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Lactation Disorders



AUTHOR: CRISTINA. GOBELLO



EDITOR MICHELLE. KUTZLER



BASIC INFORMATION image



DEFINITION


Partial or complete failure to produce or secrete milk to meet puppies’ demands. They include agalactia (complete failure to produce milk), hypogalactia (partial failure), and galactostasis (accumulation of milk within the mammary gland due to failure of ejection [let-down] from the gland). Primary agalactia is extremely rare, but a delay in milk let-down is more frequent.



SYNONYMS


Agalactia or agalactosis; hypogalactia or hypolactation



EPIDEMIOLOGY


SPECIES, AGE, SEX: Postpartum female dogs, young bitches seem more prone. These disorders have not been described in cats.


GENETICS & BREED PREDISPOSITION: Any breed potentially can be affected. A genetic component may be present with agalactia.


RISK FACTORS: Inadequate nutrition, stress, anxiety, premature delivery or caesarean section, progesterone therapy, and systemic illness may trigger hypogalactia or poor milk let-down with galactostasis.


ASSOCIATED CONDITIONS & DISORDERS: Lactation disorders can coexist with other puerperal diseases, such as mastitis, metritis, and endotoxemia.



CLINICAL PRESENTATION


HISTORY, CHIEF COMPLAINT: History reveals the previous occurrence of (premature) parturition or caesarean section. Inadequate neonate weight gain, and crying and restless puppies are frequent complaints due to insufficient lactation. Few puppies nursing or abrupt weaning may precede galactostasis.



PHYSICAL EXAM FINDINGS



• Hypogalactia and agalactia: mammary development and milk appearance at nipple squeezing are scarce or absent.

• Galactostasis: engorged, firm and painful mammary glands, which may be associated with nipple anatomic abnormalities.


ETIOLOGY AND PATHOPHYSIOLOGY



• Normal milk production is the consequence of an endocrine cascade of estrogens, progesterone, and prolactin as well as other ancillary hormones. Idiopathic primary agalactia may represent a disruption of the pituitary/ ovarian/mammary gland axis of unknown etiology.

• Failure of milk let-down (secondary agalactia) can be due to stress, anxiety, premature delivery, progesterone therapy, or systemic illness.


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


Crying puppies and a dam that is reluctant to nurse are suggestive of either primary or secondary agalactia. Consideration of environment where lactation is occurring and physical examination of the mammary glands help differentiate the two causes.



DIFFERENTIAL DIAGNOSIS



• Mastitis

• Mammary tumors

• Pseudocyesis

• Care should be taken, as mastitis and mammary tumors can coexist with lactation disorders.


INITIAL DATABASE



• History and physical findings (as already described)

• CBC is normal if no concurrent inflammatory illness is present.


ADVANCED OR CONFIRMATORY TESTING



• Diagnosis is confirmed by exclusion of other diseases. Occult primary illness may require serum biochemistry profile, vaginal discharge examination, and ultrasound of the uterus.

• Cytologic evaluation of milk reveals cell counts > 3000 cells/μL with macrophages and neutrophils when inflammation (see p. 688) is present.


TREATMENT image



TREATMENT OVERVIEW


Agalactia treatment mainly consists of the administration of galactagogues (prolactin increasing drugs). Failure of milk letdown requires treatment of primary cause (see Mammary Disorders, Non-Neoplastic, p. 688; Pyometra, p. 1014; Sepsis, p. 954.) Conversely, galactostasis could be treated with prolactin-decreasing drugs (dopamine agonists or antiserotonergics) if there are no puppies to nurse.



ACUTE GENERAL TREATMENT


Primary agalactia has no effective treatment, so puppies frequently need to be hand reared. Hypogalactia or secondary agalactia can be treated with:


• Metoclopramide, 0.1-0.2 mg/kg SQ q 6-8 h

• Domperidone, 2.2 mg/kg PO q 12 h for 4-6 days, is a safer choice than metoclopramide, as it does not cross the blood-brain barrier and therefore has no central side effects.

• Failure of milk let-down can be treated with nasal oxytocin spray 10 minutes before lactation q 8 h.

• Anxious bitches may benefit from mild tranquilization with phenothiazine compounds (e.g., acepromazine, 0.1-0.25 mg/kg PO or 0.05-0.1 mg/kg IM or SQ), which also increase prolactin release.

• In cases of galactostasis, reduction of milk production can be achieved by the administration of cabergoline, 5 mcg/kg PO q 24 h for 5-7 days. Diuretics and analgesics may also be beneficial when there are puppies to nurse and lactation cannot be interrupted.


NUTRITION/DIET


Diminishing food intake (half) and water for 2 or 3 days may contribute to resolving galactostasis.



BEHAVIOR/EXERCISE



• In hypo/agalactia cases, be sure puppies suckle vigorously so that a natural stimulation of the glands occurs.

• Galactostasis may benefit from wrapping mammary area with an elastic bandage to protect from trauma. Any stimulation on the mammary glands (e.g., padding, touching, or milking) should be avoided if lactation is going to be terminated.


DRUG INTERACTIONS


High metoclopramide doses (5 mg/kg) for more than 5 days usually cause behavioral side effects such as excitation and aggression. Domperidone provokes minimal (soft stools) to no side effects.



POSSIBLE COMPLICATIONS


When gross inflammatory changes of the mammary glands accompany the accumulation of milk, mastitis may be present.



PROGNOSIS AND OUTCOME image


Primary agalactia has a poor prognosis for lactation, and neonates should be hand reared. Failure in milk let-down and galactostasis typically respond to treatment or resolve spontaneously.



PEARLS & CONSIDERATIONS image



COMMENTS


Lactation disorders do not pose a risk for the female’s life, although they may cause considerable neonatal losses.



PREVENTION



• Provide gradual increase of food intake during the second half of pregnancy, and 125%-159% maintenance requirements after whelping.

• Be sure mammary development is adequate before caesarean section, and slowly and calmly introduce (preferably by the owner) the puppies to the dam after surgery.

• Gradual weaning prevents galactostasis.

• Considering the possible genetic component of primary agalactia, breeding affected bitches should be weighed against the potential of perpetuating the problem.


CLIENT EDUCATION


Teach clients to recognize lactation disorders early so puppies can be saved.



SUGGESTED READING



Anderson PO, Valdés V. A critical review of pharmaceutical galactagogues. Breastfeed Med. 2007;2:229.


Davidson A. Frustrating case presentations in canine theriogenology. Vet Clin North Am Small Anim Pract. 2001;31:411.



Lameness image



AUTHOR: DAVID A. PUERTO



EDITOR ETIENNE. CÔTÉ



BASIC INFORMATION image



DEFINITION


Alteration of gait caused by structural or functional abnormality in one or more limbs



SYNONYMS


“Favoring leg,” limping



EPIDEMIOLOGY



RISK FACTORS



• Obesity

• Overnutrition during growth

• Trauma

• Genetics


ASSOCIATED CONDITIONS & DISORDERS



• Neurologic disorders

• Metabolic disorders

• Neoplasia

• Certain infectious diseases


CLINICAL PRESENTATION


DISEASE FORMS/SUBTYPES: Lameness is most often secondary to pain. However, lameness also commonly occurs secondary to neurologic, mechanical, metabolic, or endocrine dysfunction.


HISTORY, CHIEF COMPLAINT: Thorough history is critical:


• Determine which limb is affected

• Abnormal gait or limping observed by owner

• Difficulty rising

• Improves or worsens with exercise

• Holding leg up (in contrast to neurologic deficit)

• Shifting leg lameness

• Acute or gradual onset

• Progression over time


PHYSICAL EXAM FINDINGS



• Complete general physical looking for any evidence of systemic abnormalities (e.g., fever)

• Complete orthopedic and neurologic examinations (see pp. 1315 and 1311).

Orthopedic examination must include assessment of:


○ Abnormal posture

○ Joint effusion

○ Bone, joint pain, or muscle pain

○ Muscle atrophy

○ Thickening or bony prominences at or near joints

○ Crepitus

○ Abnormal range of motion in joints

• Observation at a walk and trot for gait abnormalities to help localize the limb that is affected:
○ Failing to bear full weight on limb

○ Short stride

○ Head bob (“down on sound”: head moves down when patient bears weight on normal limb then up with weightbearing on affected limb to decrease weight on affected limb) with forelimb lameness

○ Toeing in or out

○ Dragging feet or scuffing nails

○ Bunny hopping (hindlimb weakness)

○ Stumbling

○ Ataxia

○ Hypermetria

• When both hind limbs are affected, weight may be shifted onto forelimbs, resulting in arched posture and abduction of the elbows.


ETIOLOGY AND PATHOPHYSIOLOGY



• Lameness secondary to pain from the musculoskeletal system: pain causes decreased weight bearing of the affected limb and shortness of stride. Severe acute pain may cause non-weight bearing on affected limb.

• Mechanical lameness: may be caused by abnormal length or angulation of bones, joints, ligaments, or tendons.

• Endocrine-related lameness: hyperadrenocorticism may cause myopathy, and diabetes mellitus may cause peripheral neuropathy.

• Neurologic disorders may cause ataxia, paresis, or pain manifesting as lameness.


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


Accurate diagnosis of lameness combines a thorough history, clinical exam, and consideration of signalment of the patient. An orthopedic exam (see p. 1315) is indicated in every case, and additional tests such as radiographs are selected based on abnormalities identified in the exam and medical history.



DIFFERENTIAL DIAGNOSIS



• Immature (<12 months) dogs and cats:
○ Forelimb:
▪ Trauma (soft tissue, bone, joint)*

▪ Osteochondritis dissecans (OCD) of the shoulder

▪ OCD of the elbow

▪ Ununited anconeal process (UAP; component of “elbow dysplasia”)

▪ Fragmented medial coronoid process (FMCP; component of “elbow dysplasia”)

▪ Elbow incongruity

▪ Avulsion of flexor muscles

▪ Premature growth plate closure

▪ Retained cartilage core

▪ Panosteitis

▪ Hypertrophic osteodystrophy (HOD)

▪ Infection (local or systemic)*

▪ Nutritional imbalance*

▪ Congenital abnormalities* (i.e., radial agenesis, congenital elbow luxation)

▪ Atlantoaxial instability

○ Hind limb:
▪ Trauma*

▪ Hip dysplasia

▪ OCD stifle

▪ OCD hock

▪ Patellar luxation*

▪ Avulsion of long digital extensor

▪ Aseptic necrosis of femoral head

▪ Panosteitis

▪ HOD

▪ Infection (local or systemic)*

▪ Nutritional imbalance resulting in overnutrition felt to be a factor in many developmental orthopedic diseases and dysplasias, or under-nutrition [nutritional secondary hyperparathyroidism/rickets] and development of pathologic fractures.*

▪ Congenital abnormalities* (tibial agenesis in cats)

• Mature (>12 months) dogs and cats*:
○ Forelimb:
▪ Trauma*

▪ Elbow luxation

▪ Shoulder luxation

▪ Degenerative joint disease*

▪ Bicipital tenosynovitis

▪ Contracture of infraspinatus or supraspinatus

▪ Mineralization of supraspinatus tendon

▪ Elbow incongruity

▪ Cervical disk disease*

▪ Brachial plexus injury*

▪ Inflammatory joint disease*

▪ Polyneuritis

▪ Polymyositis

▪ Infection (local or systemic)*

▪ Neoplasia of bone or soft tissue*

○ Hind limb:
▪ Trauma*

▪ Hip luxation*

▪ Stifle luxation*

▪ Patellar luxation*

▪ Superficial digital flexor luxation

▪ Hip dysplasia

▪ Degenerative joint disease*

▪ Cruciate ligament disease*

▪ Avulsion of long digital extensor tendon

▪ Panosteitis

▪ Iliopsoas muscle injury

▪ Thoracolumbar disk disease

▪ Lumbosacral disease

▪ Inflammatory joint disease*

▪ Achilles tendon injury*

▪ Polyneuritis

▪ Polymyositis

▪ Hypertrophic osteoarthropathy

▪ Aortic thromboembolism*

▪ Infection (local or systemic)*

▪ Neoplasia of bone or soft tissue*


INITIAL DATABASE



• Complete orthopedic and neurologic examination

• Radiographs of affected limb(s)


ADVANCED OR CONFIRMATORY TESTING



• CBC

• Serum biochemistry panel

• Urinalysis

• Arthrocentesis (see p. 1199)
○ Can aid in distinguishing degenerative joint disease from infectious, inflammatory, or immune-mediated joint disease

○ Culture and sensitivity: joint fluid should be cultured in blood culture medium for highest yield

• Immunologic testing: rheumatoid factor, antinuclear antibody test

• Serologic evaluation for infectious disease (Lyme disease, Rocky Mountain spotted fever, ehrlichiosis)

• Ultrasound of tendons or muscles

• CT, MRI: CT is most useful for bones and joints, whereas MRI is most useful for soft tissue and spinal disease.

• Arthroscopy: can be used for both diagnostic and therapeutic purposes

• Arthrotomy

• Soft-tissue or bone biopsy

• Force plate and gait analysis

• Nuclear scintigraphy: used for localizing disease such as a difficult-to-diagnose lameness or metastatic tumors

• Electromyography (EMG) (see online chapter: Electromyography and Nerve Conduction Velocity): useful for evaluating neuromuscular conditions

• Muscle or nerve biopsy (see p. 1305)


TREATMENT image



TREATMENT OVERVIEW


Treatment of lameness requires a multi-modal approach to alleviate pain and treat the underlying disorder causing the lameness.



ACUTE GENERAL TREATMENT


Lameness is a clinical sign, not a specific disease. Therefore treatment is based on determining the underlying cause.



CHRONIC TREATMENT



• Depends on underlying cause

• Adjunctive/supportive treatment:
○ Weight loss if indicated

○ Glycosaminoglycan administered intramuscularly or intraarticularly

○ Nonsteroidal antiinflammatory drugs (NSAIDs) such as meloxicam, deracoxib, firocoxib, etodolac, or carprofen

○ Amantadine as an N-methyl-d-aspartate (NMDA) receptor antagonist or other agents such as tramadol or gabapentin can be used as adjunctive medications for pain management.

○ Intraarticular corticosteroids can be administered for severe arthritis unresponsive to other therapies but carry risk of introducing infection and/or cartilage damage.

○ Stem cell therapy derived from autogenous adipose tissue has recently been described and become available.


NUTRITION/DIET


Nutritional and dietary therapeutics include eicosapentaenoic acid (EPA)-rich diets and nutraceuticals such as chondroitin and glucosamine.



BEHAVIOR/EXERCISE


Behavioral and physical activity recommendations include moderation of physical activity, physical rehabilitation (see p. 1329), stretching, and eliminating environmental risks such as slippery walking surfaces, stairs, and need for jumping.



DRUG INTERACTIONS


Glucocorticoids potentiate the gastrointestinal ulcerogenic effects of NSAIDs; this combination is contraindicated.



POSSIBLE COMPLICATIONS


NSAIDs may be associated with gastrointestinal irritation in some patients. They should also be used cautiously in animals with preexisting renal disease.



RECOMMENDED MONITORING


Repeat examination if response to therapy is not appropriate or if lameness progresses



PROGNOSIS AND OUTCOME image


Highly variable, depending on underlying cause of lameness. For example, most cases of panosteitis in growing dogs resolve spontaneously over time (prognosis excellent), whereas lameness due to osteosarcoma of a long bone has a poor long-term prognosis.



PEARLS & CONSIDERATIONS image



COMMENTS


Attention to signalment, history, and thorough examination are essential for generating “short list” of differential diagnoses.



PREVENTION


Weight management has been proven to reduce the incidence and severity of osteoarthritis and clinical signs in patients with orthopedic disease.



SUGGESTED READING



Hulse DA, Johnson AL. Orthopedic examination. In: Small animal surgery. St Louis: Mosby; 1997:719-729.



Laryngeal Masses



AUTHOR: MICHAEL B. MISON



EDITOR RANCE K. SELLON



BASIC INFORMATION image



DEFINITION


Proliferation of laryngeal tissues due to benign or malignant processes



EPIDEMIOLOGY



SPECIES, AGE, SEX



• Laryngeal masses are rare in dogs and cats but occur most often in middle-aged to older animals.

• Benign lesions may be seen in younger animals.

• There is a higher incidence of laryngeal tumors in male dogs and cats.

ASSOCIATED CONDITIONS & DISORDERS: Laryngeal masses can lead to acute or chronic upper airway obstruction.



CLINICAL PRESENTATION


DISEASE FORMS/SUBTYPES: Benign or malignant masses



HISTORY, CHIEF COMPLAINT



• Acute or progressive history of inspiratory stridor

• Voice change

• Dyspnea

• Cough

• Exercise intolerance

• Gagging and/or dysphagia

• Ptyalism

• Cyanosis

• Collapse

• Mass in the neck


PHYSICAL EXAM FINDINGS



• May be normal, with mass as an incidental finding at time of endotracheal intubation

• Inspiratory dyspnea, with gasping if severe

• Inspiratory stridor

• Palpable mass in the ventral laryngeal area in some

• Coughing and/or gagging due to laryngeal compression

• Weakness


ETIOLOGY AND PATHOPHYSIOLOGY



• Laryngeal tumors cause luminal obstruction by external compression or internal obstruction.

• Primary:
○ Benign:
▪ Oncocytoma

▪ Laryngeal cyst

▪ Laryngeal polyp

▪ Rhabdomyoma

▪ Lipoma

○ Malignant:
▪ Squamous cell carcinoma (most common)

▪ Mast cell tumor

▪ Fibrosarcoma

▪ Rhabdomyosarcoma

▪ Lymphoma

▪ Osteosarcoma

▪ Melanoma

▪ Mixed cell tumor

• Metastatic:
○ Lymphoma

○ Plasma cell tumor

○ Thyroid neoplasia


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


Diagnosis often hinges on direct observation of the larynx in an anesthetized or heavily sedated patient with stridor or voice changes.



DIFFERENTIAL DIAGNOSIS



• Laryngeal paralysis (dogs > cats)

• Laryngeal collapse

• Elongated soft palate (dogs, especially brachycephalic)

• Nasopharyngeal polyp (cats)

• Pharyngeal or laryngeal foreign body

• Granulomatous masses


INITIAL DATABASE



• Results of a CBC, biochemistry panel, and urinalysis are usually unremarkable.

• Cervical radiographs may show a soft-tissue opacity in the area of the larynx, leading to laryngeal distortion or decreased laryngeal luminal space. The normal larynx of dogs, especially if mineralized, should not be confused with an abnormality (foreign body or other on a lateral cervical radiograph).

• Ultrasonography may allow identification of laryngeal masses because of the distortion of normal structural/anatomic relationships. It may also allow for fine-needle aspirates to be taken.

• Thoracic radiographs may have evidence of metastasis or aspiration pneumonia.


ADVANCED OR CONFIRMATORY TESTING



• Note: Patients with large laryngeal masses may be at the cusp of respiratory collapse despite showing only moderate dyspnea (inspiratory).
○ These patients may be unable to recover from anesthesia without respiratory distress/suffocation. Therefore, before sedation/anesthesia for evaluation of the upper airway in patients suspected of having airway obstruction:
▪ An appropriate-sized endotracheal tube must be available.

▪ A tracheostomy kit should be available.

▪ Hair should be clipped from the ventral neck (preparation for tracheostomy if needed).

▪ A contingency plan should be discussed with the owner if the mass is nonresectable (e.g., recover with tracheostomy versus euthanize on the table).

• Laryngoscopy with animal under general anesthesia to directly visualize the mass

• Tissue biopsy specimen can be obtained by open surgical technique or endoscopically.
○ Masses may also be aspirated for cytologic analysis.

○ A misleading cytologic or histologic diagnosis of lymphoid hyperplasia may be initially obtained by needle cytology or pinch biopsies in patients with primary laryngeal neoplasia.

• Ultrasound may help visualize the mass and aid fine-needle aspiration.

• CT or MRI can better show the extent of the mass and possible involvement of other regional structures.


TREATMENT image



TREATMENT OVERVIEW



• Remove/reduce laryngeal luminal obstruction.

• Treatment depends on the extent of the lesion and type of mass.


ACUTE GENERAL TREATMENT


Stabilize the patient:


• Oxygen by face mask, oxygen cage, or nasal cannula if needed (see p. 1319)

• Tracheostomy if in severe distress from near complete obstruction (see p. 1344)


CHRONIC TREATMENT



• Small, benign lesions may be surgically excised by submucosal resection or partial laryngectomy.

• Laryngeal lymphoma is amenable to treatment with chemotherapy.

• Large invasive lesions or malignant tumors are best removed surgically by total laryngectomy combined with a permanent tracheostomy.
○ Permanent tracheostomy can palliate signs of respiratory distress in nonresectable cases or cases managed conservatively. Rarely successful in small individuals (cats, small dogs), because tracheal lumen becomes recurrently obstructed with secretions.

• Certain tumors may be better treated with radiation therapy. Consultation with an oncologist can be beneficial.


POSSIBLE COMPLICATIONS



• Postoperative swelling

• Dysphagia and/or gagging

• Pharyngeal dehiscence

• Laryngeal stenosis/webbing

• Hypoparathyroidism/hypothyroidism (if removed during laryngectomy)

• Tumor recurrence or metastasis

• Obstruction or self-trauma of tracheostoma


RECOMMENDED MONITORING



• Monitor closely for upper airway obstruction secondary to postoperative pharyngeal swelling.

• Withhold water and food for at least 24-48 hours in the postoperative period.

• Exercise should be restricted for 2-4 weeks.

• Routine laryngoscopic reevaluation is recommended to identify tumor recurrence or laryngeal stenosis.

• Periodic physical and radiographic evaluation is recommended to check for recurrence or metastasis.


PROGNOSIS AND OUTCOME image



• The prognosis is good for benign lesions if complete resection is possible.

• Prognosis for malignant laryngeal tumors is guarded:
○ Advanced disease is often present at the time of diagnosis.

○ May not be surgically resectable


PEARLS & CONSIDERATIONS image



COMMENTS



• A CO2 laser works well for surgical dissection and results in less inflammation and hemorrhage.
○ When using a laser, make sure the endotracheal tube is protected from the laser beam.

• Some patients may benefit from placement of a feeding tube for postoperative nutritional support (see pp. 1267-1273).


PREVENTION


There is no means of preventing the development of laryngeal masses.



TECHNICIAN TIPS


When preparing for examinations of animals with laryngeal disease, handy items to have nearby include a laryngoscope, tongue depressor (to move the soft palate), an extra endotracheal tube (in case a first becomes occluded with blood and mucus), long cup biopsy forceps, formalin, 22- or 23-gauge needles of varying lengths (1-inch, l 1/2-inch, spinal needles) and 6- or 12-mL syringes and microscope slides (for aspiration cytology), and cotton-tip swabs (or alternatively, gauze sponges and forceps or suction) for clearing mucus or blood.



CLIENT EDUCATION


Vocalization is lost after total laryngectomy.



SUGGESTED READING



Jakubiak MJ, et al. Laryngeal, laryngotracheal, and tracheal masses in cats: 27 cases (1998-2003). J Am Anim Hosp Assoc. 2005;41:310-316.


Saik JE, et al. Canine and feline laryngeal neoplasia: a 10-year survey. J Am Anim Hosp Assoc. 1986;22:359.


Withrow SJ. Cancer of the larynx and trachea. In: Withrow SJ, Vail DM, editors. Withrow and MacEwen’s small animal clinical oncology. ed 4. St Louis: Elsevier; 2007:515-517.



Laryngeal Paralysis image



AUTHOR: KAREN M. TOBIAS



EDITOR RANCE K. SELLON

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