Syringomyelia in the Cavalier King Charles spaniel (CKCS) dog
Syringomyelia (SM) is defined as a condition that results in the development of fluid-containing cavities within the parenchyma of the spinal cord as a consequence of abnormal cerebrospinal fluid movement through the foramen magnum (1). Although the exact etiology and pathogenesis are unknown, SM is thought to develop secondary to an obstruction of cerebrospinal fluid (CSF) flow at the level of the foramen magnum (2). A cause of SM in veterinary medicine is a reduced volume of the caudal fossa secondary to an inappropriately small occipital bone (2,3). This malformation of the caudal fossa is known as a Chiari-like malformation (CM), a condition that appears similar to Chiari type I malformation in humans. Other documented etiologies causing SM in the dog include spinal trauma (4) and neoplasia in the region of the brainstem or foramen magnum (5,6). Recent data suggest that CM in the Cavalier King Charles spaniel (CKCS) is inherited (3,7). The incidence of CM in the CKCS breed is an estimated 95% and current studies suggest that SM is present in more than 50% of dogs with CM (7) with approximately 35% of affected dogs exhibiting clinical signs (2). Along with the CKCS breed, this condition has been reported in Pekingese dogs, Maltese terriers, miniature dachshunds, fox terriers, lhasa apsos, pomeranians, Yorkshire terriers, and a Samoyed dog (4,8–10). Occasionally, the presence of CM/SM is found as incidental findings while investigating another neurologic condition (11).
The 2 following cases, recently presented to the Ontario Veterinary College Teaching Hospital, illustrate the variability in clinical signs that can be observed in dogs afflicted with CM/SM.
A 3-year-old, spayed female CKCS was presented with a progressive 6-month history of mild paraparesis, cervical hyperesthesia, and frequent episodes of aggressively scratching at her neck and face. Magnetic resonance imaging (MRI) of the brain revealed CM with severe cerebellar crowding secondary to a caudal occipital malformation, kinking of the brainstem, caudal cerebellar herniation, occlusion of CSF passage through the foramen magnum, and SM affecting the cervical spinal cord (Figure 1). Treatment was initiated with prednisone 0.5 mg/kg orally twice daily and gabapentin (Neurontin, Pfizer Canada, Kirkland, Quebec) 10 mg/kg orally 3 times daily. Specific to the central nervous system, corticosteroids are thought to decrease the production of phospholipase A2 (11), a powerful regulator of inflammatory cascades, inhibit the expression of cytokines, and decrease the release of substance P (13,14). Gabapentin and Pregabalin (Lyrica, Pfizer), second generation antiepileptics, have shown promise for alleviating pain within the central nervous system (15,16). While their mechanisms of analgesia remain unknown, they are believed to decrease the release of glutamate, an excitatory neurotransmitter, via binding to the alpha2-delta subunit on voltage dependant calcium channels in the dorsal horn (17,18). Convincing evidence has shown that these calcium channels are involved in the persistence of pain (19). At 1-month and 3-month recheck examinations her cervical pain had significantly improved and her scratching episodes had ceased. She has since been tapered off prednisone but remains on gabapentin.
A 2-year-old, castrated male CKCS was presented with a 2-month history of progressive pelvic limb ataxia, right thoracic limb monoparesis, cervical hyperesthesia, and scratching at his right shoulder. Magnetic resonance imaging of the brain revealed CM with severe cerebellar crowding, kinking of the caudal brainstem and moderate ventricular dilatation (not shown). He was affected with severe SM, predominantly in the caudal cervical spine affecting spinal cord white and grey matter, presumably accounting for the right thoracic limb monoparesis (Figures 2 and and3).3). Treatment was initiated with prednisone 0.5 mg/kg orally twice daily and gabapentin 10 mg/kg orally twice daily. At a 3-month recheck examination, his pelvic limb ataxia had improved; however, he remained monoparetic in the right thoracic limb and mildly painful in his cervical spine.
Syringomyelia (SM) that accompanies a Chiari-like malformation (CM) is thought to be a consequence of abnormal CSF flow at the foramen magnum secondary to a decrease in caudal fossa volume and compression of the subarachnoid space (20–22). The causative mechanism of SM is a relative increase in pulse pressure in the spinal cord compared to that in the nearby subarachnoid space due to an induced pressure difference secondary to an obstruction in the subarachnoid space (23). Normally, the pulse pressure in the CSF is transferred to the spinal cord and equals the inherent pressure within the cord and the 2 cancel out to maintain a homeostatic environment. However, when an obstruction in the subarachnoid space is present such as a caudally displaced cerebellum in CM type I in humans, there is a mismatch of the pulse pressure between the CSF and spinal cord (24,25). This leads to a medullary-subarachnoid pressure dissociation with transiently higher pressure in the spinal cord than the CSF allowing a distention of parenchmyal tissue and injury to the tissue causing an extravasation of plasma infiltrate into the syrinx (24–26).
The most consistent clinical sign seen in SM-affected dogs is pain localized to the cervical spine (11,27,28). Many owners report that their dog exhibits postural pain characterized by sudden vocalizing after jumping (28). Syringomyelia-affected dogs behave as if they experience allodynia (pain arising in response to an otherwise nonpainful stimulus) and dysesthesia (intense burning sensation) (28). For example, affected dogs appear to dislike being touched in certain areas around their ears, neck, top of head, and they may be unable to tolerate grooming or wearing a neck collar (28). Allodynia and dysesthesia are 2 characteristics consistent with neuropathic pain syndrome described by humans affected with CM/SM (29).
Neuropathic pain syndrome, a clinical syndrome due to abnormal somatosensory processing in the peripheral and central nervous systems, is complex and relies on anatomical, physiological, and neurochemical causes. Once initially thought to be primarily due to damage to the spinothalamic tract (21,30) or the spinoreticular tract (31), researchers studying pain-related somatosensory evoked potentials following CO2 laser stimulation in humans. It was concluded that the spinothalamic tract is intact in most patients, while the cellular function of the dorsal grey horn of the spinal cord is impaired (32).
While the exact pathophysiology is unknown, there are 3 important phenomena critical to the development of neuropathic pain, central sensitization, central disinhibition, and phenotypic change (33–35). Central sensitization is the state of heightened sensitivity of dorsal grey matter neurons during repetitive C-fiber nociceptive stimulation such that their threshold of activation is reduced, and their responsiveness to synaptic inputs is augmented (36). Long-term effects of central sensitization are due to an augmented release of glutamate, an excitatory amino acid, and substance P, a peptide thought to be responsible for pain modulation and perception. These neurotransmitters activate voltage-gated calcium channels resulting in a calcium influx from voltage sensitive ion channels as well as from intracellular stores. The intracellular calcium increase results in activation of calcium-dependent kinases such as protein kinase C and A, and tyrosine kinase (37). These changes activate phosphorylation of membrane receptors and ion channels that can alter neuron excitability for minutes to hours after the initiating stimulus (38). Central disinhibition results from the loss of spinal cord inhibitory interneuron transmitters such as GABA and glycine and consequently shifts the balance towards an increased excitatory state, which can manifest clinically as spontaneous or evoked pain to an otherwise innocuous stimulus (allodynia) (36,39,40).
Currently, a diagnosis of CM and SM in dogs is made most often with MRI of the brain and spinal cord (3,4,11). Obtaining both sagittal and transverse images is necessary for identifying the characteristic changes associated with CM and for measuring the width and length of SM. Magnetic resonance imaging changes consistent with CM in dogs include a small caudal fossa secondary to a hypoplastic or dysplastic occipital bone, cerebellar crowding, compression and/or herniation of the cerebellar vermis and medulla through the foramen magnum, and minimal to absent CSF signal between the caudal cerebellum and brainstem (2,11,27,28). Additionally, kinking of the brainstem at the level of the cerebellum and ventricular dilation may be present (11,27,28). Magnetic resonance imaging findings consistent with SM in dogs include detecting a distinct cavity of fluid within the parenchyma of the spinal cord. On T1-weighted imaging this fluid will appear hypointense to isointense to surrounding spinal cord tissue and hyperintense to surrounding spinal cord tissue on T2-weighted imaging (41). Transverse and parasaggital images allow for the assessment of width, dorsal horn involvement, and longitudinal extent of the cavity (28). Maximum syrinx width is the strongest predictor of pain, scratching behavior, and scoliosis; 95% of CKCS with a maximum syrinx width of 0.64 cm or more will have associated clinical signs (28).
Treatment of dogs with CM/SM is aimed at medically or surgically relieving pain and other neurologic signs thought to be associated with the condition. Depending on the severity of clinical signs, 3 categories of drugs that have shown some benefit include analgesics (NSAIDs, Gabapentin, Tramadol), drugs targeted at decreasing CSF production (Omeprazole, Acetazolamide), and corticosteroids (1,2). For dogs that exhibit signs consistent with neurogenic pain (neck and back pain on palpation, abnormal scratching, episodes of sudden vocalizing, allodynia) the authors recommend Gabapentin at 10 mg/kg orally every 8 to 12 h as a primary treatment. Side effects include sedation and occasional vomiting and anorexia. For episodes of severe pain nonresponsive to Gabapentin, Prednisone is added at anti-inflammatory doses of 0.5 mg/kg orally every 12 to 24 h as it effectively targets pain mediators such as substance P in the central nervous system (13,14). The length of treatment depends on clinical response. While the majority of affected dogs are maintained for the long-term on Gabapentin, Prednisone is usually discontinued after approximately 7 to 10 d, as long as the clinical symptoms are controlled. However, for recurrent episodes of acute and severe neck and back pain, Prednisone is continued for a longer period of time at the lowest acceptable dose. Owners with dogs that are severely affected and/or are unresponsive to medical management may consider surgery.
Surgical management is frequently performed in humans with CM/SM to alleviate clinical symptoms (42). The most common procedure is a foramen magnum (FM) decompression (suboccipital decompression). This procedure involves the removal of a portion of the supraoccipital bone overlying the cerebellum and the rostral extent of C1. The largest case series of dogs undergoing this procedure reported 81.25% of dogs had improvement or resolution of clinical signs (43). However, the study also found that 25% of dogs undergoing suboccipital decompression had a recurrence of clinical signs within the follow-up period, and this recurrence was presumed to be due to scar tissue formation at the surgical site. This recurrence rate is consistent with that reported in humans (42). A modified surgical technique, FM decompression with cranioplasty, aims to alleviate scar tissue formation by securing a titanium mesh to the perimeter of the supraoccipital craniectomy (43). Early reports of this procedure are favorable; however, long-term data are unknown.
Overall, the prognosis for CM/SM-affected dogs depends on the severity of clinical signs and on the response to medication. Chiari-like malformation and syringomyelia is a progressive condition in those dogs that are affected clinically. Some dogs will need constant dose adjustments to adequately treat their symptoms. Unfortunately, some dogs afflicted with severe and disabling pain do not respond to medical management and are not surgical candidates, in which cases a thorough evaluation of their quality of life is necessary.
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Articles from The Canadian Veterinary Journal are provided here courtesy of Canadian Veterinary Medical Association
Eosinophilic Diseases of Dogs
Murdoch, Western Australia, Australia
Eosinophils are important components of the immune system, and are often involved in hypersensitivity disorders and parasitic infestation.1 Eosinophilia is defined as an increase in the total eosinophil count in blood or tissue. Although the upper reference range for blood concentration of eosinophils in dogs is 0.75 x 109/L, significant circulating eosinophilia is considered to be present when the count exceeds 2.2-2.5 x 109/L.2 This most commonly occurs as a leukaemoid response, or when eosinophil counts increase to a high levels in response to an underlying cause (see Table).2 The most common underlying causes for an eosinophilic leukaemoid response in people are atopy and helminth infestation.1 Dogs with Angiostrongylus vasorum (lungworm) or Dirofilaria immitis (heartworm) have been shown to have significant eosinophilia in a significant percentage of infected dogs.2,3 However, in one survey performed by our centre of Perth metropolitan Rottweiler breeding kennels, it does not appear that the presence of low numbers of intestinal parasites predispose to higher eosinophil counts. A few dogs had intestinal parasites present (one or more of Trichuris, Isospora, Giardia and Sarcocystis), but none were considered clinically affected.
Dogs are most commonly identified with eosinophilia secondary to dermatological diseases (such as sarcoptic mange), inflammatory bowel disease and pulmonary diseases, all of which may have a hypersensitivity component.4-7 Interestingly, atopic dermatitis does not seem to cause a significant eosinophilia in dogs.6,8 Paraneoplastic eosinophilia is commonly reported, as is eosinophilic CNS disease.2,6,9-12 Dogs may also have significant organ infiltration with eosinophils (such as with eosinophilic bronchopneumopathy), but no circulating eosinophilia.5 This may be due to the short circulating half-life of these cells.7 Diurnal variation may also play a role, as circulating eosinophil numbers in healthy dogs have been shown to peak in late evening, and be at their lowest at noon.13
In both our local survey and in a large published analysis of eosinophilia, Rottweilers have been shown to be predisposed to eosinophilic disease.6 A number of the Rottweilers that we surveyed had increased eosinophilic counts, but no identifiable parasitic, allergic or neoplastic disease, and there was no age or sex predisposition. However, certain kennels did seem to have increased incidence of eosinophilia, suggesting there may be a heritable component. German shepherds also appear to have an increased incidence of exaggerated eosinophil responses to normal stimuli.6 Cavalier King Charles spaniels, Alaskan malamutes and Siberian huskies appear predisposed to eosinophilic stomatitis, intestinal and airway disease.5,14-16
Rottweilers are also over-represented in the published reports of hypereosinophilic syndrome (HES).2,17 HES is a rare syndrome that has been described in people, cats and less commonly in dogs.1,2,17-19 The criteria for the definition of idiopathic HES used in people are an eosinophil count persistently greater than 1.5×109/L, damage to end-organs such as the heart and lungs, no ascertainable cause for the eosinophilia and no evidence of clonality.1 The prognosis for this condition is considered universally poor. However, there have been individual reports of good survival times with spontaneous resolution reported in one dog and resolution with hydroxyurea and prednisolone treatment in another.17, 18 Recently we have seen two related dogs (Rottweilers) that fulfilled the criteria for HES, but recovered with no, or very short-term, treatment. This suggests that there may be a similar disease to the ‘benign HES’ identified in people. Differentiation of HES from eosinophilic leukaemia (EL) is difficult, but generally demonstration of >5% blast cells in the bone marrow is necessary for diagnosis of EL.1
The exact mechanisms for eosinophilic production are unknown, but interleukin-5 (IL-5), IL-3 and GM-CSF all inhibit eosinophil apoptosis and have specific receptors on eosinophils and basophils.1,2 Production of IL-5 by neoplastic lymphocytes has been implicated as one potential cause of paraneoplastic eosinophilia. Basophils are also primed by IL-3 and therefore basophilia often accompanies eosinophilia.2 Eosinophilic bronchopneumopathy has been identified as being mediated by CD4+ lymphocytes with a concurrent decrease in CD8+ lymphocytes, suggesting a T helper (Th)-2 mediated response.5 Further investigations of the molecular signaling mechanisms in affected animals is warranted, as this may allow for establishing simple tests to allow differentiation between allergic, infiltrative eosinophilic and neoplastic disease in dogs of all breeds.
Whatever the mechanism of initial production by the bone marrow, eosinophils are then attracted into tissues by local chemo-attractant molecules.1 This is generally a Th-2 mediated response, and may be appropriate in cases of parasitism, as the cytotoxic components of eosinophils may destroy the parasite. Eosinophils contain many toxic inflammatory mediators.1 Eosinophil cationic protein in particular appears to promote the activity of other toxic mediators in target tissue.20 In addition, eosinophils produce compounds capable of increasing vascular permeability, stimulating mucus secretion and smooth muscle contraction.17 If eosinophilia is inappropriately stimulated (i.e., in the absence of helminths), the accumulation of eosinophils has the potential to cause significant damage to the target organs.
Table. Potential causes of eosinophilia in dogs.
Pneumomonyssoides caninum (?)
Flea allergy dermatitis
Eosinophilic infiltrative disorders:
Suppurative processes (chronic upper respiratory disease, pneumonia, metritis, mastitis, lower urinary tract infection)
Mast cell tumour
Solid tumours (myxosarcoma, basal cell tumour, squamous cell carcinoma, salivary gland adenocarcinoma, sweat gland adenocarcinoma)
Soft tissue trauma
Renal failure (?)
Acute gastroenteritis (?)
Pemphigus foliaceous (?)
Immune mediated haemolytic anaemia (?)
Chronic renal failure (?)
Pulmonary oedema (?)
Diabetes mellitus (?)
Juvenile nephropathy (?)
1. Rothenberg. NEJM 1998 338:1592-1600
2. Lilliehook, Tvedten. VCNA (SA Practice) 2003 33:1359-1378
3. Willesen, et al. Vet J 2007 Epub
4. Guilford In: Strombeck’s Small Animal Gastroenterology. 3rd edn. 1996:451-456.
5. Clercx, et al. JVIM 2000 14:282-291
6. Lilliehook, et al. JSAP 2000 41:248-253
7. Corcoran, et al. JSAP 1991 494-502
8. Hayshiya, et al. J Vet Med A Physiol Path Clin Med 2002 49:27-31
9. Ozaki, et al. Vet Path 2006 43:339-344
10. Marchetti, et al. Vet Clin Path 2005 34:259-263
11. Salvadori, et al. JSAP 2007 48:466-499
12. Bennett, et al. Aust Vet J 1997 75:786-789
13. Lilliehook. Vet Clin Path 1997 26:113-117
14. Rajamaki, et al. Vet J 2002 163:168-181
15. German, et al. JSAP 2002 43: 533-538
16. Calvert, et al. JAAAHA 1988 311-320
17. Sykes, et al. JVIM 2001 15:162-166
18. Perkins, Watson. Aust Vet J 2001 79:686-689
19. Aroch, et al. Vet Rec 2001 149:386-389
20. Young, et al. Nature 1986 321:612-616
(click the speaker’s name to view other papers and abstracts submitted by this speaker)Caroline Mansfield, BSc, BVMS, MACVSc, MVM, DECVIM-CA
Department of Veterinary Clinical Sciences
Murdoch, Western Australia, Australia
Guinea pigs make excellent pets with unique personalities, and because they are docile and rarely bite, they are often a good “first” pet for children. They have also been used for years as a research model for human medicine. As a result, much is known about their biology and care. Familiarity with common illnesses of guinea pigs and their causes can help improve the care of these popular pets in both the clinic and home settings.
Guinea pigs are very sociable animals. They have a variety of vocalization patterns, including purrs and whistles (especially at feeding time). If in pain, they may scream or squeal.1 When startled, they may freeze temporarily or frantically run around their enclosure. Healthy guinea pigs are bright-eyed and alert and may appear tense or nervous at presentation.
Unfortunately, like many rodents, guinea pigs hide signs of illness for as long as possible. Guinea pig owners, like all animal owners, should be encouraged to bring their pet in for routine evaluations. This will give the veterinary staff the opportunity to educate the client about good husbandry practices and appropriate nutrition, which can help avoid many of the health issues associated with guinea pigs.
Treating guinea pigs can be challenging. Guinea pigs react fearfully to novel stimuli and may refuse to eat foods that they were not introduced to at an early age. Adding medication to food or water may alter the taste enough to lead the animal to refuse to eat and drink, as can the stress of hospitalization alone. The challenge increases when some clients choose not to pursue recommended treatments because of an “I can replace it cheaper than I can treat it” attitude.
If possible, the client should bring the guinea pig into the hospital in its own cage with a supply of its regular food. If the animal is ill, the enclosure and diet may answer some questions as to why. Prior to treating a guinea pig, it is important to be familiar with normal physiologic data for these patients.
When a guinea pig is brought to the clinic, every effort should be made to keep it away from the noise of barking dogs and other hospital traffic. The hospital should have a good exotic animal formulary as well as other reference texts specific to the species. Guinea pigs should be handled gently, placing one hand under the thorax/abdomen while supporting the hindquarters with the other hand to prevent damage to the internal organs.
Bacterial pneumonia, commonly caused by Bordetella bronchiseptica and Streptococcus pneumoniae, frequently leads to death in the guinea pig.2 Stress, pregnancy, poor husbandry, and exposure to carrier animals (i.e., dogs and rabbits) may increase the risk of the guinea pig contracting the disease.3,4 Signs may include dyspnea, anorexia, depression, poor haircoat, and ocular and nasal discharge.5 Supportive care should be implemented to keep the animal comfortable and hydrated.
Force-feeding may be necessary to provide nutritional support. If so, it is important to handle the animal as gently as possible. A mixture of one part protein powder of vegetable origin (e.g., soy, rice), one part instant breakfast powder (not chocolate), one part baby food cereal, and one part Nutri-Cal (EVSCO Pharmaceuticals, Buena, NJ) thinned to paste consistency with water can be fed in 3- to 5-ml amounts at 6- to 8-hour intervals. The formula can be given orally into the side of the mouth through a syringe, thinning as necessary with water. Soy-based enteral formulas, softened guinea-pig pellets, and vegetable baby food can also be used for force-feeding. Feeding tubes can damage the soft palate; therefore, they should be used with care. Regardless of the method of feeding, it is important to add vitamin C daily to the guinea pig’s diet.6,7
If blood tests are to be conducted, small samples of blood may be obtained from an ear vein or saphenous vein, with larger samples obtained from the jugular vein. However, because the restraint necessary for blood collection can prove too stressful, the veterinarian may opt to treat based on clinical signs.a
Antibiotics effective against gram-positive bacteria, such as penicillin and erythromycin, may destroy the normal flora of the guinea pig’s intestinal tract, leading to enterotoxemia. Recommended antibiotics for guinea pigs include chloramphenicol and enrofloxacin. One study showed that Bordetella vaccines developed for other species, particularly pigs, may be used in guinea pigs.8
Guinea pigs suffering from ringworm or infested with fleas, lice, or skin mites may exhibit signs of pruritis, excoriation, rough haircoat, alopecia, thickened skin, and secondary bacterial skin infection. It is important to remember that ringworm and the Trixacarus caviae mite are transmissible to humans.7 Good sanitation and personal hygiene are the best methods for preventing the transmission of zoonotic diseases from rodents. The bedding in cages should be changed frequently. If a rodent shows signs of a zoonotic disease, the owners should be advised to avoid close contact with the pet until the situation is resolved; especially immunosuppressed individuals should avoid contact with these pets.
Flea powders that are safe for use with cats may be used to help control flea infestation. Ringworm can be treated with topical antifungal creams applied once daily for up to 4 weeks and/or systemic antifungal drugs added to food or water.3Lice and mites can be treated with ivermectin.7
Alopecia may be seen in sows during the late stages of pregnancy, and animals housed in groups may chew each others’ hair, which is “barbering” behavior.3 If the animal is stressed, it may engage in hair-pulling. These conditions may require treatment, depending on the cause. For example, if the behavior is caused by stress (e.g., the cat is caught sitting on top of the cage and reaching through the bars), the cause of the stress needs to be removed. However, if the barbering is a result of dominant-subordinate behavior and is not resulting in trauma, hay or a chew toy can be offered as a distraction. If this distraction technique does not work, separating the animals may be necessary.
Poor sanitation, abrasive substrate, wire cage bottoms, obesity, and trauma are all contributing factors in the development of pododermatitis, a condition causing swollen, painful feet. The feet may become ulcerated and infected by Staphylococcus spp.9 The guinea pig will vocalize and be unwilling to move. The animal can be treated with foot soaks, debridement of tissue, and systemic antibiotics, but treatment is not always successful.2,7 To prevent pododermatitis, the client should be educated about proper sanitation, bedding, and diet. Trimming the guinea pig’s nails to prevent them from curling back into the soles of the feet should be performed as needed.
The incisors, premolars, and molars of the guinea pig are open rooted. Since the teeth grow continually, if they do not occlude properly, they may cause trauma to the oral mucosa or trap the tongue. Unlike other pet rodents, malocclusion of the premolars and molars is more common than malocclusion of the incisors in guinea pigs.5 Visual examination of the mouth of a guinea pig is difficult, but an otoscope can help detect problems in the cheek teeth.b Malocclusion of the incisors is much easier to see. Signs include slobbering, weight loss, and moist dermatitis. A lack of vitamin C in the diet may contribute to malocclusion; however, this problem seems to have a strong genetic component. After the guinea pig is anesthetized, the teeth can be trimmed with a Dremel tool (Dremel, Mount Prospect, IL) or a slightly abrasive burr.7Clients should be warned that this is a continuous problem that will require routine care throughout the life of the guinea pig.
Digestive System Problems
Anorexia, weight loss, diarrhea, and dehydration are signs indicative of antibiotic-induced enterotoxemia. The normal flora present in the guinea pig intestinal tract are primarily gram-positive; therefore, antibiotics that are effective against gram-positive bacteria, such as ampicillin, penicillin, erythromycin, and gentamicin, can destroy the normal flora and may result in enterotoxemia.6 Treatment of enterotoxemia requires supportive care (e.g., warmth, fluid therapy, nutritional support). Some veterinarians feed live culture yogurt to these patients to increase healthy bacteria in the gut.
Bacterial enteritis caused by Salmonella spp, Escherichia coli, or Clostridium perfringens is diagnosed by bacterial culture of the feces. It is usually contracted as a result of poor husbandry practices, such as failure to maintain clean environmental conditions, to provide a fresh supply of water, or to thoroughly wash any fresh vegetables or fruits fed to the guinea pig.7 Treatment includes supportive care, keeping the animal hydrated, and antibiotic therapy.
Diarrhea may also be caused by parasites. Cryptosporidium wrairi is a protozoal parasite transmitted via the fecal-oral route. C. wrairi may cause weight loss, diarrhea, and death, primarily in very young animals.3,9 Guinea pigs may also host other protozoal parasites, such as Eimeria caviae and nematodes, but clinical disease rarely presents.7 Good sanitation procedures may help control reinfestation.
Urinary obstruction from congealed ejaculate has been noted in older male guinea pigs. Urinary calculi are more common in older females. Signs may include dysuria, anuria, hematuria, and a hunched posture.2 Diagnosis is based on clinical signs and radiographic evidence of calculi. Treatment includes systemic antibiotic therapy and surgical removal of stones. Preventive measures are not well known7; however, alfalfa hay is sometimes thought to contribute to the formation of urinary calculi because of its high calcium content.10
Dystocia may occur in obese sows, sows pregnant with a large litter or a single large fetus, or sows bred for the first time when older than 6 months due to fusion of the pubic symphysis.2 Uterine inertia may also lead to dystocia and may be treated with oxytocin. However, dystocia caused by fusion of the symphysis will likely require delivery by cesarean section.7 Straining without producing a pup, depression, and foul discharge from the vulva are signs of dystocia.
Other Common Problems
Cervical lymphadenitis, also referred to as lumps, is usually caused by Streptococcus zooepidemicus. The guinea pig may present with swelling or abscesses of the cervical lymph nodes. The infection may be a result of bite wounds,2 but abrasions to the oral mucosa caused by malocclusion or coarse feed products may contribute to the problem.7 Treatment options include surgical excision of the affected nodes, draining the purulent material from the abscess, and flushing the wound with 2% chlorhexidine solution. Systemic antibiotic therapy using enrofloxacin has proven effective. Until the wounds have healed, the affected animal should be housed separately from other guinea pigs.2
Ketosis, a metabolic disease in which large amounts of ketone bodies accumulate in the blood and tissue, usually occurs in obese sows during late gestation. Male guinea pigs, however, can also develop ketosis. Clinical signs include anorexia, lethargy, hypoglycemia7 (<60 mg/dl), dyspnea, convulsions, and death. Good nutrition, including fresh water and a good-quality guinea pig diet supplemented with grass hay and fresh vegetables and fruit can help prevent ketosis, as will monitoring food intake to prevent obesity. Sows may refuse to eat if their diet is changed during pregnancy. Supportive care, fluid therapy, and intravenous administration of 1 to 2 ml 50% dextrose in 3 to 5 ml saline can be used to treat ketosis; however, the mortality rate is very high.6
Like primates, guinea pigs require vitamin C as part of their diet. A deficiency of this vitamin can lead to the development of scurvy within 2 weeks.6 Signs of scurvy include lethargy, joint swelling and lameness, vocalization, loose teeth, anorexia, rough haircoat, and diarrhea. Affected animals are at an increased risk for secondary bacterial infections. Scurvy can be prevented by feeding the animal a high-quality guinea pig diet supplemented with vitamin C. However, vitamin C is not a stable ingredient, and food not used within 90 days of the milling date is unsatisfactory. Keeping the food refrigerated is recommended. Fresh fruits and vegetables high in vitamin C, such as oranges, kale, and dandelion greens, should be fed daily. Dandelion greens should be from a reliable source that does not use chemical sprays (many grocery stores now stock edible dandelion greens). Uneaten fruit and vegetables should be removed to prevent spoilage. Vitamin C can also be added directly to the drinking water, but the water level should be monitored in case the guinea pig is put off by the flavor. The water should be changed daily. Multivitamin drops should not be used for vitamin C supplementation because other vitamins may be toxic to the guinea pig.6
Guinea pigs are susceptible to heat stroke. According the Animal Welfare Act, guinea pigs should not be housed at temperatures below 60°F (16°C) or above 85°F (29°C). A temperature range of 65°F to 75°F (18°C to 24°C) is recommended.2 Guinea pigs suffering from heat stroke salivate, have rapid respiration, and have an elevated body temperature. Coma and death may result. A guinea pig with heat stroke should be bathed with cool water to begin reducing its body temperature. The veterinarian should be contacted immediately. Fluid therapy and corticosteroid administration may be necessary.7
Administration of Common Therapies
Because guinea pigs do not vomit and, therefore, do not have the risk of aspiration as seen in cats and dogs, fasting the pet prior to anesthesia administration is not necessary. Guinea pigs can be induced and maintained with isoflurane gas using a facemask and a nonrebreathing circuit.6 Facemask induction requires little restraint. Ketamine, alone or in combination with diazepam and acepromazine, can also be used. It is important to keep in mind that rodents have a fast metabolism; therefore, they excrete injectables rapidly. Even when in a deep plane of anesthesia, the pedal reflex will be present. During recovery, the animal should be kept warm and turned from side to side every 15 minutes to prevent dependent edema.
Medications should be administered through 21-gauge or smaller needles to prevent tissue irritation, injecting no more than 0.3 ml into any intramuscular site. Butterfly catheters are helpful when giving subcutaneous injections. Placing the guinea pig on a towel during administration can provide some warmth and can limit their movement. Intravenous placement can be difficult; a 23-gauge or smaller catheter may be placed in the saphenous vein after shaving the site and prepping with alcohol. Applying a warm compress or shining a low-watt light over the area may help distend the vein.
Intraosseous catheter placement can be achieved using a 22-gauge needle. The site should be surgically prepped and the needle inserted with a twisting motion into the greater trochanter of the femur. The catheter should be secured with tape or suture material, and the guinea pig should be closely monitored to prevent it from chewing at the site.4
Providing skilled and knowledgeable care to hospitalized guinea pigs can be both challenging and rewarding. The staff should educate owners about the special care these pets require. Preventing problems before they occur is essential to the health and well-being of these unique animals.
Ballard B, Cheek R (eds): Exotic Animal Medicine for the Veterinary Technician. Ames, Iowa State University Press, 2003.
Carpenter JW: Exotic Animal Formulary, ed 3. Philadelphia, WB Saunders, 2005.
Harkness JE, Wagner JE: The Biology and Medicine of Rabbits and Rodents, ed 3. Media, PA, Lippincott Williams & Wilkins, 1988.
Hillyer EV, Carpenter JW (eds): Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery, ed 2. St. Louis, WB Saunders, 2004.
aFor more information about guinea pig venipuncture, including restraint techniques and safe sample sizes, see “Basic Techniques in Rodent Medicine” on page 768 of this issue.
bFor more information about conducting an oral examination in a guinea pig, including useful equipment, see “Basic Techniques in Rodent Medicine” on page 768 of this issue.
The website for the veterinary profession
AORTIC THROMBOEMBOLISM IN DOGS – SIGNS AND
Author : Victoria Doyle
Categories : Vets
Date : February 20, 2012
Victoria Doyle looks at how ATE can be a complication of other diseases, highlighting clinical and neurological signs, and diagnosis and treatment methods AORTIC thromboembolism (AtE) is less commonly seen in dogs compared to cats.
However, it is an important differential diagnosis for dogs presenting with a range of clinical signs. ATE is seen more often in large-breed dogs, including border collies, Labradors and greyhounds, although there is an apparent predisposition in cavalier King Charles spaniels (CKCS). Male dogs tend to be over-represented. Middle-aged to older dogs are usually affected, with a mean age of nine years (range five to 14 years)1 .
ATE is seen in dogs with a range of underlying causes that may lead to a hypercoagulable state. This disease process includes cardiac disease, hyperadrenocorticism (HAC; pituitary or adrenaldependent or iatrogenic), immune-mediated haemolytic anaemia (IMHA), disseminated intravascular coagulation (DIC), sepsis, bacterial endocarditis, parvovirus infection, hypertension, neoplasia, and protein-losing enteropathy (PLE) and nephropathy (PLN)1-
6. No underlying cause may be identified in up to 38 per cent of cases1. In cats, the primary underlying cause of ATE is cardiac disease (hypertrophic, restrictive or dilated cardiomyopathy)7. Neoplasia, paraneoplastic thrombocytosis, foreign body and idiopathic causes have rarely been reported in the feline species
8. 1 / 6 Pathogenesis
Thrombosis occurs due to the disruption of blood flow, injury to the vessel wall and disruption of the balance of procoagulant and anticoagulant factors. Cardiac disease can disrupt blood flow due to venous congestion, and the integrity of theendothelium may be affected 2. Arrhythmias will cause abnormal intracardiac blood flow, which can precipitate thrombus formation 2. HAC is proposed to cause thrombosis due to increased levels of clotting factors in the blood, lossof antithrombin III (ATIII) and an increase in plasminogen activator inhibitor2. Hypothyroidism causes atherosclerosis, which leads to an increased risk of thrombosis in both dogs and humans 6.
Up to 80 per cent of cases with IMHA have thromboembolic disease due to a number of factors, including hypoalbuminaemia, thrombocytopenia and use of corticosteroids 9.
DIC is a complex pathological process that causes spontaneous haemorrhage and thrombus formation via plasmin and thrombin activation, as well as consumption of clotting factors and platelets 3. DIC also causes activation of cytokines leading to fibrinolysis, damage to blood-vessel walls, causing platelet aggregation, and inhibition of natural anticoagulants including ATIII3. Neoplasia can lead to a predisposition to clot formation due to platelet activation, a reduction in neutralisation of clotting factors and their clearance from the body, a reduction in fibrinolysis, and an increased production of factor X activator2. PLE and PLN cause hypercoagulability due to the loss of ATIII, which is of a similar size to albumin. Dogs with a serum albumin of less than 20g/L are highly likely to have reduced ATIII1.
Hypoalbuminaemia may also affect platelet aggregation leading to hypercoagulability.
CKCS have a high prevalence of cardiac disease, abnormal platelet morphology, femoral artery occlusion and connective tissue disorders that may predispose them to thromboembolic disease1,
10. Clinical and neurological signs
Clinical presentation of a dog with an ATE is more variable than in cats. Cats tend to have a peracute presentation with ATE due to the dislodging of a cardiac thrombus, which embolises and occludes the aorta. This triggers a cascade of events, including the release of vasoactive substances, culminating in the constriction of the collateral vasculature in the pelvic limbs11. In dogs, presentation can be acute onset of mono or para-paresis/plegia with absent femoral pulse, 2 / 6 but in many cases it is chronic with exercise-induced pelvic limb weakness/ataxia1. Femoral pulses were reported present on clinical examination, although reduced in quality in up to 54 per cent of cases1. There are multiple potential causes for this, including the presence of extensive collateral circulation involving the lateral circumflex femoral, the distal caudal femoral, the caudal gluteal and the deep femoral arteries 1,
The different underlying causes of ATE in dogs may allow a more gradual formation of the ATE, which allows further collateral circulation to form1,
12. The clinical signs in dogs may be exacerbated during defecation, as increased abdominal pressure may further compromise perfusion to the pelvic limbs. It is uncommon for dogs to have cyanotic footpads or nail beds. Pain may not be a feature, or may be difficult to localise, especially in chronic cases, but also occasionally in dogs with acute presentations1. A thorough clinical examination may identify a potential underlying cause for the ATE.
On neurological examination, conscious proprioceptive deficits were reported present in 54 per cent of cases1. Interestingly, the patella reflex is more frequently, and more markedly, affected in dogs with ATE compared to cats where it is usually spared 1. The pedal withdrawal in dogs is less often affected than cats. This may be due to anatomical variation between the species in the arterial supply to the pelvic limbs1.
Haematology and serum biochemistry are required to assess potential underlying causes and may suggest the requirement for more specific testing, including ACTH stimulation tests or a thyroid panel. Creatinine kinase (CK) and aspartate aminotransferase (AST) are useful additions to the serum biochemistry as they are frequently elevated, especially in acute cases1 , 2 . However, they
may only be mild to moderately elevated or within the normal range, especially in chronic cases. The coagulation profiles are often within the normal range1 . Plasma D-dimers can be measured and are usually elevated in dogs with thromboembolic disease13. D-dimers form from the breakdown of a stabilised clot and are only seen with active coagulation and fibrinolysis13. Studies have shown that D-dimers are more sensitive than fibrin degradation products (FDPs) for thromboembolic disease13. Urine analysis, including a urine protein: creatinine ratio (UPCR), is required to assess for protein loss via the kidneys. Systemic blood pressure and fundic examination to exclude the possibility of hypertension as an underlying cause of the ATE are also important. Echocardiography is indicated if there is a cardiac murmur, and an electrocardiogram (ECG) is important if an arrhythmia is detected on clinical examination. Screening the thorax and abdomen with radiographs and ultrasound for primary neoplasia or metastatic disease are a vital part of the investigation. Abdominal ultrasound may also show the presence and extent of the thrombus in the distal aorta (Figures 1 and 2).
3 / 6 Colour flow Doppler is useful to assess whether there is any flow past the thrombus (Figure 3)
Magnetic resonance imaging (MRI) of the caudal abdomen can also be used to detect the
thrombus. A filling defect may be seen within the distal aorta on T2-weighted images or with time of flight angiography (Figures 4,5 and 6)
14. MRI can also detect ischaemic changes in affected musculature. As canine ATE is often more chronic than feline, collateral arteries can form and these may also be evident on MRI14. Computed tomography (CT) angiography can also be used to detect the filling defect in the distal aorta15. The presence of an ATE can be confirmed on postmortem and histopathology (Figures 7 and 8). However, small thrombi lyse shortly after death and can be overlooked.
Analgesia and fluid therapy to correct dehydration or electrolyte imbalances are important in the initial stages. Medication is directed towards the underlying cause of the ATE when one is found.
Thrombolysis using streptokinase (a humanlicensed plasminogen activator) has been shown to eradicate the thrombus in three dogs with ATE and reduce the size of the thrombus in another16.
Plasminogen activators have not been successful in all dogs2. Side effects include reperfusion injury, cerebral thromboembolic events and clinical haemorrhage, so their use is not without risks.
Heparin and aspirin have both been used to reduce the risk of further clot formation; however, neither have a veterinary licence3. The use of heparin also carries risks of haemorrhage, but this can be reduced with the use of low molecular weight heparin, although the optimal dose has not been determined.
Concurrent use of heparin with aspirin will increase the risk of haemorrhage. The dose of aspirin likely to be effective is debated – some authors advocate the use of ultra lowdose aspirin therapy (0.5mg/ kg/day) to prevent thromboembolic disease in patients with IMHA, while others have shown this dose is ineffective in healthy dogs.
Clopidogrel, a new humanlicensed anti-platelet drug, has been used successfully, alone and in combination with ultra low-dose aspirin, in dogs with IMHA9. A restricted exercise regime to prevent increased demand on perfusion to the pelvic limbs is also prudent. However, short periods of gentle exercise may encourage perfusion to the limbs and re-canalisation of the thrombus.
The prognosis for dogs presenting with acute or chronic signs of ATE is more favourable than for cats with ATE. Only 33 to 39 per cent of cats are reported to survive until discharge17. However, up to 53 per cent of dogs can survive until discharge1,
2. After discharge, the reported mean survival time for cats is between 117 days to 345 days 7,
17. The median survival in dogs has been reported at 270 days (range 45 to still alive at 780 days), which is similar to cats 1. Those dogs that survive to discharge tend to have a gradual improvement in their clinical signs. Those with a more chronic 4 / 6
history usually remain stable 1.
The difference in prognosis between cats and dogs may be due to the potential for development of collateral circulation in dogs and the variety of underlying causes possible. Unfortunately, further thrombus formation is possible even if the underlying cause is treated and the dog is receiving antiplatelet therapy, so relapses are a possibility 2. Conclusions
While ATE is less commonly seen in dogs compared to cats, it is an important complication of a range of different diseases. The clinical signs seen in dogs are significantly different from those in cats. The clinician must remain aware of the possible clinical signs that can be seen in dogs and institute further diagnostic procedures if the clinical suspicion of ATE arises. The most successful treatment for ATE in dogs is not known, although different options are available that can be trialled with owner consent. The short-term prognosis is more favorable than in cats, but the long-term prognosis may be comparable.
The author would like to thank Brian Smyth at the RVC for the pathology images, the imaging department at the AHT for the diagnostic images, and Alberta de Stefani at the AHT for her help in preparing the manuscript.
1. Goncalves R et al (2008). Clinical and neurological characteristics of aorticthromboembolism in dogs, J Small Anim Pract 49(4): 178-184.
2. Boswood A, Lamb C R and White R N (2000). Aortic and iliac thrombosis in six dogs, J Small Anim Pract 41(3): 109-114.
3. Fox P R, Petrie J and Hohenhaus A E (2005). Peripheral vascular disease. In Textbook of Veterinary Internal Medicine, Ettinger S J and Feldman E C (eds), Elsevier Saunders, St
4. Boswood A (1996). Resolution of dysrhythmias and conduction abnormalities following
treatment for bacterial endocarditis in a dog, J Small Anim Pract 37(7): 327-332.
5. Sykes J E et al (2006). Clinicopathologic findings and outcome in dogs with infective
endocarditis: 71 cases (1992-2005), J Am Vet Med Assoc 228(11): 1,735-1,747.
6. MacGregor J M et al (2004). Cholesterol-based pericardial effusion and aortic
thromboembolism in a 9-year-old mixed-breed dog with hypothyroidism, J Vet Intern Med
7. Laste N J and Harpster N K (1995). A retrospective study of 100 cases of feline distal
5 / 6 aortic thromboembolism: 1977-1993, J Am Anim Hosp Assoc 31(6): 492-500.
8. Reimer S B, Kittleson M D, and Kyles A E (2006). Use of rheolytic thrombectomy in the
treatment of feline distal aortic thromboembolism, J Vet Intern Med 20(2): 290-296.
9. Mellett A M, Nakamura R K and Bianco D (2011). A prospective study of clopidogrel
therapy in dogs with primary immune-mediated hemolytic anemia, Journal of Veterinary
Internal Medicine 25(1): 71-75.
10. Buchanan J W, Beardow A W and Sammarco C D (1997). Femoral artery occlusion in
cavalier King Charles spaniels, J Am Vet Med Assoc 211(7): 872-874.
11. Smith S A and Tobias A H (2004). Feline arterial thromboembolism: an update, Vet Clin North Am Small Anim Pract 34(5): 1,245-1,271.
12. Guglielmini C et al (2008). Internal thoracic artery-caudal epigastric artery as a collateral pathway in a dog with aortic occlusion: a case report, Vet J 178(1): 141-145.
13. Nelson O L and Andreasen C (2003). The utility of plasma D-dimer to identify thromboembolic disease in dogs, J Vet Intern Med 17(6): 830-834.
14. Brofman P J and Thrall D E (2006). Magnetic resonance imaging findings in a dog with
caudal aortic thromboembolism and ischemic myopathy, Vet Radiol Ultrasound 47(4): 334-338.
15. Kirberger R M and Zambelli A (2007). Imaging diagnosis – aortic thromboembolism
associated with spirocercosis in a dog, Vet Radiol Ultrasound 48(5): 418-420.
16. Ramsey C C et al (1996). Use of streptokinase in four dogs with thrombosis, J Am Vet
Med Assoc 209(4): 780-785.
17. Smith S A et al (2003). Arterial thromboembolism in cats: acute crisis in 127 cases
(1992-2001) and long-term management with lowdose aspirin in 24 cases, J Vet Intern Med
Discover why Bella & Duke dog parents swear by their Bella & Duke fresh-frozen raw dog food and introduce your mutt to the ultimate flavour enhancer for dogs – bone broth!
NATURAL RAW DOG FOOD
why bella & duke?
Our raw dog food includes only the best ingredients and combines them into a diet that gives your dog all the nutrients he or she needs to be healthy.
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Our packaging is 100% polypropylene – that also means it is 100% recyclable by councils and 100% reusable as well. It may look like plastic, it may feel like plastic, but it is the safest recyclable food packaging we can find. Just pop it into your recycling bin and it can be sorted. Or find another use for it yourself!
We set out to make the best dog food
We looked at the nutrition a dog needs, how their digestion system works. We looked at the food groups that were excluded from dog foods for expense or just because myth said dogs did not like them. Then we realised that dogs (like humans) want variety, so we created 8 different menus based on different animals or fish. Then we worked out how we could pack and ship them to you each month so you could serve them when you needed to.
Our Dog Menu
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Did you know that dogs cannot digest grains?
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What is Bone Broth?
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Dogs evolved over millions of years to eat a specific type of diet. Modern diets have ignored evolution and contain ingredients that dogs would not choose in their natural state. The most obvious example are grains which are the core constituent of kibbles.
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Alternative names for prolactin
In everyday language, prolactin is referred to as the ‘milk hormone’; PRL; luteotropic hormone; LTH
What is prolactin?
Prolactin is a hormone named originally after its function to promote milk production (lactation) in mammals in response to the suckling of young after birth. It has since been shown to have more than 300 functions in the body. These can be divided into a number of areas: reproductive, metabolic, regulation of fluids (osmoregulation), regulation of the immune system (immunoregulation) and behavioural functions.
In humans, prolactin is produced both in the front portion of the pituitary gland (anterior pituitary gland) and in a range of sites elsewhere in the body. Lactotroph cells in the pituitary gland produce prolactin, where it is stored and then released into the bloodstream. Human prolactin is also produced in the uterus, immune cells, brain, breasts, prostate, skin and adipose tissue.
How is prolactin controlled?
One of the main regulators of the production of prolactin from the pituitary gland is the hormone called dopamine, which is produced by the hypothalamus, the part of the brain directly above the pituitary gland. Dopamine restrains prolactin production, so the more dopamine there is, the less prolactin is released. Prolactin itself enhances the secretion of dopamine, so this creates a negative feedback loop.
Oestrogen is another key regulator of prolactin and has been shown to increase the production and secretion of prolactin from the pituitary gland. Studies have shown small increases in prolactin in the blood circulation of women during stages of their reproductive cycle where oestrogen levels are at their highest. This is also the case during and after pregnancy, which makes sense, since a higher level of circulating prolactin is needed to cause lactation to start.
In addition to dopamine and oestrogen, a whole range of other hormones can both increase and decrease the amount of prolactin released in the body, with some examples being thyrotropin-releasing hormone, oxytocin and anti-diuretic hormone.
What happens if I have too much prolactin?
The condition of having too much prolactin circulating in the blood is called hyperprolactinaemia. The most common causes of hyperprolactinaemia include pregnancy, medications that reduce dopamine action in the body, thyroid underactivity and benign pituitary tumours (known as prolactinomas). Symptoms can include the unwanted production of milk, disturbances to the menstrual cycle and symptoms due to oestrogen deficiency (in women) or testosterone deficiency(in men). The vast majority of patients with a prolactinoma can be treated successfully using drugs which mimic the action of dopamine. The most commonly used is cabergoline.
What happens if I have too little prolactin?
The condition of having too little prolactin circulating in the blood is called hypoprolactinaemia. This condition is very rare and may occur in people with pituitary underactivity.
A decrease in the amount of prolactin secreted can lead to insufficient milk being produced after giving birth. Most people with low prolactin levels do not have any specific medical problems, although preliminary evidence suggests they might have reduced immune responses to some infections.
When Cats and Dogs Won’t Milk
When mothers won’t milk, it’s critical – but quick intervention can be the remedy.
Prolactin is the hormonal stimulant that initiates lactation at birth. Females who have plenty of glands but no milk lack the prolactin stimulation to start producing milk. This is common in moms who have C-sections, as there is no birthing process to stimulate prolactin release. Bulldogs in particular struggle with this, as the puppies’ large heads often preclude them from free whelping.
Reglan (Metoclopramide) causes the release of prolactin in the postpartum female or queen. It’s reliable and quick to effect – within hours! Reglan is mostly used to stop vomiting, so it’s readily available. You can give Reglan at 0.5 mg/kg every six hours, with Oxytocin every two hours, to help get lactation started. Prolactin stimulates the gland to produce milk, and the Oxytocin lets the milk out of the gland into the duct. The empty gland asks mom for more milk production. Results usually occur within 12 hours.
Herbs are helpful and reliable when a mom’s not milking or not producing enough milk. Fenugreek and Chaste tree fruit are herbal products that reliably boost milk production. Both are in Oxy Momma and dosed according to label. With very little or no milk production, we will double the dose for three days to jump start lactation. It is works and saves puppies.
Breeders’ Edge® Oxy Momma™ is a postnatal vitamin herb chew that contains Fenugreek, Chaste tree fruit, and Motherwort in a form that quickly brings moms into milk. You can expect increased production within 72 hours. Use for seven days before birth for queens or females that have had milking issues in the past or before planned C-Sections to bring Mom into milk. We don’t start before 14 days as milking before birth increases their risk of mastitis.
Prevent Kitten and Puppy Loss
When you’re dealing with milk production issues, keep in mind that the kittens and puppies still need nutrients! If you can’t bring the milk in within six hours, you have to bottle feed with a kitten or puppy milk replacer every two hours. As the queen or female produces more milk, you can transition the kittens or puppies back to their mother.
If you need help, call us at 1-800-786-4751.
Don Bramlage, DVM, Director of Veterinary Services at Revival Animal Health
Can Bulldogs give birth naturally?
(Yesterday…in my clinic .. – I performed C-cection … Bulldog. ..aren’t they pretty?..):
Can Bulldogs give birth naturally?
A frequently asked question – many bulldogs can self whelp, however conditions such as primary inertia and small litters can cause the need for veterinary intervention. I prefer to trust in today’s skilled veterinarians and modern advances in surgery to avoid any possible whelping problems and request that bulldog puppies are delivered by caesarean section. If you have bred puppies before in any other breed it is quite possible to try to safely self whelp a bulldog bitch as your past experience would identify if you needed to seek help. Whelping a bulldog as your first breeding experience without experienced help is not recommended for novices.
Up to 6 hours after care for mum and pups, incubation of the pups ensuring they get the best start in life.
Planning is the key to a successful delivery and healthy pups. I take all the pressure off the owner by looking after the bitch a day or so before she is due to give birth, I will know when it is the right time … for the caesarean section, delivering too early can cause great complications.