

AUTHOR: SHARON. WELCH

EDITOR SAFDAR A. KHAN

1ST EDITION AUTHOR: MOAZZAM. KHAN

BASIC INFORMATION image

DEFINITION

Acute and often self-limiting toxicosis of dogs resulting from ingestion of macadamia nuts. It is characterized by paresis, depression, vomiting, ataxia, tremors, hyperthermia, abdominal pain, lameness, and/or stiffness. Toxicosis can occur after ingestion of commercially available macadamia nuts or macadamia nut-containing cookies or candies.

EPIDEMIOLOGY

SPECIES, AGE, SEX

• Currently, the syndrome has been described in dogs only.
• All breeds, ages, and both sexes are susceptible.

RISK FACTORS

• Dogs develop signs of toxicity after ingesting 2.2-62.4 g/kg macadamia nuts.
• Dogs will readily eat large amounts of chocolate-coated macadamia nuts.

GEOGRAPHY AND SEASONALITY

• Macadamia nuts are obtained from Macadamia integrifolia and Macadamia tetraphylla trees, mostly cultivated in Hawaii in the United States.
• Toxicosis can occur year round, although it is more likely to occur during holiday seasons.

CLINICAL PRESENTATION

DISEASE FORMS/SUBTYPES

• Severity and onset of signs will depend on amount of macadamia nuts ingested.
• Majority of dogs show clinical signs within 12 hours after ingestion.
• Clinical signs usually resolve within 24-48 hours.

HISTORY, CHIEF COMPLAINT

• History of exposure to macadamia nuts
• Evidence of macadamia nuts in the vomitus or in the stool
• Hind limb weakness, depression, vomiting

PHYSICAL EXAM FINDINGS

• Hind limb weakness with no evidence of central nervous system involvement, musculoskeletal pain, or trauma
○ Rarely, generalized weakness is possible.
○ Forelimb weakness without hind limb weakness is inconsistent with macadamia nut toxicosis.
○ Respiratory muscle paralysis likewise has not been a feature of macadamia nut toxicosis in dogs.
• Mild tremor of hind limbs
• Depression
• Vomiting
• Ataxia
• Hyperthermia (due to tremor; not true fever)

ETIOLOGY AND PATHOPHYSIOLOGY

• Exact cause and mechanism of macadamia nut toxicosis are not clear.
• Evidence suggests that the syndrome is dog specific.
• Toxic principle in macadamia nuts is not known at this time.

DIAGNOSIS image

DIAGNOSTIC OVERVIEW

Diagnosis is based entirely on history and physical signs: observed or suspected ingestion of macadamia nuts, especially if concurrent signs (paresis, ataxia, stiffness, hyperthermia, and/or vomiting within 12 hours of exposure) are present, is sufficient to warrant treatment.

DIFFERENTIAL DIAGNOSIS

• Rule out other toxicoses that can cause hind limb weakness, ataxia, and vomiting:
○ Ethylene glycol
○ Cholinesterase inhibitor pesticides: organophosphates and carbamates
○ Marijuana (dogs)
○ Phenoxy herbicide (2,4 D)
○ Coral snake bite
○ Bromethalin (dogs)
• Rule out nontoxic causes for hindlimb weakness and ataxia (see p. 837):
○ Systemic disturbances (e.g., anemia, acid-base or electrolyte abnormalities, cardiac arrhythmias)
○ Neuromuscular disorders (polyradiculoneuritis, myasthenia gravis, tick paralysis, botulism)
○ Orthopedic disorders
○ Trauma
○ Right-to-left shunting patent ductus arteriosus (weakness confined to hind limbs)

INITIAL DATABASE

• Abdominal radiographs (may show a large amount of ingesta in the gastrointestinal tract)
• Examination of stomach contents for presence of macadamia nuts (if vomiting occurs)
• Rectal palpation may show presence of macadamia nuts in feces.
• Body temperature
• A complete medical examination is needed if concurrent ingestion of other harmful compound is suspected and to rule out any preexisting condition.

ADVANCED OR CONFIRMATORY TESTING

Serum biochemistry profile: mild elevation in serum triglycerides and serum alkaline phosphatase may be noted but is nonspecific.

TREATMENT image

TREATMENT OVERVIEW

Treatment is general and supportive: induction of emesis and administration of activated charcoal if ingestion is suspected or confirmed and patient is stable. Management of complications of severe intoxications (e.g., nursing care if recumbent; treatment of hyperthermia) is applied as needed. Most clinical signs resolve within 24-48 hours with or without treatment.

ACUTE GENERAL TREATMENT

• Decontamination of patient:
○ Emesis (within 2-4 hours after ingestion in dogs not showing overt clinical signs; see p. 1364); or
▪ Apomorphine (0.03-0.04 mg/kg IV or IM, or crush tablet portion with water and instill into conjunctival sac, rinse after emesis); or
▪ Hydrogen peroxide 3% (2 mL/kg, max 45 mL PO, repeat in 10-15 minutes if no vomiting)
○ Activated charcoal:
▪ Give after inducing emesis or if a few hours have elapsed after exposure; administer activated charcoal (1-4 g/kg) with a cathartic such as 70% sorbitol (3 mL/kg) orally.
○ Warm tap water enema (5-10 mL/ kg) with large ingestion may help move the macadamia nuts more quickly through the gastrointestinal tract.
○ Supportive care:
▪ Administer IV fluids as needed.
▪ Thermoregulation (cold bath, cooling fans if needed)

RECOMMENDED MONITORING

Serum electrolytes, biochemistry profile, and triglycerides in severely affected dogs

PROGNOSIS AND OUTCOME image

• Generally, excellent prognosis
• Dogs recover with or without treatment within 24-48 hours

PEARLS & CONSIDERATIONS image

COMMENTS

• Consider concurrent methylxanthine (chocolate) toxicosis if macadamia nuts were covered with chocolate and large amounts of macadamia have been ingested.
• Mild uncomplicated cases may resolve with home observation for 12 hours.

PREVENTION

Keep macadamia nuts out of reach of dogs

SUGGESTED READING

Gwaltney-Brant SM. Macadamia nuts. In: Peterson ME, Talcott PA, editors. Small animal toxicology. ed 2. St Louis: Saunders Elsevier; 2006:817-821.

Malassezia Dermatitis image

AUTHOR: ADAM P. PATTERSON

EDITOR MANON. PARADIS

BASIC INFORMATION image

DEFINITION

An extremely common pruritic dermatosis caused by the overgrowth of Malassezia spp. yeast. Most infections are caused by the lipophilic unicellular organism Malassezia pachydermatis.

SYNONYMS

Malasseziasis, yeast dermatitis

EPIDEMIOLOGY

SPECIES, AGE, SEX: Very common in dogs of all ages; uncommon in cats of any age; either sex

GENETICS & BREED PREDISPOSITION: May occur in any breed of dog or cat. Terriers, shih tzus, dachshunds, shar-peis, spaniels, hounds, and German shepherd dogs seem predisposed, likely to underlying conditions favorable to yeast overgrowth. Devon Rex cats are more susceptible.

RISK FACTORS

• Excessive sebum production, poor sebum quality, cutaneous moisture accumulation (particularly in skin folds), a disrupted epidermal surface, and altered host immune defenses. These alterations are often the result of primary underlying diseases (e.g., allergy, endocrinopathy).
• Specific disorders that predispose to cutaneous yeast overgrowth include allergic skin disease (e.g., atopic dermatitis, food allergy, flea allergy, contact allergy), endocrinopathies (e.g., iatrogenic or spontaneous hyper-adrenocorticism, hypothyroidism, hyperthyroidism, diabetes mellitus), primary or secondary cornification disorders, folliculitis (e.g., pyoderma, demodicosis, dermatophytosis), ectoparasitism (e.g., demodicosis, sarcoptic mange, notoedric mange), metabolic diseases (e.g., superficial necrolytic dermatitis, zinc-responsive dermatosis), nutritional deficiencies, cutaneous or internal neoplasia, and in cats, retroviral infections.

CONTAGION & ZOONOSIS: Malassezia yeasts have been transmitted from the contaminated hands of dog-owning health care workers to infants in an intensive care nursery, causing mycotic sepsis. Therefore Malassezia yeast should be considered a potential zoonotic agent, especially in immunoincompetent individuals.

GEOGRAPHY AND SEASONALITY: Malassezia dermatitis may occur more frequently in humid geographic regions, and/or with underlying causes that worsen seasonally (e.g., atopic dermatitis).

CLINICAL PRESENTATION

DISEASE FORMS/SUBTYPES

• Localized dermatitis: involving the face (perioral, muzzle, ears), ventral aspect of the trunk (neck, axillae, inguinal area), perineal region (ventral tail, perianal area), and paw (interdigital web and nail fold)
• Generalized dermatitis: involving several regions as noted above

HISTORY, CHIEF COMPLAINT: Intense pruritus: most common chief complaint. Rancid offensive odor; an oily coat; hair loss (alopecia); redness (erythroderma); thickened, elephant-like skin (lichenification); scaling (dander); and/or relapsing and remitting dermatitis unresponsive to antibiotics or glucocorticoids are also frequently noted.

PHYSICAL EXAM FINDINGS

• Skin lesions reflect existing pruritus and seborrhea and are not specific to Malassezia dermatitis.
• Lesional skin may be erythematous, hyperpigmented, hyperkeratotic, lichenified, scaly, greasy or dry, alopecic, saliva-stained, and excoriated. Hyperpigmented lichenification implies chronicity.
• Intertriginous areas (skin folds) are typically affected. Occasionally, yellow/orange to slate gray seborrheic plaques are present in body folds.
• A brown waxy discharge may be evident in the nail folds, signifying paronychia.
• A brown discoloration around the base of white nails may be seen in dogs with Malassezia pododermatitis.
• Follicular casts (keratosebaceous material adhered to the proximal hair shaft) might be suggestive of an underlying keratinization disorder.
• Cats, particularly Devon Rex, may present with alopecia, erythema, and greasy exudation of the axillae, groin, and paws.

image MALASSEZIA DERMATITIS Malassezia dermatitis in a miniature poodle. Alopecia, erythema, and lichenification on the ventral neck.

(Copyright Dr. Manon Paradis.)

ETIOLOGY AND PATHOPHYSIOLOGY

Malassezia spp. yeasts are part of the normal skin microflora. They become opportunistic invaders when changes occur in the cutaneous microclimate (e.g., lipid composition, relative humidity) or defense mechanisms (e.g., epidermal barrier dysfunction, immunosuppression). Once colonization takes place, yeasts may release proteases and lipases that alter cutaneous homeostasis, allowing for continued yeast overgrowth. In some atopic dogs with cytologic demonstration of yeasts, Malassezia may elicit a type-1 cutaneous hypersensitivity reaction.

DIAGNOSIS image

DIAGNOSTIC OVERVIEW

Malassezia dermatitis should be considered in any pruritic dog or cat. Confirmation requires typical clinical signs, cytological demonstration of yeast, and most importantly, response to antifungal therapy. Underlying primary conditions must be identified and corrected. Importantly, Devon Rex cats may not have an identifiable predisposing disease.

DIFFERENTIAL DIAGNOSIS

Since Malassezia dermatitis is a secondary complication of underlying disorders in most cases, the chief differential diagnosis consists of identifying whether the underlying disorder (see Risk Factors, above) exists in an uncomplicated state or if secondary Malassezia dermatitis is present.

INITIAL DATABASE

• Skin cytologic analysis is performed on every case with compatible historical/physical findings.
○ Cytologic examination specimens can be obtained by direct impressions, acetate tape preparations, or dry or wet swabs.
○ Malassezia are ovoid, monopolar budding yeasts that resemble the shape of footprints or peanuts. They are 3-8 mcm in diameter (the same size as, or slightly smaller than, a red blood cell).
○ Yeasts are best visualized using high power (40x) or oil immersion (100x).
• Multiple skin scrapings to exclude superficial and deep ectoparasites
• Especially with cats: dermatophyte culture to exclude ringworm

ADVANCED OR CONFIRMATORY TESTING

• Biopsy and histopathologic analysis: rarely necessary
○ Suggestive but nonspecific findings include parakeratotic hyperkeratosis, epidermal hyperplasia, superficial perivascular dermatitis, and possibly eosinophilic microabscesses.
○ Occasionally, yeast may be found in the superficial keratin layer and/or in hair follicles.
○ Other histopathologic findings may represent changes associated with the underlying dermatosis.
○ Loss of surface scale during processing may decrease the chance of finding yeast organisms.
• Elimination diet trial to exclude food allergy
• Intradermal and/or immunoglobulin (Ig)E serologic testing if history and clinical findings are supportive of atopic dermatitis
• CBC, serum chemistry panel, and urinalysis to screen for internal diseases
• Hormonal testing (e.g., screening tests for hyperadrenocorticism, hypothyroidism, and diabetes mellitus)
• Feline retroviral testing

TREATMENT image

TREATMENT OVERVIEW

The main goal your job is to reduce pruritus and remove seborrhea. This is accomplished by killing yeast and controlling for underlying primary diseases and risk factors.

ACUTE GENERAL TREATMENT

• Keratomodulating (antiseborrheic) and antiyeast topical therapies (e.g., sulfur/salicylic acid, phytosphingosine, benzoyl peroxide, selenium sulfide, boric/acetic acid, miconazole, clotrimazole, ketoconazole, terbinafine, enilconazole, lime sulfur, or chlorhexidine) can be applied daily to weekly depending on the formulation used (e.g., shampoo, solution, lotion, spray, wipe, powder).
• Systemic antifungal therapy may be warranted for severe infections or those not responding to sole topical therapy. Duration of systemic therapy should persist beyond (e.g., 1-2 weeks) clinical and cytologic improvement (usually a minimum of 3-4 weeks). Griseofulvin has no effect against Malassezia species.
○ Ketoconazole, 5-10 mg/kg PO q 24 h with food; other azoles better suited for cats, or
○ Itraconazole, 5-10 mg/kg PO q 24 h with (capsules) or without (suspension) food, or
○ Fluconazole, 2.5-5 mg/kg PO q 24 h (generic available in some countries), or ○ Terbinafine, 30 mg/kg PO q 24 h with food
• Because dogs with Malassezia dermatitis frequently have concurrent staphylococcal pyoderma, treating any secondary bacterial infection with oral antibiotics at an appropriate dose and duration (minimum 21 days) will help improve cutaneous signs.

CHRONIC TREATMENT

• Therapy for underlying predisposing diseases
• Topical keratomodulating and/or antiyeast therapy at reduced frequencies of application if possible
• Azole pulse therapy can be used for remitting and relapsing episodes of Malassezia dermatitis, as these drugs concentrate in the skin. Typically, the same initial dose is prescribed for 2 consecutive days per week or given daily for 1-week-on/1-to-4-weeks-off cycles after the initial induction dose described in Acute Treatment above.

DRUG INTERACTIONS

Azole therapy may alter the metabolism or distribution of other prescribed medication by inhibiting cytochrome P450 metabolizing enzymes and P-glycoprotein transporting pumps. Terbinafine does not inhibit these enzymes. Specifically, azoles cannot be given with macrocyclic lactones (e.g., avermectins); if so, dosage reduction and close monitoring is required (see p. 706).

POSSIBLE COMPLICATIONS

• Idiosyncratic cutaneous adverse reactions to topical therapies (e.g., pruritus, erythroderma, papular rash, pustulation, vesiculation, necrosis, ulceration) may occur on the patient or person applying therapy and must be considered along with reassessment of possible underlying causes in “refractory” cases of Malassezia dermatitis.
• The patient may have adverse reactions to systemic azoles (e.g., vomiting, diarrhea, hepatotoxicity, vasculitis, lightening of haircoat, pruritus). Ketoconazole may inhibit cortisol synthesis at doses greater than 10 mg/kg/d.

RECOMMENDED MONITORING

• Clinical signs and skin cytology every 2-4 weeks during therapy
• Other monitoring recommendations are at the discretion of the clinician, based on underlying predisposing diseases.

PROGNOSIS AND OUTCOME image

• Failure to detect and treat underlying problems will result in partial treatment success, treatment failure, or relapse.
• For incurable diseases (e.g., primary cornification disorders), therapy for Malassezia dermatitis may need to be lifelong.

PEARLS & CONSIDERATIONS image

COMMENTS

• Malassezia dermatitis is one of the most overlooked causes of pruritus in the dog.
• Malassezia dermatitis tends to occur in body areas rich in sebaceous glands and high in relative humidity, and is commonly associated with allergic dermatitis.
• How many yeast are cytologically significant? Finding any yeast from typical clinical lesions is significant.
• Dogs with atopic dermatitis may be hypersensitive to Malassezia, resulting in yeast numbers disproportionate to the level of pruritus experienced by the animal.
• Skin culture for Malassezia yeast is not recommended in clinical practice, as these organisms are residents on the skin.
• Biopsy with histopathologic evaluation is not considered superior to cytologic evaluation for the diagnosis of Malassezia dermatitis (most of the surface scale is lost during biopsy processing) but may be useful in the diagnosis of primary skin disorders in addition to which Malassezia dermatitis is a secondary phenomenon.
• Do not use selenium sulfide on cats; it is too irritating to their skin.
• Enilconazole is not approved for small-animal use in some countries.
• Griseofulvin has no effect against Malassezia species.
• Cats tend to have gastrointestinal upset with oral ketoconazole, so other systemic antifungals are preferred.
• When given in tablet or capsule form, the azole drugs, ketoconazole and itraconazole, are best absorbed systemically if administered with food; failure to do so may reduce bioavailability of these drugs by up to 40%.

PREVENTION

Correctly identifying and treating for all underlying predisposing factors favorable to yeast overgrowth

TECHNICIAN TIPS

Technicians managing patients with Malassezia dermatitis should be proficient in collection and examination of cytologic skin samples, and capable of instructing owners on appropriate use of topical therapy.

SUGGESTED READING

Åhman S, Perrins N, Bond R. Treatment of Malassezia pachydermatts-associated seborrheic dermatitis in Devon Rex cats with itraconazole-a pilot study. Vet Dermatol. 2007;18:171-174.

Chen TA, Hill PB. The biology of Malassezia organisms and their ability to induce immune responses and skin disease. Vet Dermatol. 2005;16:4-26.

Negre A, Bensignor E, Guillot J. Evidence-based veterinary dermatology: a systematic review of interventions for Malassezia dermatitis in dogs. Vet Dermatol. 2008;20:1-12.

Malignant Fibrous Histiocytoma

AUTHOR: JOHN. FARRELLY

EDITOR: KENNETH M. RASSNICK

BASIC INFORMATIONimage

DEFINITION

An uncommon primary tumor made up of fibrous and inflammatory cells thought to arise from a primitive mesenchymal cell. It is not to be confused with malignant histiocytosis (histiocytic sarcoma), a disease of localized or multisystemic histiocytic infiltration (see p. 535).

SYNONYMS

Epithelioid sarcoma, giant cell fascial sarcoma, giant cell tumor, reticulum cell sarcoma

EPIDEMIOLOGY

SPECIES, AGE, SEX: Malignant fibrous histiocytoma is an uncommon tumor of the skin and subcutaneous tissue of dogs and cats, and can also occur in the spleen in dogs. This tumor type has been reported at injection sites in cats (see p. 610).

GENETICS & BREED PREDISPOSITION: Golden retrievers and rottweilers may be overrepresented.

CLINICAL PRESENTATION

DISEASE FORMS/SUBTYPES

• Different pathologic types include storiform-pleomorphic, inflammatory, and a giant cell variant. The giant cell variant, which occurs in dogs but is very rare in cats, is associated with metastasis and a poor prognosis.
• Malignant fibrous histiocytoma has been reported at injection sites in cats (see p. 610).

HISTORY, CHIEF COMPLAINT

• Pets with malignant fibrous histiocytomas in the skin and subcutaneous tissue usually present for a progressively enlarging mass noticed by the owner.
• Dogs with malignant fibrous histiocytomas of the spleen usually present for signs related to an abdominal mass or abdominal hemorrhage.

PHYSICAL EXAM FINDINGS

• Malignant fibrous histiocytomas in the skin and subcutaneous tissue often present as firm, palpable masses. Occasionally they are hairless or ulcerated.
• Regional lymphadenomegaly may be present secondary to inflammation or (rarely) lymph node metastasis.
• Dogs with splenic tumors may present with abdominal mass, pain, or abdominal enlargement.

ETIOLOGY AND PATHOPHYSIOLOGY

• Malignant fibrous histiocytomas are typically firm, slow-growing tumors that commonly infiltrate into surrounding soft tissues and along fascial planes. Overall they have a moderate metastatic potential, but some variants or grades may be more likely to metastasize (see prognosis).
• Lesions caused by malignant fibrous histiocytoma depend on the location of the primary tumor.
• These tumors are considered a separate entity from the other histiocytic diseases. Peripheral tumors can metastasize, but usually to the lungs.

DIAGNOSISimage

DIAGNOSTIC OVERVIEW

Definitive diagnosis can only be confirmed via histopathologic analysis, although additional testing such as diagnostic imaging is often helpful in defining the extent of the tumor.

DIFFERENTIAL DIAGNOSIS

• Other skin and subcutaneous tumors:
○ Soft-tissue sarcoma
○ Mast cell tumor
○ Others
• Other splenic tumors:
○ Hemangiosarcoma
○ Lymphoma
○ Others

INITIAL DATABASE

• Fine-needle aspirate cytologic analysis may help identify the tumor type before other diagnostics.
• Three-view thoracic radiographs to rule out pulmonary metastases
• Radiographs of the affected area may reveal involvement of underlying bone.
• Abdominal ultrasound to identify splenic tumors and rule out metastasis. However, abdominal ultrasound cannot be relied on to differentiate malignant fibrous histiocytoma from other splenic tumors.
• Fine needle aspirate of draining lymph nodes to help rule out metastasis

ADVANCED OR CONFIRMATORY TESTING

• CT or MRI may be necessary to delineate the local extent of the tumor and plan for surgery or radiation therapy.
• Biopsy: diagnosis of malignant fibrous histiocytoma is based on histopathologic evaluation of tissue.
○ Special stains may be necessary to differentiate malignant fibrous histiocytoma from other soft-tissue sarcomas, especially poorly differentiated tumors.
○ Care should be taken to differentiate these tumors from other histiocytic tumors, including histiocytic sarcoma and malignant histiocytosis (see p. 535). These other tumors usually have a different prognosis and recommended course of treatment.
○ Histopathologic grade of the tumor is necessary for determining the prognosis and treatment of most soft tissue sarcomas (see p. 610).
▪ Histopathologic grading typically involves using the general grading system for soft-tissue sarcomas based on mitotic rate, percent necrosis, and degree of differentiation.
▪ Tumors are graded as low, intermediate, or high grade.
▪ In most cases, high-grade tumors are larger and more invasive, but gross size and invasiveness cannot be used as a substitute for histopathologic grading.

TREATMENTimage

TREATMENT OVERVIEW

Definitive treatment is based on complete eradication of the primary tumor whenever possible. However, additional treatment such as chemotherapy may be indicated to prevent or delay metastases or in dogs with high-grade tumors, the giant-cell variant of this tumor or tumors that have already metastasized. Palliative treatment options, such as palliative radiation, may help control pain or discomfort in patients with advanced tumors or in patients where definitive treatment cannot be tolerated.

ACUTE AND CHRONIC TREATMENT

• Aggressive surgical resection, radiation therapy, and/or chemotherapy may be used for treatment (see p. 610).
• Chemotherapy may be indicated to delay or prevent metastasis for malignant fibrous histiocytoma affecting the spleen, high-grade tumors, or giant-cell variants of malignant fibrous histiocytoma.

POSSIBLE COMPLICATIONS

Complications of treatment depend on types of treatments and location of the primary tumor.

RECOMMENDED MONITORING

After appropriate local treatment, follow-up examination should be done routinely to monitor for recurrence (every 2-3 months) and metastasis (thoracic radiographs at 6 months and 1 year). High-grade tumors may require more frequent monitoring (at least every 2-3 months) for metastases during and after chemotherapy administration.

PROGNOSIS AND OUTCOME image

• Prognosis is excellent for histologically low- to intermediate-grade tumors with appropriate treatment. This includes either surgical resection with clean histopathologic margins or incomplete resection combined with radiation therapy.
• Dogs with the giant-cell variant of this tumor often have metastases at the time of diagnosis or soon afterward, and prognosis is usually poor despite treatment. Few cats with this variant develop metastases.
• Dogs with splenic tumors are more likely to develop metastases and therefore have a poor prognosis.
• High-grade malignant fibrous histiocytoma: like other soft-tissue sarcomas, prognosis is considered guarded based on the increased likelihood for metastases.

PEARLS & CONSIDERATIONS image

COMMENTS

Aside from the giant-cell variant, malignant fibrous histiocytoma should be considered like other soft tissue sarcomas (see p. 1034) in treatment and prognosis. Tumors at injection sites in cats should be treated like injection-site sarcomas (see p. 610).

CLIENT EDUCATION

Pet owners can be educated to monitor their pets for palpable or visible masses and have them evaluated in a timely fashion. Early detection may allow for easier treatment via surgery and may help avoid the need for radiation therapy.

SUGGESTED READING

Liptak JM, Forrest LJ. Soft tissue sarcomas. In: Withrow SJ, Vail DM, editors. Small animal clinical oncology. Philadelphia: WB Saunders; 2007:425-454.

Waters CB, et al. Giant cell variant of malignant fibrous histiocytoma in dogs: 10 cases (1986-1993). J Am Vet Med Assoc. 1994;205:1420-1424.

Malnutrition

AUTHOR: SARAH K. ABOOD

EDITOR: KATHRYN E. MICHEL

BASIC INFORMATION image

DEFINITION

Malnutrition is the inappropriate intake of nutrients, resulting in nutritional deficiencies or excesses.

EPIDEMIOLOGY

SPECIES, AGE, SEX: Malnutrition can affect animals of any species, age, life stage, or lifestyle.

GENETICS & BREED PREDISPOSITION: No specific genetic link or breed disposition is known for malnutrition associated with nutritional deficiencies. An increased prevalence of obesity resulting from excessive caloric intake has been associated with basset hounds, beagles, Cairn terriers, Cavalier King Charles spaniels, cocker spaniels, long-haired dachshunds, Labrador retrievers, and Shetland sheepdogs.

RISK FACTORS

• Animals fed vegetarian, homemade, or single-food diets may be at risk for nutrient deficiencies (see p. 686).
• Animals with a history of chronic vomiting or diarrhea could have altered digestion or absorption, resulting in decreased nutrient assimilation.
• Drugs such as corticosteroids, cancer chemotherapeutic agents, antibiotics, or diuretics may adversely affect nutritional homeostasis.
• Neutering, decreased physical activity, age or calorie-dense foods may predispose dogs or cats to obesity.

GEOGRAPHY AND SEASONALITY: Inadequate food or water intake during severe weather conditions may result in nutrient deprivation.

ASSOCIATED CONDITIONS & DISORDERS

• Decreased protein/calorie intake negatively effects immune function.
• Increased risk of orthopedic problems or diabetes mellitus (cats) with prolonged excessive food intake

CLINICAL PRESENTATION

DISEASE FORMS/SUBTYPES

• Weight loss, emaciation, low body condition score (1 or 2 on a scale of 1-5 or 1-9). Weight gain, obesity, high body condition score (4 or 5 on a scale of 1-5 or 8 or 9 on a 1-9 scale)

HISTORY, CHIEF COMPLAINT

• Nutrient-deprived animals present with a history of failure to thrive and inappetence or anorexia.
• Overnourished or obese animals often present with clinical signs associated with lameness or endocrinopathy.

PHYSICAL EXAM FINDINGS: Nutrient-deprived animals are often in poor physical appearance: thin body condition; dry, coarse haircoat; flaky skin; hyperkeratosis; muscle wasting; broken or missing teeth; skeletal abnormalities; pressure sores; poor wound healing. Obese animals are also in poor physical condition with fat deposition over the ribs, hips, tail head, and throughout the abdomen. Some are unable to adequately groom themselves, which can result in an unkempt hair coat, dry skin, skinfold dermatitis, and the inability to walk, run, or jump.

ETIOLOGY AND PATHOPHYSIOLOGY

• Inadequate or excessive nutrient intake results in malnutrition.
• Decreased nutrient intake diminishes immune cell response and production, as well as protein turnover, tissue synthesis, and wound healing.
• Altered drug metabolism results from protein/calorie malnutrition and may increase or decrease both drug efficacy and drug toxicity.
• Although not well documented in hospitalized veterinary patients, malnutrition is thought to increase morbidity and mortality.

DIAGNOSIS image

DIAGNOSTIC OVERVIEW

The diagnosis of malnutrition is made on the basis of a thorough diet history and the physical examination findings.

DIFFERENTIAL DIAGNOSIS

Gastrointestinal disease: protein-losing enteropathy, lymphocytic-plasmacytic enteritis, inflammatory bowel disease

INITIAL DATABASE

• A thorough diet history should include sufficient information to purchase all food items necessary to feed the patient exactly as the owner does at home.
• The physical examination should include a body weight, body condition score (1-5 or 1-9 scale), and muscle mass score (1-3 scale).
• Laboratory evaluation plays a limited role in diagnosing nutrition-related problems.

TREATMENT image

TREATMENT OVERVIEW

The goals of treatment are to correct nutrient deficiencies or excesses and return patient to a normal plane of nutrition and a more appropriate body weight and body condition.

ACUTE GENERAL TREATMENT

• Stabilize patient: rehydrate, correct electrolyte imbalances, hemodynamic abnormalities, and hypothermia before initiating nutritional support.
• Determine whether the gastrointestinal tract is functional and how nutrition support is to be delivered (enteral or parenteral).
• For patients unable or unwilling to prehend, choose the type of feeding tube for enteral delivery that fits your patient (e.g., gastrotomy tube for patients with persistent regurgitation or vomiting, esophagostomy tube for facial trauma). See pp. 1267 and 1273.
• Estimate an initial daily caloric goal for resting energy needs based upon animal’s current weight (rather than an ideal weight), using the equation: 70 × BWkg0.75
• For patients weighing between 15 and 30 kilograms, use the equation: 30 × BWkg + 70. This provides a reasonably accurate assessment of resting energy needs.
• Select a diet or food type that meets the nutritional needs of the patient.
• Determine a feeding regimen (continuous or intermittent feedings) that will deliver the estimated caloric goals over a 24-hour period.
• Administer nutrition to patients by assisted feeding until patient is eating at least 50% resting energy needs.
• Plan to get the animal eating its own food in its own environment as soon as possible.

CHRONIC TREATMENT

• Identify dietary, animal-related, owner-related or environmental issue(s) that caused or contributed to the nutritional deficiency or excess.
• Educate owner(s) about nutritional needs of their animal, given the species, age, life stage, and lifestyle.
• Provide information about, or resources for, complete and balanced homemade diets (website formulation services, laboratory analyses, and continuous monitoring).
• Provide information and support for owners considering a weight management program for their animal.

DRUG INTERACTIONS

Medical therapies instituted for primary conditions will be altered without adequate nutrition support.

RECOMMENDED MONITORING

Client education and repeated follow-up is critical for animals enrolled in weight management programs, or those who are fed homemade or raw meat diets.

PROGNOSIS AND OUTCOME image

• Prognosis is good to excellent with immediate identification and correction of nutrient deficiencies or excesses.
• Prognosis is poor to good with prolonged identification and correction of nutrient deficiencies or excesses.

PEARLS & CONSIDERATIONS image

COMMENTS

• Obesity prevention is much easier than obesity management. Client education campaigns should focus on prevention at every well-pet visit.
• Obesity management programs should be directed by veterinarians and delivered by trained, licensed veterinary technicians who are excellent communicators.
• Pet owners interested in feeding homemade or raw meat diets should consult with a veterinarian, identify a balanced recipe to use, and plan on regular monitoring of both their pet and the diet (see online chapter: Malnutrition: Home-Prepared Diets).

PREVENTION

• Complete nutritional assessments should be performed daily on hospitalized patients to identify patients at risk of malnutrition before it occurs.
• Clients should be educated on the basic nutrient needs of animals, considering species, age, life stage, and environmental conditions.

TECHNICIAN TIPS

• Technicians can be instrumental in providing client education about the proper diet and feeding management of dogs and cats and in overseeing patients enrolled in weight management programs.
• In the outpatient setting, technicians should ensure that every patient is weighed, body condition scored, and has a diet history taken.
• In the inpatient setting, technicians can aid in identifying patients at risk of malnutrition.

CLIENT EDUCATION

• Consultation for customized homemade diet formulations is available through the American College of Veterinary Nutrition (ACVN.org), or diets can be purchased at www.balanceit.com or www.petdiets.com.
• Homemade diet recipes can be analyzed through the Nutrition Laboratory in the Diagnostic Center for Population and Animal Health at Michigan State University: 517-353-9312.

SUGGESTED READING

Abood S, McLoughlin M, Buffington T. Enteral nutrition. In: DiBartola SP, editor. Fluid, electrolyte, and acid–base disorders small animal practice. ed 3. St Louis: Saunders Elsevier; 2006:601-620.

Buffington T, Holloway C, Abood S. Manual of veterinary dietetics. St Louis: Elsevier, 2004.

Chan DL. Nutritional requirements of the critically ill patient. Clin Tech Small Animal Pract. 2004;19:1-5.

Eirmann L, Michel K. Enteral Nutrition. In: Silverstein D, Hopper K, editors. Small animal critical care medicine. St Louis: Saunders, 2009.

Freeman L, Chan D. Total parenteral nutrition. In: DiBartola SP, editor. Fluid, electrolyte, and acid–base disorders small animal practice. ed 3. St Louis: Saunders Elsevier; 2006:548-600.

Remillard RL, Armstrong PJ, Davenport DJ. Assisted feeding in hospitalized patients: enteral and parenteral nutrition. In Hand MS, Thatcher CD, Remillard RL, Roudebush PR, editors: Small animal clinical nutrition, ed 4, Topeka: Mark Morris Institute, 2000.

Malnutrition, Home-Prepared Diets

AUTHOR: LISA P. WEETH

EDITOR KATHRYN E. MICHEL

DEFINITION

Feeding of an unbalanced diet of uncooked and cooked foods as a sole source of nutrition; this practice is becoming more common among pet owners.

SYNONYMS

Home-cooked diet, homemade diet

EPIDEMIOLOGY

SPECIES, AGE, SEX: Dogs more likely to be fed home-prepared diets than cats. Young and reproductive animals at increased risk for deficiencies and excess. All animals at risk of illness from foodborne pathogens.

GENETICS & BREED PREDISPOSITION: Dogs and cats: all breeds affected. Dogs: large and giant breeds at increased risk of developmental orthopedic disease. Cats: taurine-deficient cardiomyopathy and/or central retinal degeneration. CONTAGION & ZOONOSIS: Dogs and cats: Salmonella, Escherichia coli, Campylobacter, Toxoplasma, Cryptosporidium

ASSOCIATED CONDITIONS & DISORDERS: Poor skin and coat, obesity, vomiting, diarrhea, pathologic fractures, seizures, pancreatitis (high-fat diet), oral trauma, intestinal obstruction/perforation

CLINICAL PRESENTATION

DISEASE FORMS/SUBTYPES

• Incidental: no clinical signs

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