Small patients bring huge problems

 

Dr Milena Zlatarova

Clinica Zaivet

Sofia, Bulgaria

 

Meet Betty, 2 year old intact gerbil, living with a sibling. She was presented by the owner for unusual abdominal swelling.

On ultrasound examination the abdominal cavity was filled with large anechoic contents. We discussed the possible differencials with the owner and decided to  step on surgery.

Standard diagnostic laparotomy was performed. Some special preparations were needed, because she weighted 97g. Heating pad, gloves with warm water to maintain hypothermia. We used premedication with meloxicam 0.5mg/kg p.o., warmed saline s.c.,  induced with Isoflurane 4% and continued at 2%.

 

 

After the procedure Betty was bright alert and the weight was 61 g.2 weeks later we removed the stiches and she is 68g now

 

 

Our second patient is Strahil – 3 year old intact male, weight 0.081kg, with previous history of inflammation of the scent gland. It was treated topically with iodine and dermazin cream with no improvement. We decided to

proceed to surgery. The histology examination of the leason wasn’t performed due to financial issues.

 

 

 

 

 

 

 

Misha, 15g female panda mouse was the smallest patient ever being operated in our cabinet. She was sent by collegues for something protruding from the anus. It turned out that  the uterus was protruding from the vagina. We had to proceed to surgery.

This is Misha 10 days later for suture removal.

 

 

 

 

 

Meet Dorothy, 7 months intact female hamster. She was brought for a lump on the left eye. The owner first refused any microbiology or surgery and just wanted eyedrops.  We provided Tobramycin 0.3% 3-4 times daily. A week later  The eye was closed and the owner wanted  emergency treatment. We treated surgically the absces and gave NSAID and enrofloxacin, because microbiology was still denied due to financial issues.

 

A week later Doty was fine almost no sign of illness at all.

Colchicine intoxication in a dog

    Dr Denica Djodjeva

        Sofia, Bulgaria

 

Abstract

Colchicine is extracted from Colchicum autumnale (autumn crocus, or meadow saffron) and Gloriosa superba (glory lily). It is a lipid-soluble alkaloid that is isolated from the plant and is one of the main agents used in the treatment of crystal arthropathy gout, immune-mediated disorders such as Behçet’s disease (characterized by vasculitis), familial Mediterranean fever (characterized by polyserositis and amyloidosis), and neutrophilic dermatoses.  Because colchicine stimulates enzymes called collagenases, which break down collagen protein and inhibit liver cells from making amyloid A, in dogs and cats colchicine is used off-label to reduce scarring processes such as liver cirrhosis, amyloidosis, Shar-Pei fever, fibrosis following placement of a glaucoma drainage device, to prevent granuloma formation following tracheal stent placement and to prevent urethral stricture formation. In birds, it has also been reportedly used to treat hyperuricemia.

Colchicine is rapidly absorbed after oral administration. The pharmacokinetics involves the intestines, liver, and kidneys.  Rapidly absorbed from jejunal and ileal enterocytes, colchicine is partially locally metabolized by enterocytes. The bulk of absorbed colchicine is further metabolized by the liver and excreted in bile. The time to peak concentration in humans is 0.5 to 2.0 h, decreasing rapidly within 2 h. Colchicine undergoes extensive enterohepatic recirculation before being fecally excreted and is distributed to all tissues in the body, where it binds to intracellular tubulin and has a dissociation half-life of 20–40 hours. The accumulation in the kidney, liver, spleen, gastrointestinal wall, and leucocytes may lead to toxicity.  Because of the high degree of tissue uptake, only 10% of a single dose is eliminated within 24 hours, and elimination from the body may continue for 10 days or more. The long half-life and enterohepatic recirculation explain colchicine’s prolonged effect. However, the severity and mortality rate of the poisoning is usually related to the dose ingested. The lowest lethal oral dose reported for dogs is 0.13 mg/kg. Fatalities in the first few days result from shock, respiratory or cardiac arrest, or rapidly progressive multiple organ failure. The most common side effects start 2-5 hours after ingestion and are associated with gastrointestinal upset, vomiting, and diarrhea and are very rare but colchicine can suppress neutrophil production and can cause bone marrow suppression.

Introduction

To date, there are only a few described cases in the veterinary literature of colchicine intoxication in a dog. The main symptoms associated with ingested medication are severe abdominal pain, diarrhea, nausea, vomiting, and in more severe cases, DIC and MODS. There is no specific antidote, and the therapy is symptomatic and supportive. If

colchicine ingestion is suspected, giving active charcoal or gastric lavage would be beneficial if too much time has not passed since ingestion.

Three clinical phases of intoxication are described, each of which is associated with the corresponding expected complications and symptoms.

1. Gastrointestinal / 10-24 hours – characterized by abdominal pain, nausea, vomiting, and diarrhea. Hypovolemic state and hypotension due to severe dehydration, and peripheral leukocytosis.
2. Multiorgan phase / 2 – 7 days – bone marrow hypoplasia with strong leukopenia and thrombocytopenia; oliguric renal failure; cardiac arrhythmias and arrest; electrolyte and metabolic disorders such as hyponatremia, hypocalcemia, hypokalemia, hypophosphatemia; changes in mental status, seizures; respiratory distress, hypoxia.
3. Recovery, if death has not occurred/ after 7 days – leukocytosis; risk of alopecia.

Manifestations of Colchicine Toxicity reported in humans

Gastrointestinal:	Abdominal pain; Nausea/vomiting; Diarrhea; Paralytic ileus; Hepatocellular damage; Pancreatitis
Respiratory:	Respiratory distress; ARDS
Hematological:	Leukocytosis (first stage); Bone marrow hypoplasia; Coagulopathy; Hemolytic anemia
Skin:	Rash; Alopecia
Cardiovascular:	Hypovolemia; Hypotension; Depressed myocardial contractility; Peripheral vasodilation; Arrhythmias; Myocarditis
Renal:	Proteinuria/hematuria; Acute renal failure
Metabolic:	Metabolic acidosis; Hyponatremia; Hypocalcemia; Hypophosphatemia; Hypomagnesemia
Fertility:	Azoospermia; Sterility
Miscellaneous:	Fever; Hypothermia
Neuromuscular:	Mental status changes; Coma; Ascending paralysis; Seizures; Peripheral neuropathy; Rhabdomyolysis

 

The Case of Lady: A Pomeranian’s Struggle with Colchicine Toxicity

Lady’s clinical journey commenced when her owners discovered that she had ingested up to three tablets of colchicine, each containing 0.5 mg of the drug. The ingestion occurred less than 24 hours before her admission, and the rapid onset of clinical symptoms constitutes an emergency, requiring immediate veterinary intervention.

Upon evaluation, Lady presented with a constellation of acute gastrointestinal symptoms including diarrhea, nausea, vomiting, abdominal pain, fatigue, and a notable refusal to eat. Each of these symptoms indicates a severe systemic response, triggered by the colchicine overdose. Colchicine is known to affect multiple organ systems, primarily targeting the gastrointestinal tract, bone marrow, liver, and kidneys. The rapid decline in Lady’s health condition pretty good shows the nature of colchicine toxicity, which can escalate quickly if not addressed promptly.

The prognosis for Lady remains questionable due to the timing of her ingestion and the associated clinical signs. In veterinary practice, the prognosis in cases of colchicine toxicity is influenced by various factors, including the extent of ingestion, the duration since exposure, and the promptness of medical treatment. Given that less than one day has elapsed since the incident, there remains a crucial window of opportunity for effective medical intervention. Treatment protocols typically include decontamination procedures such as emesis induction and activated charcoal administration to reduce further absorption of the toxin but in a time manageable time after the ingestion. In this case, these procedures were not performed due to time elapsed since ingestion.   Supportive care, including intravenous fluids and anti-emetics, may be required to manage dehydration and electrolyte imbalances that commonly accompany gastrointestinal distress.

Test and Investigations:

In the realm of clinical diagnostics, the role of point-of-care (POC) examinations cannot be underestimated. For Lady, a range of POC exams were scheduled, including a complete blood count (CBC), basic metabolic panel (BH), and electrolytes, alongside imaging studies such as abdominal ultrasound and X-ray. Notably, Lady’s irregular vaccination status necessitated the inclusion of a CPV/CCV/G test, which ultimately returned negative results.

Laboratory findings highlighted evidence of dehydration, accompanied by increased liver enzyme levels—a possible reflection of hepatic distress or injury. These findings warrant immediate attention, as dehydration can exacerbate underlying conditions and complicate treatment protocols. Concurrently, the elevated liver enzymes may suggest an underlying metabolic or infectious process that requires further exploration.

The abdominal ultrasound provided crucial insights into Lady’s condition. Importantly, the examination did not reveal any free fluid, which often serves as a potential marker for various abdominal pathologies, such as perforation or significant intra-abdominal hemorrhage. However, the ultrasound did unveil a thickened intestinal wall and signs of inflammation in the small intestine, coupled with increased peristalsis. These findings are suggestive of an inflammatory condition, such as enteritis, which could stem from a variety of etiologies including infectious agents or inflammatory bowel disease.

Complementing the ultrasound findings, the X-ray examination corroborated the absence of any foreign body, thus eliminating a critical differential diagnosis that could account for Lady’s symptoms. The combination of these imaging modalities and laboratory tests contributes to a more comprehensive understanding of her moment health status.

Treatment and Problem-Solving Plan for Hemorrhagic Gastroenteritis due to colchicine intoxication

Hemorrhagic gastroenteritis is a serious condition characterized by inflammation and bleeding, which can lead to significant morbidity. Despite a few cases of colchicine intoxication described, Lady’s case presented a structured treatment and problem-solving plan implemented during the hospitalization and her critical condition. The approach utilized involved a combination of symptomatic therapies, intensive monitoring, nutritional support, and hygiene care tailored to address the complexities arising from her illness.

Upon admission, Lady exhibited clinical signs, including lethargy, refusal of food and water, and vital signs indicative of distress: arterial blood pressure at 150 sys (Doppler measurement), heart rate at 120 bpm, respiratory rate at 21/min, and hypothermia at 36,5 C°, MMC- pink, CRT>2sec. Immediate interventions commenced with symptomatic therapy, specifically the administration of antacids and antiemetics, complemented by antibiotics, supportive care, and warming. Regular monitoring of vital signs was imperative, enabling prompt detection of any deterioration in her condition.

The antibiotic regimen consisted of Ampicillin at a dosage of 20 mg/kg every six hours and Metronidazole at 10 mg/kg every twelve hours. This dual therapy aimed to combat potential intestinal, and bacterial translocation and infections while addressing gastrointestinal stability. Pain relief was managed through a multimodal approach, incorporating buprenorphine, metamizole sodium, hyoscine butylbreomide, and a constant rate infusion (CRI) of lidocaine at dose 1mg/kg/h, ensuring Lady’s comfort during her recovery.

Nause, vomiting, and regurgitation were challenging symptoms in this gastrointestinal upset condition. The combination of maropitant, pantoprazole, ondansetron, and metoclopramide facilitated a significant alleviation of these distressing symptoms, allowing for the resumption of feeding and subsequent recovery. Maropitant, administered at a dosage of 1 mg/kg every 24 hours, serves as a potent antiemetic, specifically targeting the neurokinin-1 (NK1) receptors in the central nervous system. Its use was instrumental in controlling nausea and vomiting episodes and also may act as mild pain control medication. In conjunction with maropitant, pantoprazole was prescribed at a dosage of 1 mg/kg every 24 hours. As a proton pump inhibitor, pantoprazole plays a crucial role in reducing gastric acid secretion, preventing the potential for gastric irritation and ulcers that may result from chronic vomiting. The synergistic effect of combining maropitant with pantoprazole not only addressed the challenges posed by nausea but also provided a protective mechanism for the gastrointestinal tract, promoting an environment for healing. Additionally, ondansetron was incorporated into Lady’s treatment regimen at a dosage of 0.3 mg/kg every 12 hours. Ondansetron’s mechanism of action, which involves blocking serotonin receptors in the central nervous system and the gastrointestinal tract, proved valuable in achieving comprehensive control over Lady’s nausea and vomiting episodes. Recognizing the importance of gastrointestinal motility in managing nausea, metoclopramide was also included in Lady’s therapy as CRI at a dosage of 2mg/kg for 24 hours. Administered to enhance peristalsis, metoclopramide not only functions as an effective antiemetic but also facilitates gastric emptying. This dual action was particularly beneficial in this case, as it mitigated the regurgitation and associated complications. Achieving coordinated motility ensured that Lady’s digestive system could efficiently process the food that would be introduced once her nausea was under control. Once adequate control of nausea and regurgitation was established, the placement of a nasoesophageal tube permitted the safe initiation of feeding and administration of additional probiotic therapy. This intervention was pivotal in delivering necessary nutrition while circumventing the challenges related to oral intake, which could have exacerbated Lady’s condition.

S-adenosyl-methionine (Transmetil ®) is known due to its hepatoprotective properties.  It’s crucial role in detoxification, metabolism, and the synthesis of various biochemicals essential for digestion, growth and potent antioxidants within hepatic tissues, can offer significant benefits in restoring liver function and mitigating cellular damage. At the moment of presence Lady’s liver enzymes were elevated (AST 549 U/I, ALP 1031 U/I). In this case dose of 10mg/kg every twelve hours was used due the hospitalization.  Colchicine is lipid- a soluble alkaloid, and to enhance its safe excretion and mitigate its adverse effects, the use of Intralipid emulsion of 20% has been included in the treatment.  Administered at a rate of 1.5 mL/kg over 15 minutes, followed by a continuous infusion of 0.25 mL/kg/min over two hours, Intralipid serves to expedite colchicine clearance. The emulsion encapsulates the lipophilic drug, facilitating its removal from the body system and subsequent elimination. Due to the hypoproteinemic and albuminemic state (ALB 28.5 g/L; TP 38.6 g/L) coupled with electrolyte imbalance (K 3.6- 3.44mmol/L; Cl 91.9mmol/L; Na 135mmol/L) the administration of amino acid solution has emerged as a vital solution. Amino acids are the building blocks of proteins and play an essential role in addressing the underlying hypoproteinemic and hypoalbuminemia state and recovery from malnutrition. The amino acid glutamine has been recognized for its role in maintaining the gut barrier and modulating electrolyte absorption in the intestines. A serum albumin level of 28.5 g/L indicates a clear departure from the normal range, which typically hovers between 30 to 40 g/L. The context of hypoproteinemia and albuminemia often underscores systemic issues such as malnutrition, liver dysfunction, or protein loss through renal or gastrointestinal pathways. The noted total protein concentration of 38.6 g/L appears low as typical total protein levels fall within the range of 60 to 80 g/L in a healthy individual. However, the focus remains on the significance of low albumin as it plays a crucial role in maintaining oncotic pressure and transporting various substances in the bloodstream. A deficit in albumin can lead to interstitial edema, impaired wound healing, and diminished immune response, exacerbating a patient’s overall clinical condition. In conjunction with hypoproteinemia, the electrolyte profile reveals imbalances: a potassium level fluctuating between 3.6 and starts dropping to 3.44 mmol/L, chloride at 91.9 mmol/L, and sodium at 135 mmol/L, which is a complication described in human clinical cases of colchicine intoxication. These values highlight a tendency to hyponatremia, which can lead to neurological disturbances, and hypokalemia, which can adversely affect cardiac function and muscle contraction.

One of the critical complications arising from HGE is anemia, often characterized by a marked decrease in red blood cell (RBC) count, hemoglobin (HGB) levels, and hematocrit (HCT). Platelet count (PLT) except as a consequence of colchicine intoxication could be indicative of starting DIC or a hypercoagulable state. Recent clinical assessments have indicated RBC levels ranging from 4.61 x 10^12/L to 3.69 x 10^12/L, HGB decreasing from 109 g/L to 89 g/L, HCT dropping from 28% to 23%, and PLT counts diminishing from 21 x 10^9/L to 18 x 10^9/L. The prevalence of anemia in HGE patients necessitates prompt and comprehensive management of potential complications, including the risk of a hypercoagulable state. In managing anemia associated with HGE, the administration of tranexamic acid at a dosage of 10 mg/kg every 12 hours has emerged as an effective therapeutic intervention. Tranexamic acid, an antifibrinolytic agent, functions by inhibiting fibrinolysis, thus promoting clot stability and reducing bleeding tendencies. In the context of HGE, where the loss of blood can lead to both acute anemia and a coagulopathy, tranexamic acid serves a dual purpose: it treats active bleeding while simultaneously preventing the progression to a hypercoagulable state that can occur due to a compensatory increase in coagulation factors. Supportive measures need to include close monitoring for signs of coagulopathy, which can arise due to microvascular changes associated with both the inflammatory response and anemia itself.  Because of that D- dimer was measured and was in normal ranges of 174ng/ml.

Fluid therapy was also critical, compensating for dehydration resulting from vomiting and diarrhea while restoring electrolyte balance; this was further supported with a per-axis supplement to correct hypokalemia and hypochloremia.

Other complications as pancreatitis were observed. The CPL measurement of 702 mcg/L indicates a severe elevation that signals significant pancreatic distress, which may correlate with the severity of pancreatitis and potential progression toward complications. Furthermore, systemic complications including acute respiratory distress syndrome (ARDS) and multi-organ failure can arise as the body attempts to respond to the inflammatory mediators released from the damaged pancreas.

Despite the initial treatment, Lady’s condition showed minimal improvement on the first days of hospitalization, characterized by persistent refusal to eat, regurgitation, and laboratory findings indicative of leukocytosis, anemia, thrombocytopenia, and hypoproteinemia. By the seventh day of hospitalization, Lady demonstrated remarkable improvement. She regained her appetite but still with the NE tube and exhibited heightened vitality and mobility, signifying a positive response to the comprehensive treatment strategy instituted. A careful transition to home care entailed a tailored prescription that included antibiotics, an anemia supplement, probiotics, and regular clinical check-ups.

Drugs affecting colchicine toxicity

 

Interactions with colchicine	Representative drugs
CYP3A4 inhibitors (↑ toxicity)	Almorexant, alpha, amiodarone, amprenavir, aprepitant, atazanavir, boceprevir, casopitant, ceritinib, chloramphenicol, cimetidine, ciprofloxacin, clarithromycin, clotrimazole, cobicistat, conivaptan, crizotinib, cyclosporine, dalfopristin, danazol, darunavir, dasatinib, deferasirox, delavirdine, diltiazem, dronedarone, erythromycin, fluconazole, fluoxetine, fluvoxamine, fosamprenavir, fosaprepitan, fusidic acid, grapefruit juice, idelalisib, imatinib, indinavir, interferon alpha, isoniazid, itraconazole, ketoconazole, lapatinib, lopinavir, lomitapide, miconazole, natural, nefazodone, nelfinavir, paroxetine, posaconazole, propoxyphene, quinupristin, ritonavir, saquinavir, simeprevir, telaprevir, telithromycin, tipranavir, troleandomycin, verapamil, voriconazole, etc
P-glycoprotein inhibitors (↑ toxicity)	Atorvastatin, budesonide, clarithromycin, cyclosporine, diltiazem, erythromycin, grapefruit juice, hydrocortisone, itraconazole, ketoconazole, lovastatin, propafenone, quinidine, ranolazine, saquinavir, simvastatin, tacrolimus, verapamil, etc
CYP3A4 inducers (↓ toxicity)	Aminoglutethimide, armodafinil, barbiturates, bexarotene, bosentan, carbamazepine, dabrafenib, dexamethasone, efavirenz, enzalutamide, eslicarbazepine, etravirine, fosamprenavir, fosphenytoin, griseofulvin, lumacaftor, modafinil, nafcillin, nevirapine, oxcarbazepine, phenytoin, primidone, rifabutin, rifampin, rifapentine, St. John’s wort, etc
P-glycoprotein inducers (↓ toxicity)	Phenytoin, curcumin, carbamazepine, genistein, St. John’s wort extract, quercetin, rifabutin, etc

Expected Outcome

In the event of colchicine overdose, the prognosis is often considered dubious, primarily due to the drug’s potent mechanism and the body’s capacity to metabolize and excrete it. Following significant exposure, patients are at considerable risk for developing disseminated intravascular coagulation (DIC), characterized by widespread activation of the coagulation cascade leading to the formation of small blood clots throughout the body’s small vessels. This pathological process can severely impact organ function and culminate in multiple organ failure. Clinically, the anticipated symptoms would include gastrointestinal distress, cardiovascular instability, and hematological anomalies. The toxicological implications of colchicine are further exacerbated by its narrow therapeutic index and long half-life, which complicates both clinical monitoring and the treatment regimen.

Actual Outcome

In a divergence from the expected prognosis, after seven days of aggressive therapy, the patient demonstrated remarkable clinical recovery. Intensive supportive care measures, including intravenous fluids, symptomatic therapy, and close monitoring of organ function, culminated in the complete restoration of health. This outcome highlights not only the resilience of the body in the face of potentially lethal drug toxicity but also underscores the critical importance of timely intervention and appropriate medical management.

Conclusion

In conclusion, this case serves as an important reminder of the unpredictable nature of drug toxicity and the potential for recovery even in seemingly dire circumstances. While the expected outcomes of colchicine overdose typically carry a grim prognosis due to all possible complications and the risk of DIC, and multiple organ failure, the actual outcome observed here emphasizes the effectiveness of proactive therapeutic measures. Given the underreported clinical cases, it is difficult to create a protocol for the treatment of colchicine poisoning, so I hope this material will help in the future creation of one and help in better management of this rare intoxication condition.

Enemy at the Gates: Hypothermia, the underestimated anesthesia complication

Dr Denica Djiodjeva

Central Vet Clinic

Sofia, Bulgaria

Hypothermia is one of the most frequent and major anesthetic complications, occurring in at least 40% of patients. Unfortunately, too little attention is paid to this condition, which is associated with many pathophysiological changes that affect the patient before, during and after surgery. In a dog, hypothermia is considered a temperature below 37° C. As with prolonged procedures and operations, the risk increases. These are operations in which the abdominal cavity is open for a long time, in small animals under 2 kg, weak, cachectic, pediatric and geriatric patients.

Thermoregulation is a process in which the body strives to maintain a constant body temperature, regardless of external conditions, which ensures normal functioning of enzymes, coagulation and immune response. The normal physiological limits for a dog and a cat are 37.5˚ C to 39.2˚ C for a dog and 37.8˚ C to 39.5˚ C for a cat. For mild hypothermia, 37.0˚ C to 37.7˚ C is accepted; moderate, 35.8˚ C to 37.0˚ C ; severe, 33.6˚ C to 35.8˚  C ; and critical, less than 33.6˚ C or less. The normal body temperature (head and body) is about 38° C, and that of the peripheral parts is 2-4° C lower. Animals and humans, in addition to maintaining their body temperature within certain limits, can also produce it. Their body is conditionally divided into two parts, central (core), which generates heat, and peripheral, which regulates. The body’s regulatory mechanisms work to keep heat within normal limits. Under normal conditions, the production of heat is the result of the metabolic processes of the internal organs. When the blood passes through them, it warms up and reaches the periphery of the body through the cardiovascular system. The main organ that plays the role of a thermostat is the hypothalamus. When the blood passes through it, its temperature depends on what the body’s response will be in order to maintain the balance between heat gain and loss. From the hypothalamus, through afferent and efferent nerve pathways, vasoconstriction is induced, which occurs before the activation of other energy-consuming reactions, such as shivering. It is important to mention that the efferent response includes both types of regulation – behavioral and autonomic. Behavioral is the strongest response to rewarming, but requires awareness, which is absent during anesthesia. For this reason, the patient must rely on autonomic defense mechanisms, such as maintaining normal blood pressure, vasoconstriction, etc. When local anesthesia is used, vasoconstriction is reduced in the area, where it is administered and this increases heat loss. In addition to central thermoreceptors for heat and cold (in the hypothalamus, spinal cord, abdominal organs, brain stem, muscles), there are also peripheral ones in the skin.

According to the second law of thermodynamics heat can only flow by temperature gradient from the body that is warmer towards the periphery or the environment that is colder, therefore, the body can never be heated from the periphery to the core which is usually warmer than the outside.

As already mentioned, when the animal is under anesthesia, the thermoregulatory mechanisms are blocked. Anesthesia slows down behavioral defense mechanisms, reduces metabolic needs, hypothalamic function and muscle tone. Heat loss begins within the first minutes of premedication because all sedatives and tranquilizers block the hypothalamus. The highest heat loss is during the first 20 minutes of induction, due to its distribution from the center to the periphery of the body. For this reason, it is very important to prevent heat loss at the beginning of the anesthesia, through various methods that will be mentiont later.

At first, the main mechanisms of heat loss are four.

 

Convection- This is one of the most common ways of losing heat, which occurs when body heat is dissipated into the surrounding space through the air. The larger the surface of the body, the greater the heat loss. In animals, hair greatly interferes with this mechanism and it is important, with a larger shaved area and an open abdominal cavity during prolonged surgery.         Conduction – occurs in direct contact of surfaces with different temperatures. For example, when lying on a cold operating table. This mechanism is especially important, when the patient is lying on a wet and cold surface.  

Radiation- The transfer of heat from one surface (e.g. the body) to another without direct physical contact. Radiation is received from the sun by any object exposed to sunlight. The heat load from solar radiation,  can be significant in hot environments, where animals are exposed to sunlight for prolonged periods. When an animal is standing in bright sunlight, the amount of solar radiation absorbed may substantially exceed its own metabolic heat production.

Evaporation – evaporation of water at the surface of the body or respiratory tract results in heat loss and it’s approximately 22% of total body loss. 0.58 kilocalories of heat is lost for each gram of evaporated water. In human the evaporation is manifested like sweating but in animals due to the lack of sweat glands, it is expressed by panting. To prevent evaporation from the respiratory tract and a drop in body temperature during anesthesia, the oxygen flow can be reduced if this is compatible with the circuit used and the needs of the patient.

The main physiological disorders that occur with hypothermia are related to reduced liver metabolism, compromised cardiovascular system, reduced ventilation and oxygenation, compromised renal function, reduced cerebral flow. All these factors also influence the slower post-anesthesia recovery. In human medicine, there are many more studies on the subject and more specifically on the direct impact of hypothermia on the body. The most frequently observed are delayed pharmacokinetic and dynamics of anesthetics, impaired coagulation, a threefold increase in the risk of cardiac problems in high-risk patients, an increased likelihood of difficult wound healing and infection, leukocyte migration and suppression along with impaired phagocytosis and neutropenia.

When liver metabolism and enzyme systems are reduced, the metabolism of most anesthetics such as acepromazine, propofol is also impaired. As well as anesthetics can directly block the hypothalamus, such as acepromazine and morphine. Inhalational anesthetics are affected by hypothermia by increasing their solubility but not slowing their potency. They also reduce the intensity of shivering, as a mechanism to conserve heat. It has not been proven, whether that hypothermic patients may take longer to recover from anesthesia because of larger amounts of anesthetic that need to be exhaled. But it’s for sure known that propofol, as one of the most commonly used anesthetics, is also affected by body temperature, as for hypothermia with 3° C down, its plasma concentration increases by 30%. The only drug tested so far, which does not effect thermoregulatory responses, is midazolam. The vasodilator effect of most of the anesthetics surpasses physiological vasoconstriction, which supports thermoregulation. As with vasodilation, there is a large loss of heat that comes from the center of the body and is lost to the periphery.

The negative effect of hypothermia on coagulation and blood has three main factors. It affects – platelet function, coagulation enzyme function and fibrinolytic function. As a rule, hypothermia increases blood viscosity, which leads to deterioration of perfusion. For every 1° C decrease, the hematocrit rises by 2%. This accordingly leads to false results that can be interpreted as blood loss. Since the function of the enzyme systems is disturbed, this also affects blood clotting. PTT, PT increase significantly, there is temporary thrombocytopenia and reduced platelet function occur due to impaired synthesis of thromboxane B2. The morphology of the platelets  also changes. There is a hypothesis according to which hypothermia results in coagulopathy by reducing the availability of platelet activators. This hypothesis is supported by the following observations: (a) The generation of thrombin, a potent platelet agonist, decreases under hypothermic conditions, and (b) hypothermia results in the release of a circulating anticoagulant with heparin-like effects. (1)

Due to the vasoconstriction that occurs, the oxygenation of the tissues is reduced and hence their slower healing. Direct suppression of neutrophil function is also a factor influencing healing in addition to the immunosuppressive effect, reducing leukocyte migration, neutrophil phagocytosis and production of ILF 1, 2, 6 and TNF.

In order to avoid all complications of hypothermia, different methods are used for pre-during and post-operative warming of patients. Typically, in the preparation of the animal for surgery, towels are used to cover the table or the animal is wrapped. A heating pad is often placed on the surgical table. The use of fluid-warming devices, which largely support normothermia, is also appropriate. Various methods can be used such as putting socks on the paws, wrapping in bubble rap, placing hot water bottles, red infrared lamps. After surgery, the animal can be wrapped with a blanket and any of the methods of warming can be used. But some of the most effective methods of maintaining a normal body temperature are warm air devices and warm water beds. According to a study comparing several methods of warming and prevention of heat loss, warm air is the most effective. (2) In addition to all the listed methods, it is important to reduce the time of the operation, especially in longer abdominal operations. Avoiding placing animals on cold metal tables, warm operating room.

It is advisable to warm up by 1-2° C per hour and under constant monitoring, because complications can occur from trivial burns to more serious systemic complications. Some of the underestimated ones are the so-called “afterdrop”, in which, despite the warming, the temperature of the animal continues to fall. This is caused by the return of cold blood from the peripheral limbs to the body, which makes it difficult to reach a normal temperature. It is important in such moments to warm up the body (chest, abdomen), and not the extremities. Afterdrop can cause deterioration of physiological parameters, cardiac arrhythmias and arrest.

Rewarming shock is very unknown and underestimated complicaton, which manifests itself in a sudden vasodilation with following drop in blood pressure and cardiac output. This results in increased metabolic demands and increased perfusion requirements. In this regard, there may also be areas of impaired perfusion that are hypoxic and lactate begins to form. During rewarming, these areas are reperfused and lactate re-enters normal oxidative pathways, consuming oxygen in the process. Because of the rewarming acidosis that has occurred, appropriate fluid therapy may be considered. Shivering is a normal response of the body, with which it tries to normalize its temperature, but on the other hand, it can also lead to additional complications, because additional oxygen consumption is needed and this can cause additional hemodynamic instability. The suppression of shivering by neuromuscular blockade is an effective method for decreasing O2 consumption. This method has been described in some human studies. (3) Monitoring during the warm-up should include as many indicators as possible, such as saturation, blood pressure, ECG, lactate, glucose.

OSTEOMIELITIS OF THE MANDIBLE IN A 7-YEAR-OLD CAT -case report

 

 

 

 

 

 

 

 

 

 

Elena Carmen NENCIULESCU, DVM, MRCVS, PET STUFF Small Animal Hospital, Bucharest, Romania

Address correspondence to Dr Guzu: guzu@advetia.fr

 

History and Clinical Examination Findings

A 7-year-old 5.350 kg neutered male Domestic Shorthair cat was referred for loss of appetite and generalized weakness lasting for 10 days. The owners reported a short episode of hemorrhagic ptyalism (for 24 hours), accompanied by moans and chewing efforts. Previous injection 0.1 mg/kg and prescription 0.05 mg/kg of meloxicam PO, q 24 h, for 2 days only permitted minor transitory food intake improvement. On physical examination, the patient appeared mildly dehydrated (5%) and hyperthermic (39.4°C ). Halitosis with concurrent rostral mandibular swelling were noticed. The swelling was fluctuating, with pain elicited by palpation. A seeping sore spot was observed on the ventral aspect of the mandible (Figure 1).

 

Moderate bilateral mandibular lymph node enlargement was noted on palpation. Examination on the awake patient was very uncomfortable and the cat only allowed a brief evaluation of the oral cavity. An inflammation of the gingiva surrounding the right mandibular second incisor and the right mandibular canine teeth (402 and 404) was otherwise reported. The remaining physical examination was within normal limits. Biochemistry profile and ionogram results were unremarkable and the FIV/FeLV SNAP test was negative. Complete blood count and serum biochemistry were within normal limits.

A 22G intravenous catheter was placed on the right cephalic vein. The patient was premedicated with methadone hydrochloride 0.2 mg/kg IV and dexmedetomidine 5 µg/kg IV. The patient was induced with propofol 2 mg/kg IV, a 4.5 oral endotracheal tube was placed and then isoflurane 1.5% at a 2L/min rate of oxygen was used for maintenance. Intraoral examination under general anaesthesia and dental charting revealed severe focal periodontitis involving the right mandibular second incisor and the right mandibular canine teeth, with concurrent absence of several incisor teeth. Lateral and occlusal intraoral radiographs were obtained. Selected radiographic views are provided (Figure 2).

 

 

 

 

 

 

 

 

 

 

 

 

Diagnostic Imaging Findings

 

Radiographic study of the mandible highlighted stage 4c dental resorptive lesions of 402 and 404 (Figure 3). Three root fragments of incisor teeth were noticed (301, 302, 401). An ill-defined bone proliferation with osteolysis involving the surrounding bone was associated with extrusion of the right mandibular canine tooth (404) and concurrent enlarged periodontal space. Cytological examination under light microscope of a transcutaneous fine needle aspirate of the lesion showed degenerated neutrophils, bacteria and some phagocytic activity.

 

Treatment and Outcome

 

Within the same general anesthesia, bilateral inferior alveolar nerve blocks (intraoral approach) were performed using a mixture of 0.2 ml lidocaine 2% and 0.8 ml bupivacaine 0.5%. The surgical procedure had 2 parts – an intraoral procedure (dental extractions and biopsy of the diseased mandibular bone) and an extraoral procedure (debridement and reconstruction of the skin). For the first part, with the patient in lateral recumbency 10 mm mucosal incision was performed over the alveolar ridge on the distal aspect of the mandibular canine teeth and was prolonged mesially within the sulcus of the mandibular incisor teeth with a #15c scalpel blade. A mucogingival envelope flap was lifted using a Chompret stripper and a Molt periosteal elevator. Simple extraction of the incisor teeth was performed with a 1.5 mm dental luxator used in a circumferential motion. An external alveolar ostectomy was then performed mesially to the mandibular canine teeth (304 and 404) with a round tungsten carbide burr under irrigation over 50% of the height of the roots. 304 and 404 were extracted using a 3 mm luxator. Curettage of the alveolar sockets and of the remodeled bone was performed using a 3 mm Volkman curette for specimen submission to histology. A minimal alveolar osteoplasty (alveoloplasty) using a round diamond burr under irrigation was eventually performed before closure of the defect with a simple interrupted pattern suture with 5/0 polyglecaprone 25, by moving the flap in translation. For the second part of the procedure, the patient was placed in dorsal recumbency. Clipping and antisepsis (with iodine soap and iodine) of the mandibular and cervical cranial area were carried out before surgical draping. The cutaneous and subcutaneous tissues were debrided over a 3 x 3 cm area, then the site was thoroughly rinsed with a 0.9% NaCl solution (Figure 2). Reconstruction of the defect was undertaken using a submandibular skin flap advanced rostrally. A multi-fenestrated drain was inserted and secured ventrally. A first intent closure of the wound was considered using a simple interrupted pattern suture nylon (Figure 3). Perioperative amoxicillin-clavulanic acid 20 mg/kg was administered by slow IV injection, as well as a postoperative injection of buprenorphine 20 μg/kg IV and meloxicam 0,1 mg/kg SC. Amoxicillin-clavulanic acid 12,5 mg/kg BID for oral relay over a 10 days course and oral meloxicam SID for 5 days were prescribed postoperatively. Placement of a buster collar was recommended during the entire convalescence period.

The patient recovered uneventfully after surgery.

Discussion

Mandibular swellings may be associated with a fluid collection, such as a cyst, inflammatory seroma, hematoma or, in some cases, a subcutaneous abscess. Development of subcutaneous abscesses may be related with penetrating or migrating foreign bodies, bites or scratches incidents, especially from other cats. A dental etiology (endodontic and/or periodontal disease) must be considered whenever the location involves the oromaxillofacial area. Some local or systemic conditions (neoplastic, inflammatory, infectious, metabolic or endocrine) may trigger the condition. The differential diagnosis summarizing the main causes responsible for mandibular swellings is shown in Table 1.Main DDx of orofacial swellings in cats

The radiographic findings in this case mainly support the hypothesis of a secondary osteomyelitis with regional subcutaneous abscess due to periodontal-endodontic complications of resorptive lesions. The prevalence of dental resorptive lesions varies between 25 and 40% in the general feline population. This rate is as high as 60 to 70% in purebred cats and/or presented within a dentistry department (Girard, 2008 et 2010; Van Wessum et al, 1992). The condition combines heterogeneous, destructive and progressive lesions of the tooth, resulting in ankylosis and replacement of dentoalveolar structures by bony tissue (ghost tooth). The resorption mostly initiates at the level of the radicular cementum and progresses towards the root and/or the dental crown. Involvement of the dental crown is usually associated by a characteristic crenate-looking patching gingiva filling the enamel-dentinal defect corresponding to the progression of a granulation tissue. Many local conditions (e.g. lack of oral hygiene and development of periodontitis, tooth fracture with pulpitis, chronic gingivostomatitis, occlusal trauma) have been documented in the literature, and some systemic causes (e.g. genetic, nutritional) have been suggested as possible triggering factors in the development of the disease in the feline patient. The resulting pulpal exposure (pulpitis) and/or progression towards periodontitis may then be associated with an endodontic-periodontal lesion, significantly decreasing the oral health status. In those cases, an acute pain may sometimes be elicited by finger percussion of the jaw. A characteristic, but not specific jaw trembling reflex may then be observed. The earliest affected teeth statistically reported in the literature are the mandibular third premolars (307 and 407). (Ingham, 2001) However, all teeth may be involved, with progression towards a generalized disease possible in some individuals. Typical but non-pathognomonic presentation is possible in canine teeth (dental extrusion or occult root destruction). Several clinical and radiological classifications have been proposed by the American Veterinary Dental College (AVDC) in regard to the location and severity of the lesions. (DuPont, 2002) A similar condition has also been described in humans and dogs, but is slightly different from the feline presentation. (Heithersay, 2007; Kim, 2013; Nemec, 2012; Peralta, 2010) Despite many evoked tracks (traumatic, metabolic, infectious, nutritional or genetic), the etiology of the feline tooth resorption remains rather vague and no prophylactic approach is available to date. (Okuda & Harvey, 1992; Reiter, 2005; Girard, 2008) It seems that metabolism of vitamin D may play a key role in the odontoclastic activation process. (Booij-Vrieling, 2009)

 

When facing an oromaxillofacial swelling, it is important to consider the specificity of the area, in particular the proximity of oral, nasal, orbital, nodal, vasculo-nervous or salivary structures. Reclining the lips and tongue, allowing a more detailed inspection of the gingiva, vestibule, floor of the mouth, as well as the ventral and lateral aspects of tongue is therefore essential. Fine needle aspiration should be performed whenever possible as cytological examination could bring additional information that could further guide diagnostic and therapeutic approach. Evidence shows a favorable predictive value of about 69% even in case of neoplastic conditions. (Ghisleni, 2006) The histopathological examination remains cornerstone, in order to confirm the diagnosis given the high rate of secondary infection in or near the oral cavity. According to the information gathered during the clinical examination and the localization of the lesion, different diagnostic imaging tools could be considered. The conventional extraoral radiography has two major disadvantages compared to the dental radiography: superimposed images and lack of sensitivity in the exploration of dental conditions (Chapnik, 1989). The CT scan provides good information in regard to the extension of any swelling condition. However, only 42 to 57% of the dental resorptive lesions are diagnosed on the CT scan when compared to the intraoral radiography (Lang et al, 2016) Therefore, dental radiographs still constitute the gold standard imaging method to diagnose tooth resorption. New diagnostic imaging devices such as the cone-beam computed tomography scan (CBCT) might be an interesting alternative in the exploration of these dento-alveolar conditions in the future. (Naitoh et al, 2010 ; Soukup, 2015 ; Creanga, 2015)

 

Extraction of the affected tooth by resorptive lesions remains the treatment of choice. (DuPont, 2005) According to the topography of the lesions, conservative techniques (glass ionomer restoration) have historically been described in early forms, localized to the collar and dental crown. However, the outcome for those teeth remained poor, with inevitable progression of the disease in the majority of the cases. In advanced forms, with associated root ankylosis, and for which tooth extraction would be an additional trauma for healthy tissue (e.g. high risk of mandibular fracture), crown-root amputation may constitute an acceptable alternative. The use of dental rotary instruments is mandatory. However, this option remains controversial for FIV or FeLV positive patients, as potentially at high risk of osteomyelitis, and systemic infectious spread. Specific cases affected by internal or localized forms to the root apex may be eligible to standard root canal treatment +/- apicoectomy as in other species, but fast progression of the disease known in the feline patient is a negative prognostic factor and therefore extraction is the only therapeutic option.

When treating perioral wounds, choosing between first, second or even third intention healing strategies, the following must be taken into consideration: the size of the defect, the possible infection associated, the risk of tissue contraction, fibrosis and dehiscence, as well as more specific patient or systemic considerations. When infected, a surgical wound debridement with abundant sterile rinsing of the area should be considered first. It is generally accepted that leaving a wound heal by second intention is not recommended near a sphincter, or any orbicular muscle such as those constituting the lips due to the wound contraction associated, and possible restricted mobility. (Ishii & Byrne, 2009) Excessive tension should be avoided by proper use of reconstructive techniques and more specifically locoregional flaps described in the oromaxillofacial area. (Guzu et al, 2021) A random flap advanced rostrally using lateral releasing incisions and incremental subcutaneous dissection allows for simple reconstruction of the cutaneous defect in the intermandibular area. (Swaim in: Verstrate, 2012) Placement of walking sutures reduces the dead space between the flap and the underlying tissue while decreasing the tension on the wound. Depending on the different size and location of the defect, axial flaps (labial, angular oris), free cutaneous flaps, or even free vascularized flaps using microvascular anastomosis techniques are also appropriate surgical treatment options. (Tong & Simpson, 2012; Smith, 1991; Smeak, 1992; Bradford, 2011, Walsh & Gregory in: Verstraete, 2012) The survival of all those flaps does not rest on the presence of an underlying granulation tissue, but simply on the absence of major contamination. Drainage is generally recommended, in order to reduce the risk of fluid collection formation (hematoma, seroma, infection) which may compromise the vitality of the flap. (Wardlow & Lanz in: Tobias, 2012)

Conclusion:

Dental resorptive lesions constitute a potential source of discomfort, affecting approximately 30% of the cats in the general population. Early diagnosis and treatment remain particularly challenging for any practitioner. Despite many hypotheses regarding the initiating factors leading to its development, no preventive or conservative strategies are available to provide long-term control of the disease. Extraction of the affected teeth is the gold standard treatment, capable of slowing down the extension of the lesions to the adjacent teeth and preventing possible infectious complications. A better understanding of the mechanisms associated with the formation of dental resorptive lesions may improve its medical and surgical management in the future.

 

 

References

1. Verhaert L, Van Wetter C. Survey of oral diseases in cats in Flanders. Vlaams Diergeneeskd Tijdschr (2004) 73:331–40

2. Girard N, Servet E, Biourge V, Hennet P. Periodontal health status in a colony of 109 cats. J Vet Dent (2009) 26:147–55. doi:10.1177/089875640902600301

3. Girard N, Servet E, Biourge V, Hennet P. Feline tooth resorption in a colony of 109 cats. J Vet Dent. 2008 Sep;25(3):166-74.

4. Bilgic O, Duda L, Sánchez MD, Lewis JR.Feline Oral Squamous Cell Carcinoma: Clinical Manifestations and Literature Review. J Vet Dent. 2015 Spring;32(1):30-40.

5. Gracis M, Molinari E, Ferro S. Caudal mucogingival lesions secondary to traumatic dental occlusion in 27 cats: macroscopic and microscopic description, treatment and follow-up.J Feline Med Surg. 2015 Apr;17(4):318-28. doi: 10.1177/1098612X14541264. Epub 2014 Jul 7

 

Congenital pathology of duplicated ureter from left kidney with CKD in geriatric dog Chao – Chao

Dr. Mila Kisyova

veterinary clinics “Dobro hrumvane!”- Sofia, Bulgaria

• Introducion

Normal anatomy of the kidneys:

The kidneys are paired, bean-shaped structures located in the retroperitoneal space directly beneath the sublumbar muscles. The cranial pole of the right kidney lies in the renal fossa of the caudate liver lobe and is located more cranially than the left kidney. The cranial pole of the left kidney lies lateral to the ipsilateral adrenal gland, which is closely associated with the cranial aspect of the left renal vessels. The left kidney is generally more mobile than the right kidney. Each kidney has a cranial and caudal pole and a ventral and dorsal aspect .

The concave surface of the kidney is located along the medial aspect and is called the hilus. The hilus is the location where the renal artery enters the kidney and the renal vein and ureter exit. Nerves and lymphatic vessels enter at the hilus as well. Anatomically, the renal vein is located more ventrally, and the renal artery is more dorsally. In an animal of normal body condition, the kidney is typically surrounded by a substantial amount of fat; this fat is maintained even in lean animals. In obese animals, the surrounding adipose tissue can virtually hide the kidney from view, making gross evaluation difficult.

Patophysiology of duplicated ureters:

Duplicated Ureter or Duplex Collecting System is a congenital condition in which the ureteric bud, the embryological origin of the ureter, splits (or arises twice), resulting in two ureters draining a single kidney. In the case of a duplicated ureter, the ureteric bud either splits or arises twice. In most cases, the kidney is divided into two parts, an upper and lower lobe, with some overlap due to intermingling of collecting tubules. However, in some cases the division is so complete as to give rise to two separate parts, each with its own renal pelvis and ureter. Double ureters from each kidney are very rare condition in dogs. They are drain separate renal collection systems from the same kidney and open separately into the urinary or genital tract. Given the embryological migration pattern of ureters, their termination sites are often ectopic.

 

 

 

 

 

 

 

 

 

 

*) https://www.researchgate.net/figure/Classification-of-urethral-duplication-in-dogs-based-on-the-classification-in-human_fig3_250044546

 

 

 

Duplex systems can have a variety of phenotypes, and multiple classification systems have been proposed to categorise this pathology. In incomplete duplication, the two poles of a duplex kidney share the same ureteral orifice of the bladder. Such duplex kidneys with a bifid pelvis or ureter arise when an initially single UB bifurcates before it reaches the ampulla. This is likely caused by a premature first branching event that occurred before the ureter has reached the metanephric mesenchyme (MM). Much more frequent are complete duplications, which occur when two UBs emerge from the nephric duct (ND). In most cases, the lower pole of the kidney is normal and the upper pole is abnormal an observation explained by the fact that the ectopic ureteric bud (UB)  frequently emerges anteriorly to the position of the normal UB and drives the formation of the upper pole of a duplex kidney. Inverted Y-ureteral duplication is a rare condition in which two ureteral orifices drain from a single normal kidney. Inverted Y-ureteral duplication is believed to be caused by the merging of two independent UBs just before or as they reach the kidney anlagen.  A very rare H-shaped ureter has also been reported.  Although the vast majority of cases involve a simple duplication, multiplex ureters with up to six independent buds have also been described.  In some cases, the additional ureter or ureters are ectopic and fail to connect to the bladder or the kidney (blind ending ureter).

 

Report and history of the patient

We saw Jonh (11 years old, non-castrated, cryptorchid, chao- chao) for first time in our clinic for second opinion related to chronic kidney disease (CKD).  He was diagnosed with chronic renal failure by colleagues about 2 years ago. Prior to our examination, he had been taking only food supplements (Irc Vet) and Renal Food. He had polyuria and polydipsia (PU/PD). The owners said that the urine was very light in colour. Sometimes Jonny had episodes with vomiting and lose of appetite. There was data for periodic blood tests with a tendency to increase the basic renal parameters (urea and creatinine). There was no ultrasound or other type of imaging examination.

When we took Johnny’s case, we initially did a complete abdominal ultrasound and new blood tests:

1. Creatinine	456.20 mmol/L	44.30-138.40 mmol/L
2. Urea	26.32 mmol/L	3.00-8.00 mmol/L
3. ALP	272.59 U/L	10.60-109.00 U/L
4. Na	141.60 mmol/L	140.30-153.90 mmol/L
5. K	6.26 mmol/L	3.50-5.10 mmol/L
6. P	2.10 mmol/L	1.00-2.00 mmol/L
7. Albumin	31.37 g/L	25.80-39.70 g/L
8. Glucose	3.95 mmol/L	3.40-6.00 mmol/L
9. Bilirubin Total	5.07 mmol/L	0.00-5.10 mmol/L
10. Bilirubin Direct	3.05 mmol/L	0.00-3.60 mmol/L
11. ALT	31.33 U/L	8.50-109.00 U/L
12. AST	29.30 U/L	8.90-48.50 U/L

 

• Abdominal Ultrasound:

We started a standard echo-screening and the prostatic gland was normal, the bladder too. And after that on the left abdomen near the left kidney we saw a big, elongated, strange formation with anechoic  fluid with a diameter of about 3 cm.  The left and right kidneys had a good ultrasound density. Three small cysts were found in the cortex of the left kidney. There was no evidence of pyeloectasis or hydronephrosis. The corticomedullary border was good. This finding may be a pathologically altered testis, cystic formation, or pathological /duplicate/ ureter. During the first ultrasound examination, the dog was fed, so we decided to repeat the examination on an empty stomach.  For the next echo screening Jonny was on a 12- hour fasting diet but the ultrasound finding is the same as the previous examination –  the strange formation after the left kidney was there with the same size and shape. After performing the second ultrasound examination, we had suspicion for duplicate ureter.  In order to be definite in the diagnosis, it necessary to perform computed tomography (CT).

 

 

 

 

 

After the new blood tests we started a new supplements – Ipakitine/Rubenal 300/Renassense/IrcVet. But Jonny didn’t feel very well. After some days we made a new blood tests. Before that we had spoken with the owners about the ultrasound finding and we decided to do a CT and see what the exact cause of this strange ultrasound finding.

• Rusults of the CT:

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Images:

1-A – little arrows are the bought normal ureters (left and right), big arrow „А“ – duplicate/ectopic left ureter

2-B –  big arrow „А“ – duplicate left ureter

3-C – little arrows are cranial and caudal renal medula, big arrow „А“ – duplicate/ectopic left ureter draining the cranial pole of the kidney

4-D – А“ – duplicate/ectopic left ureter, about 3 cm wide along entire length

5-Е –  normal right kidney

6-F – Left kidney, big arrow „А“ – duplicate/ectopic left ureter

*) the photos are provided by colleagues from the CVK (Central Vet Clinic, Sofia)

 

Тhe conclusion of the computed tomography is the left kidney has a slightly enlarged pelvis. Two ureters originating from the left kidney are found. The ureter, originating from the left kidney, has greatly increased dimensions – a width of about 3 cm along its entire length. Before entering the bladder, it turns ventrally and then dorsally. The other ureter of the left kidney begins in the normal anatomical position and drains into the bladder in the area of the trigone. Both kidneys have no tomographic evidence of hydro/pyelonephrosis.

 

This kind of pathology of the urogenital system in dogs is very rare. In this case it was an incidental finding because for 11 years the patient had never previously undergone additional ultrasound examinations.  Certainly, this rare pathology is directly related to the rapidly progressing renal failure.

Due to the rapidly progressing renal failure, deteriorated general condition and the age of the patient, surgical intervention could not be performed.  Jonny’s prognosis is very poor.

Sourses:

• „Urethral duplication in a dog: case report [Duplicação uretral em cão: relato de caso] R. Stedile, E.A. Contesini, S.T. Oliveira, C.A.C. Beck, E.C. Oliveira, M.M. Alievi, D. Driemeie, M.S. Muccillo Faculdade de Veterinária – UFRGS Av. Bento Gonçalves, 9090 91540-000 – Porto Alegre, RS „
• „Duplex_kidney_formation_Developmental_mechanisms_a.pdf– in humans“
• Atlas of Small Animal CT and MRI by Erik Wisner, Allison Zwingenberger ,

March 2015

• Four-dimensional CT excretory urography is an accurate technique for diagnosis of canine ureteral ectopia (Tobias Schwarz, Nick Bommer, Maciej Parys, Florence Thierry, Jonathan Bouvard, Jorge Pérez-Accino, Jimmy Saunders, Maurizio Longo – onlinelibraly.wiley.com)

 

 

West Nile Virus detection in Ural owl

(case report)

Dr. Plamen M. Kirov, DVM,

Anamaria Manolea, A.S.P.A.D.A. Timisoara – Romania

 

Introduction

West Nile Virus (WNV) is a single strained RNA virus from the genus Flavivirus. It was discovered for the first time in 1937 in Uganda, causing zoonotic West Nile fever in affected animals and humans. The natural host for the virus are birds, mostly corvids(crows, ravens, and blue jays) and raptors. The disease is vector-borne and distributed by mosquitoes. It is discovered that 80% of the cases are asymptomatic, 20% become symptomatic, and mortality in birds could reach between 20 and 60%. It is agreed that the disease is a considerable factor in corvids population reduction. The mosquitoes transmit the virus by feeding infected blood and then transiting it to uninfected ones. Raptors can get infected by consuming infected chicks or birds. Between humans, the virus can be transmitted by blood or organ transfer, vertically, but not via direct contact.

Clinical signs can vary widely from non to death, with a high dependency on the species affected. Of the mammals only humans and horses show clinical signs – WNV was detected in many domestic and wild mammals, but no cases of the disease were registered. Birds with WNV demonstrate neurological signs – tremors, weakness, loss of coordination, head tilt, lethargy, blindness, and characteristic position of the legs at death.

Balkan countries by having long periods of hot weather and the presence of a lot of water sources (rivers, lakes, marshes, etc.) are the perfect environments for mosquitoes from Aedes(incl. Tiger mosquito) and Calex spp.

Clinical case

An adult Ural owl (Strix uralensis) was found by people in a passing car on rural road in Lugoj area (Timis county). The bird was in lethargic state, with difficult breathing and incoordination of movements of legs and wings.

Physical examination

During the physical examination no feather or tegument abnormalities or signs of trauma were found. Body temperature was elevated to +42oC. The bird was lethargic with difficulties to walk. The appetite appeared to be normal. Clinical diagnostic tests From the bird were taken a venous blood sample from the brachial vein, fecal, and nasopharyngeal probes. Using a panel of tests, bacterial and parasitic diseases were excluded. Since cases of WNV are detected annually in Romania and neighboring countries (Serbia and Hungary), the virological panel included West Nile Virus testing. The results obtained using epitome-binding ELISA, with a sensitivity rate of 98% for WNV antigen, are shown in Table 1.

From the obtained results we concluded that the bird is in acute state of West Nile fewer. After consulting with the local veterinary authority, the bird was kept in enclosed environment and treated with Meloxicam per os. We did a second test after a week and another one week later. The third test went negative by showing an absence of viral antigen in the three samples – nasopharyngeal, fecal, and blood. Besides the negative results and complete recovery of the bird, it was transferred to a sanctuary where will remain for a few months and eventually released back into nature in 2023

Basic anaesthesia of brachycefalic dog

Dr Denica Djodjeva

Blue Cross Veterinary Clinic

Sofia, Bulgaria

 

 

 

Quite often in our practice we have to sedate or keep under anaesthesia brachycephalic dogs and cats. This is associated with some stress for us, given the peculiarities of the breed. In this article I will try to briefly present the main key points in the anesthesia of brachycephalic breeds, which has gained great popularity in recent years. Will pay attention to their anatomical and physiological features, which are a prerequisite for complications during anesthesia, and how to avoid them and reduce the risk.

The main specificity of them is the so-called brachycephalic syndrome ( BOAS). It may include narrowed nostrils, a long soft palate, a hypoplastic trachea, or an inverted laryngeal sac. It can be re-applied and used for prolonged trauma to the pharyngeal soft tissues and trachea, which can cause soft tissue outflow or tracheal collapse. This trauma most often occurs when the animal is intubated. Gastroesophageal reflux should not be forgotten, also high vagal tone.

In severe cases of BOAS, airway obstruction may benefit from the development of pulmonary edema. The pathophysiology of post-obstructive pulmonary edema includes the effect of negative intrathoracic pressure on fluid distribution and subsequent hypoxia. High negative intrathoracic pressure causes an increase in venous return to the right atrium, which increases the pulmonary artery, while left ventricular function is reduced and afterload is increased. The end result is increased hydrostatic pressure, which aids in the movement of fluids from the capillaries in the interstitium and thus causes pulmonary outflow. Rapid recognition of this condition and taking temporary measures, such as maintaining airway patency, adequate oxygen supply and, if necessary, PPV administration. Diuretics may also be used, but it should be anticipated that hypovolaemia and hypoperfusion may occur during anesthesia and clinical delivery should be considered. And because of the risk of soft tisuue and pulmonary oedema, it’s beneficial to add an corticosteroid in low dose, as prevention. Unless there are a serious contraindications. There are different anaesthesia protocols with dexamethason or methylprednisolon, it’s a matter of personal choice.

Deep sedation in these patients is performed with excessive relaxation of the pectoral muscles and aggravation of airway obstruction. Even if the patient is aggressive, it is good to adhere to lower doses of premedication. The most commonly used combination is of a sedative component, for example an alpha-2-agonist and an opioid. A tranquilizer such as acepromazine and benzodiazepines such as diazepam or midazolam may also be used. Accordingly, the doses are at the discretion and according to the desired effect and treatment.  In the table below I quote some of the most commonly used pre- anaesthetic drugs with the value of the dose. There are no restrictions and contraindications to the use of narcotic drugs in this breed. For induction you can use a different combinations, as benzodiazepine+ propofol or benzodiazepine+ ketamine. Your choice mainly depends on what the end result you whant. In brachycefalic breeds it is recommended the induction to be smooth and fast, so the most suitable drug in this case is propofol.

Given the peculiarity of the birth, it is very important to monitor the brachycephalic patient during the pre-aesthetic period, as relaxation of the pectoral muscles further complicates breathing, reduces the number of respiratory movements and the appropriate patient does not fall into hypoxia. It is recommended that the patient be preoxygenated during the pre-anesthetic period. The administration of 100% oxygen before induction of anesthesia prolongs the time to the onset of arterial hypoxemia.

When intubating a brachycephalic patient, prepare several tube sizes, apparently up to two sizes smaller than you think would be appropriate. It will be useful if you use a laryngoscope, especially when your patient has a long soft palate, as it will help ensure good visibility to the airways.

It is common practice to maintain the patient under inhalation anesthesia during the operation. Isoflurane is most commonly used for this purpose. It should be borne in mind that, like other inhaled anesthetics, it produces a dose-dependent reduction in myocardial contractility, systemic vascular resistance and cardiac preload, followed by a reduction in mean arterial pressure (MAP) and cardiac output in a dose-dependent manner; therefore, the evaporator settings should be kept as low as possible while maintaining an adequate depth of anesthesia.

In brachycephalic breeds, there is a very strong vasovagal tone, which can cause bradycardia, which in turn can lead to AV block or even cardiac arrest. The most common reason for increased vagal tone is severe pain. Advice on this reason for good pain relief of this breed is extremely important. However, if the patient develops severe bradycardia, a use of anticholinergic in an appropriate emergency dose is indicated.

As mentioned earlier, another common complication is gastroesophageal reflux, which can occur at any stage of anesthesia. This can lead to airway obstruction and aspiration pneumonia. Advice for this reason is recommended in the anesthesia protocol to include antiemetics, unless there are serious contraindications. It is recomended to be applied proton pump inhibitors as omeprasole, 4 hours before the planed anaesthesia.

The recovery period is also not to be underestimated. Here it is important to constantly monitor the patient and be extubated, when we are sure that all reflexes have returned. Especially the swallowing one. The best time to extubate is when our patient has muscle tone in the lower jaw and tries to cough up the endotracheal tubus itself or even better if the patient is tring to chews it. It is important to be positioned in a sternal position with appropriate continuous monitoring.

The anaesthesia of these specific breeds is not so complicated, if know their features and for what to watch out for. With more carefulness and knowinge there is nothing to be afraid of.

Tabl. Most commonly used pre- anaesthetic drugs

Drug	Benefit	Side effects	Peak onset/duration of action	IM dose
Dexmedetomidine, Medetomidine	Profound sedation, reversible, some analgesic properties, drug sparing (reduction in induction drugs needed)	Dose dependent bradycardia	5-15 min IM 2- 3 min IV	Dexmedetomidine 5-15 µg/  kg   Medetomidine 3- 10 µg/ kg
Butorphanol	Mild analgesia, good sedation	Poor analgesia and should not be used for surgical patients	10–15min/lasts for 60–90min	0.1–0.4mg/kg
Buprenorphine	Moderate analgesia, mild sedation	Moderate analgesia	10- 15 min IV 15-30min IM /can be given q 6–8 h	0.01–0.04mg/kg
Methadone	Good analgesia	If given too fast, IV can cause bradycardia and respiratory depression	30min/can be given q 4 – 6 h	0.1–0.4mg/kg
Acepromazine	Good anxiolytic, sedation improved when administered with an opioid	Hypotension, unreliable sedation when used alone, not reversible	35–40min IM 10- 15 IV /can be given q 4–6h	0.01–0.05mg/kg

 

 

 

 

Diagnosis of multiple myeloma in a Labrador Retriever

Florin Cristian Delureanu

MRCVS, DVM

November 2021

 

History

A 12 years old intact male labrador retriever was presented to the practice in 05.03.2021 with a history of diarrhea and hyporexia. The diarrhea was present for few days and the appetite was decreased for about 2 weeks but there were moments when the patient was eating normally. The patient was up to date with the booster vaccination and was regulary using antyparasitic treatment.

 

Physical examination

At the moment of examination the patient was bright, alert, with normal temperature (38.7 °C), the palpable lymphnodes were normal in size, nothing abnormal detected in the oral cavity and thoracic ascultation unremarkable. A mass of approximate 5cm diameter with soft consistency, mobile, and without local reaction on the surrounding soft tissue was identified in the xiphoid area.

 

Investigations

Initially general blood tests including complete blood count, biochemistry, electrolytes and total T4 were performed as a routine screening in order to identify any abnormalities. The results from the haemoleucogram demonstrate mild microcytic hypochromic non-regenerative/ pre-regenrative anemia, neutropenia, monocytopenia and eosinopenia. On the biochemistry just hyperproteinaemia due to increased globulins was the single abnormality. Also the thyroid hormone was under the normal reference range (picture 1).

Coroborating the blood results with the history and the clinical examination the following differential diagnostic list was discussed with the owner: occult chronic blood loss, iron deficiency, inflammatory/infectiouse cause, neoplastic, immune mediated disease, endocrine (anemia secondary to hypothyroidism), gammopathies.

Aditional history: the last time when the patient went to a veterinary practice was 5 months prior for the regular booster vaccination.

Because of no evident clinical symptoms the presumption of chronic blood loss due to diarrhoea or anemia secondary to hypothyroidism was suspected. After discussion with the owner the decision of repeating blood tests in 4 days was taken. The patient was discharged with oral probiotics and was put on gastro intestinal veterinary diet to treat the diarrhoea. At reevaluation blood was collected and was send to the reference laboratory for complete blood count and blood smear interpretation, SDMA, Coomb’s test and C-reactive protein and complete thyroid panel including total T4, freeT4, cTSH, thyroglobulin autoandibody

The SDMA was normal also the thyroid panel was normal and negative on thyroglobulin autoandibody. The C-reactive protein was mildly elevated and the Coomb’s test was negative. On haematology the anemia had the same characteristics but was normocytic the reticulocytes and platelets under the normal limit. There were no modifications on the leucogram compared with the one performed at the first presentation (picture 2).

The blood film was evaluated and a mild microcytosis and no increased in polycromasia was noted. Marked rouleaux formation and occasional metarubricyte were present too and leucopenia was confirmed. Estimation of free platelets (3-8 platelets seen per HPF) suggested platelet numbers are mildly/moderately decreased with and very small platelet clumps seen was identified.

 

Based on the second blood tests (pancytopenia is observed but also marked rouleaux and occasional metarubricyte) and hyperglobulinaemia from the initial blood tests a suspicion of neoplastic disease like multiple myeloma or lymphoma less likely non-neoplastic disorders like monoclonal gammopatihes (Erlichiosis or Dirofilariasis) because the patient was regulary using antiparasitic medication and no history of travelling. In the same day results were reported to the owner and additional questions regarding the origin, travel status and lameness episodes were asked to the owner in order to find more informations. There was no history of travelling, the dog origin was United Kingdom and transitory episode of weakness were observed in the past months.

 

Further investigations

To investigate more the suspicion serum and urine protein electrophoresis, urinalysis including urine protein creatinine ratio, radiographs and bone marrow aspiration were recommended. Five days later the patient presented to the practice but the owner accepted initially just the non-invasive investigation and declined the x-rays and bone marrow aspiration. An additional in house haemoleucogram was performed at this stage to monitor the trend of the red and white blood cells (picture 3)

 

 

 

 

 

 

 

The urinalysis revealed proteinuria 3+ and a pH of 8 with active sediment and no crystals or casts, the urine beign collected via urethral catheterisation. The urine protein creatinine ratio was marked elevated (picture 4).

 

 

 

 

 

At serum protein electrophoresis hypoalbuminaemia was present with a mild increase in alpha 1 globulins and marked increase in gamma globulins migrating in a gamma region and a depletion of the globulins thereafter, consistent with a monoclonal band (picture 5)

 

 

 

 

 

 

 

 

 

The urine protein electrophoresis showed that majority of the protein was presented in the alpha-beta region and this was interpreted as overflow proteinuria secondary to the marked gammopaty present at the serum protein electrophoresis. No bands consisting with Bence Jones protein were noted but this would be masked by the overflow proteinuria (picture 6).

After these last results a highly suspicion of neoplastic disease was made. Radiography and bone marrow aspiration were recommended to confirm the disease. The owners were reluctant to put the dog under sedation because in the past he had general anesthesia and was not stable according to the previouse veterinarian. At this moment the patient was sent to a referral center to have the imagistic investigation.

 

In 09.04.2021 the patient arrived at the referral center for the last investigations. After clinical examination a firm mobile mass was noted in the caudal abdomen. Initially HLG, blood film evaluation, ionised calcium and 4Dx were performed followed by CT scan of the thorax and abdomen and fine needle aspiration of the liver, spleen and abdominal mass ultrasound guided. The ionised calcium was mild elevated (1.95 mmol/L), the 4Dx was negative. The haematology findings consist with normal white blood cell count with a slight improvement from the 5th March and a stable red blood cell count (HCT 31%) – with a mild non-regenerative anaemia. An initial review of the CT scan confirms the presence of a 4.5-5cm encapsulated mass in the caudal abdomen, with no obvious association with the intestinal wall. A small amount of free fluid is present between the liver lobes. After these investigations the patient was sent home with Fortekor as a treatment of proteinuria.

 

Seven days later the full CT report, aspirates results and blood smear interpretation were ready.

 

Cytology interpretation

 

A detailed haematology showed a mild, normocytic normochromic, poorly regenerative anaemia (HCT 36.9%, reticulocyte count 95.05×109/L). His white blood cell and platelet count were low-normal. There was no evidence to support haemolysis and leucocyte morphology was unremarkable.

Aspirates from the liver and spleen identify a population of extremely atypical plasma cells, supportive of multiple myeloma. Prominent extra medullary haematopoiesis is also noted within the spleen.

Aspirates from the caudal abdominal mass show adipocytes and a mixed inflammatory cell population, comprising of neutrophils ageing in situ and undergoing pyknosis. An atypical plasmacytoid population is identified but in low numbers, suggesting infiltration with myeloma.

 

CT findings from the report

 

Musculoskeletal:

There are multifocal osteolytic lesions throughout the entire included portion of the skeleton, including essentially all included vertebrae (thoracic, lumbar, sacral), multiple ribs, the sternebrae, the proximal humeri, the pelvis and the proximal femurs (picture 7).

 

Thorax:

No soft tissue attenuating pulmonary nodules are identified. There are multiple small (<5mm), mineral attenuating, geometrically shaped foci throughout the pulmonary parenchyma (predominately within the periphery), consistent with benign osteomata.

 

Abdomen:

An ovoid, well encapsulated mass is identified within the mesentery of the right caudal abdomen, which measures approximately 4.7cm x 4cm x 5.7cm (height x length x width) (picture 8). The mass is predominately fat attenuating, with a soft tissue attenuating rim and patchy regions of internal soft tissue attenuation (which ranges in appearance from ill-defined to linear).

 

A soft tissue attenuating (isoattenuating to the adjacent renal cortical tissue on pre-contrast), minimally contrast enhancing nodule, measuring approximately 1cm in largest diameter, is present in the right lateral renal cortex (picture 9).

 

The liver and spleen are diffusely mildly enlarged, with rounded margins, however they demonstrate normal attenuation and contrast enhancement. A mildly enlarged splenic lymph node is also present.

 

 

 

Diagnosis: Multiple myeloma – advanced stage

 

Discussion

 

Multiple myeloma is a lymphoproliferative cancer arising from plasma cells and their precursors, characterised by clonal proliferation of plasma cells infiltrating the bone marrow and then affecting other organs such as the spleen. Diagnosis of MM usually follows the demonstration of bone marrow or

visceral organ plasmacytosis, the presence of osteolytic bone lesions and the presence of urine myeloma proteins. Renal disease is present in approximately one-quarter to one half of dogs with MM, and azotemia is observed in 30% to 40% of cats.

Bence Jones proteinuria was not evident in the pacient urine protein electrophoresis due to overflow proteinuria secondary to the marked gammopaty. Bence Jones proteinuria occurs in approximately 25% to 40% and hypercalcemia is reported in 15% to 50% of dogs with multiple myeloma. The clinical signs can vary from lethargy and weakness to inappetence, weight loss, lameness, polyuria/polydipsia, bleeding diathesis and central nervouse system deficits. The patient presented with a history of mild inappetence and isolated episodes of lameness.

Chemotherapy is effective at reducing malignant cell burden and to improve the quality of life of the patient. Variouse alkylating agents such as melphalan, cyclophosphamide, chlorambucil, lomustine can be used together with steroid therapy. The most common protocol is a combination between melphalan and prednisolone. This protocol is usually well tolerated by the vast majority of the dogs, the most clinically significant toxic events beign represented by myelosuppression and delayed thrombocytopenia.

 

After the last investigations performed at the referral center the patient started to deteriorate significantly this manifested by presence of a severe swelling over the left side of the face associated with pain and ptyalis. Two days later, a chemotherapeutic protocol including melphalan, cyclophosphamide orally with intravenous dexamethasone was started. Despite this, the dog developed neutropenia and pyrexia, raising concern for sepsis. As a result, a decision was made to euthanase him one day later.

 

 

 

 

 

 

 

 

 

 

 

Idiopathic Renal Hematuria in a mongrel dog

(case report)

 

Dr. Plamen M. Kirov, DVM, MVSc, MSc

Timisoara -Romania, and Sofia-Bulgaria

 

Introduction

 

Hematuria describes a condition in which is observed presence of blood in the urine. It could be a result of diseases of the urinary tract – kidney, ureter, urinary bladder, urethra; or by diseases of the genital tract – prostate, penis, prepuce, uterus, vagina, vestibule. It can be classified as: macroscopic (visible to the naked eye), or microscopic (increased number of RBC in the urine, observed during microscopic examination). In general, hematuria can be a result of multiple reasons, as follows [1]:

 

• Urinary tract origin
  • Trauma
  • Urolithiasis
  • Neoplasia
  • Inflammations (UTI, etc.)
  • Parasites (Dioctophyma renale)
  • Coagulopathy (Warfarin intoxications, etc.)
  • Renal infarction
  • Renal pelvic hematoma
  • Vascular malformations
  • Kidney polycystic disease

 

• Genital tract origin
  • Trauma, Neoplastic or Inflammatory diseases of the genital tract
  • Estrus
  • Subinvolution of placental sites

 

 

For Idiopathic Renal Hematuria, we speak when the origin of RBC in the urine cannot be associated with any of the above-enumerated reasons and is of a renal origin. It is a very rare condition, which occurs in middle and big-sized young dogs (younger than 5 years of age), occasionally has been observed in older dogs and cats. Microscopic IRH is found by incidence during urine microscopic exams when macroscopic one is observed by the owners and described as unusual darker coloration of the urine. The condition is mostly unilateral and can be periodic – with a period of no bleeding. Since there is a release of RBC into the urine, anemia can be present in ranges from none to severe. Further, we will take a look and discuss the available treatment options.

 

 

Clinical case

 

The dog was brought to me by his owner, who observed “Cola-like” coloration of the urine in the last 2-3 days. According to the owner’s description, there are no changes of the dog’s behavior and, according to him, the micturition is normal and does not cause discomfort.

 

The patient:

• 3-year-old male mongrel dog
• 25 kg BW, normal body score
• Neutered when he was 8 months of age
• Vaccinations up to date and according to the protocol
• Living indoors
• No data for traumas
• No medications or treatments in the last 6 months

 

Physical examination

During the physical examination, no abnormalities were observed, body temperature, heart and respiratory rate, and blood pressure were in the normal ranges. No any tegument abnormalities or signs of traumas. Dog temperament was relaxed and friendly.

 

Clinical diagnostic tests

The CBC was normal, with an RBC count near the left border reference value. Tests for Babesiosis and Lyme disease were negative. A sterile probe of urine was collected by US-guided cystocentesis and examined. Urine-specific gravity was slightly elevated, presence of erythrocyte was confirmed by microscopic examination, microbiological culture was negative. Pigmenturia was excluded after centrifugation of the urine sample, which resulted in a clear separation between RBC (collected at the bottom of the test tube) and urine (supernatant).

The performed x-ray did not reveal any abnormalities (uroliths, tumors). The ultrasound examination did not result in any abnormalities in the urogenital tract – renal parenchyma was with normal structure.

Idiopathic Renal Hematuria was diagnosed by exclusion as a result of performed test procedures and obtained results.

Additional information about the diagnostic approaches for hematuria in dogs and cats can be found in [2]

 

 

 

 

 

 

Treatment options

For treating Idiopathic Renal Hematuria we have few options available, we could differentiate as:

 

• Invasive. Surgical cauterization of both ureters before the urinary bladder, and observing which kidney is the bleeding one, sclerotization of the kidney with povidone-iodine and silver nitrate [3][4] [5]. This method can be used and for bilateral hematuria. For cases with unilateral bleeding leading to severe anemia, ureteronephrectomy is recommended [1]

 

Since the dog doesn’t present anemia and invasive methods are more complex for performance and maintenance, I have directed my decision towards a non-invasive treatment option.

 

• Non-invasive. It was described that IRH results from elevated blood pressure inside the glomerular arterioles leading to their higher permeability for RBC. This was observed by multiple studies and reports and the effect of ACE2 inhibitors, especially Benazepril, over the arterioles in the renal glomerulus was demonstrated [6] [7] [8]. In addition, during my studies in FMV-Timisoara, I had the opportunity to observe the treatment of a hunting dog with IRH, using Benazepril with good results (Dr. Doru Morar, FMV-Timisoara).

 

The dog was treated with Benazepril in dose 0.40mg/kg per os every 24h. In the following days was observed visible reduction of the hematuria – by the owner’s account, urine coloration became normal. Repeated urinalysis revealed the persistent microscopic presence of RBC with a tendency of reduction during the time. Blood pressure was normal and without indications for hypotension during treatment.

 

 

Conclusion

Dogs diagnosed with IRH with absent to mild anemia can profit from treatment plan with ACE2 inhibitors – surgical methods are not widely available, are expensive, require hospitalization of the animals, and nephrectomy deteriorates the quality of life for young animals (in cases the IRH becomes bilateral this can lead to a negative outcome for the patient).

Uterine prolapse in cats – tips & tricks

Yavor Stoyanov, DVM

Yordan Yordanov, DVM

Bomed Veterinary Clinic – Sofia

Uterine prolapse is a relatively uncommon complication of parturition, occurring infrequently in cats. Ekstrand and Linde-Forsberg reported it as accounting for 0.6% of the maternal causes of dystocia. The etiology of uterine prolapse is unknown in queens. The prolapse can be complete, with both horns protruding from the vulva, or limited to the uterine body and one horn. Uterine prolapse requires immediate attention. It is an obstetric emergency.

A 1-year-old female European Shorthair outdoor cat weighing 2.5 kg was presented to our clinic with 96h after parturition. Two days before presentation his caretaker saw “something like placenta to hanging behind the cat”.

On physical examination, the animal was alert, 38.3 °C and slightly dehydrated. The pulse and respiratory rate were both within normal ranges. The prolapse of the uterus was complete, with both horns protruding from the vulva. The exposed tissue was congested and slightly edematous with a few small areas of necrosis, and was covered with debris.

The exposed uterus was palpated to rule out the possible presence within it of any abdominal organs such as the urinary bladder.

Tips & Tricks. Ultrasound examination of the abdomen and the uterine prolapse can be performed to reveal the position of the urinary bladder and the intestine.

Tips & Tricks. Topical application of Manitol 10% can be performed to reduce the oedema in prolapsed tissue.

CBC and biochemical analysis were performed. CBC showed WBC 38.8 x109/l, HGB 89 g/l, HCT 0.265 l/l.  Other parameters of the biochemical analysis and packed cell volume were all normal in range.

After premedication with domitor/buprenorphine/ketamine, anesthesia was induced with propofol after preoxygenation. An endotracheal tube was inserted and anesthesia was maintained with isoflurane. Preoperative antibiotics: Cefazoline i.v. and enrofloxacine s.c.

The surgery was performed in two steps: first the replacement of the prolapsed horns and uterus and then ovariohysterectomy.

Tips & Tricks. If the prolapsed organ is in very good condition and the cat is a valuable breeding animal you can try conservative treatment. Replacement, following by medical treatment Oxitocin (0.5-1.0 UI) and antibiotics. Complications may develop from minor laceration of the uterus to septicemia or uterine rupture.

Tips & Tricks. Do OHE! It is the safest option in this situation.

Tips & Tricks. OHE can be performed before reduction if the uterus is too contaminated or necrotic or ruptured.

In this reported case the uterus looked in good condition.

Gross debris was removed gently from the prolapsed organ by irrigation with hypertonic solution.

Then the uterus was reponeted carefully, starting from tip of the horns, one by one.

Tips & Tricks. Use some type of lubricant, like Vaseline.

Tips & Tricks. Oxytocin 0.5 IU can be administered directly in prolapsed tissue to facilitate uterine involution prior to replacement. Attention! Oxitocin make uterine tissue fragile.

Tips & Tricks. An episiotomy may be performed to assist uterine replacement.

Tips & Tricks. Cystocentesis may be performed before attempting to reposition the uterus.

Tips & Tricks. Use monofilament suture material, like PDS 2-0 for cervix ligatures. Polyfilament suture can cut the weakened uterine tissues like saw.

Apposition of vulvar lips was performed with a horizontal mattress pattern without tightening to allow vulvar discharge and normal urination.

This suture was removed after 24 h.

 

The queen recovered well. Postoperative treatment included the use of an Elizabethan collar and intravenous fluid therapy.

The day after surgery, the cat was alert, urinated normally and there was mild discharge from the vulva.

Antibiotic treatment for 5d amoxicillin/clavulanic acid -Synulox and Enrofloxacin.

Tips & Tricks. Postoperatively, urination should be monitored as swelling and pain can lead to urethral obstruction.

Conclusions

Although rare, uterine prolapse should be managed as an emergency. The treatment for uterine prolapse depends upon the severity of damage to the uterus. The prognosis following treatment for a uterine prolapse is guarded to good, depending on the timing of veterinary intervention.