Small patients bring huge problems

 

470181959_122147916800359110_3066516722040764086_nDr 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.

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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%.

 

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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.

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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.

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This is Misha 10 days later for suture removal.20251018_162628

 

 

 

 

 

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.

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A week later Doty was fine almost no sign of illness at all.20251027_090746

Colchicine intoxication in a dog

293381704_5664537806890011_4414435878500424694_n    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.

Anaesthetic management of a dog with pericardial effusion for pericardial window surgery

293381704_5664537806890011_4414435878500424694_nDr Denica Djodjeva

Central Vet Clinic

Sofia, Bulgaria

 

 

ari-spada-Cn9XO8qeJpE-unsplashVigo, 9 years old, male, labrador, non castrаted, 39 kg at the last present in the clinic. After several pericardiocentesis was decided for subtotal pericardiectomy. On the clinical examination, the dog had rapid breathing, a fast heart rate, and a normal strong pulse. On the ultrasound examination, there are already ascites, not clinically significant pericardial effusion, and the pericardium is thickened.  There was no need for pericardiocentesis. After the intravenous catheter placement, the patient was premedicated with methadone 0,1mg/ kg, ketamine 1mg/kg, midazolam 0,2 mg/ kg, and propofol 3mg/ kg to effect, intubated and pre-oxygenated at all times of surgical preparation.  An arterial catheter was placed for invasive blood pressure monitoring and arterial blood sample collection.  At the time of surgery, there was a dopamine infusion of 7mcg/ kg/ min for maintaining the blood pressure and heart contractility in normal ranges. Pain management was performed with opioid administration and intercostal block from the 4th to 7th ribs with Ropivacaine 1mg/ kg. There was fluid infusion with RLS all the time from 2- 5ml/ kg/ h depending on the personal need of the patient due to surgery. A rescue analgesia plan with CRI Lidocaine 1mg/kg/h, Ketamine 1mg/kg/h was ready and used. IPPV was performed immediately before the thoracic opening. The hemodynamic support, fluid resuscitation, and vital parameters were closely monitored during the pre-, surgical, and post-operative periods. maintaining the blood pressure in normal ranges. For the pain, there was performed intercostal block from 4th to 7th ribs with Ropivacaine 1mg/ kg. There was fluid infusion with RLS all the time from 2- 5ml/ kg/ h depending on the personal need of the patient. Rescue analgesia plan with CRI Lidocaine 1mg/kg/h, Ketamine 1mg/kg/h, Methadone 0,1 mg/kg/h was ready and used. IPPV was performed immediately before the thoracic opening. The hemodynamyc support, fluid resuscitation and the vital parameters was closely monitored during the post operative period.

The main hemodynamic goals in the anesthetic management of this patient included preservation of preload due to increased intrapericardial pressure and compromised cardiac chamber filling, control of HR to maintain atrial contribution to ventricular filling and avoid decreased CO. Another important goal was to maintain and improve contractility, which is important in patients with decreased myocardial function.

Introduction

Pericardial effusions associated with malignancy usually develop slowly, and when the volume of fluid exceeds the limit of stretch of the pericardial membrane, it results in cardiac tamponade. However cardiac effusion or tamponade may be relieved by pericardiocentesis. Malignant pericardial effusions being chronic and recurrent are best managed by pericardial window or total pericardiectomy. In this procedure, a passage is created between the pericardial sac and adjacent space, usually the pleural cavity for long-term drainage of pericardial fluid. Standard approaches for pericardial windows include a subxiphoid approach and right or left thoracotomy. In this situation, we approached through the left anterior thorax.

Physiology and pathophysiology

 

The pericardium is the natural covering of the heart, which consists of two layers. Inner visceral, which is thin and connects the epicardium of the heart, and outer, which is thicker and fibrous. The thickness of the healthy pericardium is 1-2 mm, and between the two layers, there is pericardial serous fluid, which is produced by the mesothelial cells and is drained through the lymphatic system in the right part of the heart. Normally, there is a very small amount of pericardial fluid in the pericardial sac 0, 25ml/kg in a dog. Anatomically, the pericardium is held by ligaments to the diaphragm and sternum. The heart can function normally even without its pericardial sheath because its main function is to stabilize the heart in its natural position and to limit the excess movements of the heart when the position of the body changes.

The pericardial fluid minimizes friction exerted on the epicardium from normal heart movements during the cardiac cycle and serves to balance hydrostatic pressures over the surface of the heart. The pressure exerted on the cardiac chambers by the pressure within the intra-pericardial space prevents acute distention of the chambers and helps optimize atrial and ventricular coupling and filling. The pericardial sac serves as a physical barrier against the spread of infection or neoplastic disease within the mediastinum.

There are several reasons why the function of the pericardium can be disturbed: birth defects, acute or chronic pericarditis, pericardial effusion, and tamponade. In pericardial effusion, as a consequence of an increase in the amount of fluid, the pericardial pressure also increases, which can lead to cardiac tamponade, decreased CO and blood pressure. Pericardial effusion can be caused by neoplasia, infectious organisms, congenital abnormality, or idiopathic disease. Pericardial effusion or tamponade is treated by pericardiocentesis to reduce the pressure created and ease the heart’s workload. In case of recurrent effusion, surgical removal of the pericardium is recommended.
When effusion accumulates slowly, the pericardium can enlarge to accommodate this increase in volume and, if intrapericardial pressure is low, clinical signs may not be present and cardiac function remains relatively normal. When effusion accumulates quickly or intrapericardial pressure rises quickly, surpasses the normal diastolic pressure in the right ventricle and cardiac tamponade occurs. Pericardial effusions of large volumes can also compress the lungs and trachea, causing respiratory difficulties and coughing.

In the case of developed pericarditis or a fibrosed and thickened pericardium, the work of the heart becomes difficult and limited by the harder “shell”. Once intrapericardial and intracardiac pressures increase beyond a certain limit, cardiac chamber filling and preload are reduced which causes a drop in stroke volume and cardiac output. This drop in cardiac output causes a reduction in organ perfusion, which triggers compensatory mechanisms including activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis. The resultant tachycardia, peripheral vasoconstriction, and fluid retention is an attempt to maintain systemic blood pressure, cardiac output, and organ perfusion.

Pericardial-disease-1

Anaesthetic management

Management of pericardial effusion can be divided into two groups: the pre-tamponade patients, who are hemodynamically stable, and those with tamponade who are not. Unstable patients demand urgent intervention. Since pressure caused by fluid within the pericardial sac is the underlying problem, drainage of the pericardial fluid is a lifesaving procedure.

In pericardial effusion and cardiac tamponade, impaired ventricular diastolic filling leading to a decrease in stroke volume is compensated by an increase in heart rate, contractility, and systemic vascular resistance. Cardiovascular compromise can be worsened by mechanical ventilation and when it is required, it should be instituted cautiously with the minimal inspiration pressure required to provide adequate minute ventilation. The combination of positive pressure ventilation that decreases venous return as well as vasodilation and direct myocardial depression from the anesthetic agents themselves can result in significant hemodynamic deterioration. Anesthetic considerations in these patients focus on the increase of preload and maintenance of afterload, contractility, and heart rate, and the use of low positive end-expiratory pressure (PEEP) during positive pressure ventilation.

The optimal anesthetic plan varies with the patient’s clinical condition, especially the severity of effusion. Local anesthesia is preferred for pain management, as most of the opioids and general anesthetic agents cause myocardial depression and systemic vasodilation. For intravenous induction, ketamine, midazolam, and etomidate are preferred, as the former supports the heart rate, contractility, and systemic vascular tone, and the latter has minimal effects on blood pressure.

The hemodynamic goals are to maintain adequate cardiac output by increasing chronotropy, to decrease afterload, and to decrease right atrial pressures. Dopamine and dobutamine are all appropriate first-choice inotropes. But they all increase the oxygen and metabolic requirements of the myocardium and decrease its perfusion time and so close monitoring of the hemodynamic parameters is crucial.

The role of fluid resuscitation may have a big advantage. Successful volume expansion primarily depends on the outcome measures defining it (i.e. cardiac index, end-organ perfusion, or patient symptom relief), the type of tamponade, and the overall fluid status of the patient. The effects of hypovolaemia are very obvious. A single fluid challenge is beneficial, especially in the setting of hypotension. Excess fluid administration risks worsening ventricular correlation in the patient and decreasing their cardiac output. The use of fluid as a bridging management is important in those with a poor preload and a single fluid challenge is unlikely to cause harm. Subsequent fluid bolus needed to be carefully assessed with the knowledge that they may be not of benefit.

 

Anesthesia maintenance can be accomplished with various combinations of volatile inhalational agents; intravenous opioids, propofol, and ketamine have all been used successfully. Short- or intermediate-acting muscle relaxants may be used if necessary but ideally only when the patient does not tolerate positive pressure ventilation. Continuous intravenous infusions of vasopressor or inotropic agents may be required to maintain hemodynamic stability, but they should be considered with their adverse consequences due to excessive vasoconstriction, which may restrict cardiac output. Opioids can be used for postoperative analgesia. Consideration should be given to loco regional nerve blocks (i.e., intercostal nerve blocks, serratus plane block) preferably under ultrasound control.

The formulation of a perioperative management plan for patients undergoing pericardial drainage procedures should follow general principles common to all causes of pericardial effusion. The plan should be modified specifically according to the etiology, acuity of presentation, the presence of signs or symptoms of tamponade, and the planned surgical approach.

The general perioperative hemodynamic goals are:

  • Preload: Expand intravascular volume to maintain preload (despite the high central venous pressure observed in tamponade physiology).
  • Heart rate and rhythm: Avoid bradycardia and treat any bradyarrhythmias if they occur. Maintain sinus rhythm so that cardiac output remains optimal.
  • Afterload: Maintain systemic vascular resistance (SVR), which is high in patients with tamponade because of high sympathetic nervous activity. The compensatory cardiovascular mechanisms (tachycardia and raised SVR) must be maintained during the induction of anesthesia.
  • Contractility: Maintain optimal contractility and avoid myocardial depressants.

In patients who are in a decompensated hemodynamic state, pericardiocentesis may be performed under local anesthesia.

 

Clinical case

Clinical history

Vigo, 9 years old labrador for elective pericardiectomy. After two previous pericardiocentesis, the decision for pericardiectomy was made. Previous cytological and culture examinations were negative and the diagnosis was idiopathic pericarditis. On the day of surgery, he was admitted with minimal pericardial effusion and ascites, which do not require centesis.

Physical examination

On the day of surgery, Vigo was tachypneic, with tachycardia, CRT >2 sec, pink mucous membranes, strong pulse, conscious, adequate. The only significant abnormality in the preoperative blood tests was mild hypoproteinemia, explained by the patient’s condition and effusion. Lateral thoracic access and subtotal pericardiectomy were planned and a chest tube was placed.

Induction and maintenance of anesthesia

During preoperative preparation, the patient was premedicated with methadone 0.1mg/kg, diazepam 0.2mg/kg, and ketamine 1mg/kg. Induction was done with propofol 3 mg/kg until effect and intubated with ET 11. Preoxygenation throughout the presurgical preparation for 5-10 min. Two venous and one arterial catheters were placed. The operative field was prepared for left-sided thoracotomy and cleaned with an antiseptic solution. As part of the pain management plan, there was performed local intercostal block under ultrasound guidance from the 3rd to the 7th rib space at left, using Ropivacaine 1mg/kg. During the surgery, all parameters were normal HR 115-127bpm, oscillometric blood pressure MAP 60-80mmHg, strong and regular pulse, SpO2 96-98%, T 38.6. LRS infusion 2-5 ml/kg/h. Antibiotic prevention with ampicillin 20mg/ kg intravenous. During the thoracotomy, mechanical ventilation was used with parameters on Pressure Control Mode and SIMV, 10-12 RR, PEEP 3-4mmHg, Pinsp 7-10mmHg but not exceeding total pressure more than 10- 12mmHg and reached the goal for adequate minute volume without compromising the cardiovascular system and saturation above 97%. Unfortunately, arterial blood pressure was not successfully monitored due to technical reasons, but arterial samples were taken for blood gas analysis.  Due to the surgery, it was decided to perform a pericardial window technique instead of subtotal pericardiectomy. A chest tube and nasal catheter were placed for postoperative continuation monitoring and oxygen therapy. The surgery was successful without anesthetic events.20230913_151317

 

Postoperative care

The post-operative period went well. After full awakening, Vigo received acepromazine 0.01mg/kg due to his temperament and overexcited behavior. As part of the analgesic plan, meloxicam was included in the pain management regimen. Fluid therapy was continued with maintenance 3ml/kg/h RLS. Oxygen therapy, via nasal catheter and saturation monitoring, oscillometric measurement of blood pressure, and monitoring of physiological parameters were continually performed. The prescribed therapy for the stay in the clinic remained Ampicillin 20mg/kg, Furosemide 2mg/kg, Vetmedin 5mg/kg, rescue analgesia with CRI ketamine 0.8mg/ kg/ h, lidocaine 1mg/ kg/ h, methadone. 0,05 mg/ kg/ h. The CRI was titrated till the desired effect and stopped the next morning. The chest tube was checked every 2- 4 hours for the first day and replaced on the third day. Because of the elevated liver enzymes hepatoprotection therapy was included. Broad-spectrum antibiotics, diuretics, and Pimobendan were continued at home. The follow-up from Vigo in the next control examinations is that he is feeling good.Vigo 91075-5_page-0001 20230914_191339

 

Cutaneous neutrophilic panniculitis and vasculitis in a shar-pei associated with autoinflammatory disease

Okan-KahramanDr. Okan Kahraman, DVM

İkon veterinary clinic

İstanbul/ turkey

 

CASE PRESENTATION

A 5-year-old neutered male Shar-Pei presented to the dermatology service with swelling and ulcerative crusted lesions on the flanks and chest.

PHOTO-2024-06-22-00-05-23 (1) PHOTO-2024-06-22-00-05-23 PHOTO-2024-06-22-00-05-24 (1) PHOTO-2024-06-22-00-05-24 PHOTO-2024-06-22-00-05-25 (1) PHOTO-2024-06-22-00-05-25

 

 

 

 

 

 

 

 

 

The patient was clinically diagnosed with Shar-Pei Autoinflammatory Disease (SPAID), characterized by recurrent episodes of fever and lethargy occurring once or twice annually, resolving spontaneously or with the use of non-steroidal anti-inflammatory drugs (NSAIDs).

 

Cytological examination

PHOTO-2024-06-22-00-05-26 (1) PHOTO-2024-06-22-00-05-26 PHOTO-2024-06-22-00-05-27 PHOTO-2024-06-22-00-06-10 (1)

 

 

 

 

 

 

Cytological examination of the skin lesion revealed a neutrophilic infiltrate with infectious agents (coc bacteri) , compatible with neutrophilic dermatitis-panniculitis.

Treatment and outcome:

Treatment was 1mg/kg prednisolon oral tablets (24h) 10 days than reduce dosis

Rilexine (virbac) 300 mg twice Daily 15 days

Antibacterial shampoo weekly

The neutrophilic panniculitis and vasculitis observed in this case responded well to anti-inflammatory corticosteroid therapy, implying

an underlying autoinflammatory condition as the etiology of the skin lesions.

 

1 weeks later

PHOTO-2024-06-22-00-08-29 (1)PHOTO-2024-06-22-00-08-29

 

 

 

 

 

 

 

2 moths later

PHOTO-2024-06-22-00-10-34 PHOTO-2024-06-22-00-10-35

Enemy at the Gates: Hypothermia, the underestimated anesthesia complication

denDr 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.

Cat and dog lying on the snow in cold winter

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.

images (2)

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.images (4)

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.  Temp-4a-1140x778 (1)

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.images (1)

WSAVA Offers Neurology CE to Balkan Member Associations

logo-white-backgroundArtboard-1The World Small Animal Veterinary Association (WSAVA) is offering a series of one-day seminars on neurology to its member associations in the Balkan countries.

 

The sessions will be led by Dr Thomas Flegel, Head of Neurology and Neurosurgery at the Department for Small Animals, Leipzig University, Germany. He will show delegates how to use a neurological examination to determine a problem and the most likely causes. He will then use interactive case-based workups of common neurological presentations to discuss how to approach dogs suffering from seizures or the most common spinal diseases, as well as those with peripheral neuropathies.  The sessions will take place as follows:

 

5 March Banja Luka, Bosnia and Herzegovina Contact bhuvmz@gmail.com
7 May Skopje, North Macedonia  
9 May Priština, Kosovo  
To be confirmed Tirana, Albania  
15 June Venue, Podgorica, Montenegro  

 

Dr Lea Kreszinger, a member of the WSAVA’s Continuing Education (CE) Committee and founder of a small animal clinic in Sesvete, Croatia, has organized this CE for WSAVA members in the Balkan region.  She said: “Neurological cases can be daunting for general practitioners – a fact confirmed by a recent WSAVA learning needs survey, which highlighted neurology as a key topic on which our members wanted more education.

“We’re delighted respond by offering these free one-day sessions with Dr Flegel, a highly experienced practitioner and teacher. He will demonstrate that neurology doesn’t have to be complicated and show delegates how they can improve the quality of life of dogs with neurological problems.”

WSAVA

For further information and to register, veterinarians are asked to contact their country member association.

8 years Vets on The Balkans Conference- “Vets for Cats” 2024

afisWe are delighted to announce that in 11-12th May 2024 will hold our next conference at Ramada Parc Hotel in Bucharest, Romania.

We will enjoy the knowledge of Dr Luca Ferasin, DVM PhD CertVC PGCert(HE) DipECVIM-CA (Cardiology) GPCert(B&PS) FRCVS, European  (EBVS) and RCVS Recognised Specialist in Veterinary Cardiology and Dr Ana Nemec, DVM, PhD, Dipl. AVDC, Dipl. EVDC, Assist. Prof., in Veterinary Dentistry.

 

We will have 2 more guests, local veterinarians, Dr Teodoru Soare,DVM,PhD Senior Profesor – Veterinary Pathology and Dr Elena Nenciulescu DVM, MRCVS – Veterinary Dentistry.

 

Scientific Program:

11th May

8:00-9:00 Registration and welcome coffee

9:00- A fresh approach to heart murmurs in cats.

Dr Luca Ferasin

9:45- Oral Tumors- staging and treatment options

Dr Ana Nemec

10:30-11:00- Coffee Break

11:00 -Is classification of feline cardiomyopathy truly useful?

Dr Luca Ferasin

12:30-13:30 Lunch

13:30-The most common oral tumors in cats

Dr Ana Nemec

14:45- Dr Teodoru Soare- Pathology

15:30-16:00 Coffee Break

16:00 -Clinical cases- presentations of local vets

 

12th May

9:00-A practical approach to the fainting cat.

Dr Luca Ferasin

9:45- Biopsy is always indicated: non-neoplastic oral lesions in cats

Dr Ana Nemec

10:30-11:00- Coffee Break

11:00-Beyond furosemide. Current therapeutic options in feline cardiology

Dr Luca Ferasin

12:30-13:30 Lunch

13:30- Two poorly understood clasics-feline chronic stomatitis and tooth resorption

14:45- Dr Elena Nenciulescu- veterinary dentistry

16:00-Clinical cases- presentations of local vets

17:00-TOMBOLA

 

Soon will be opened and the registration, the price for both days is 100 euro.

Thank you to our general sponsors:

Hills

Pamas Trading

Taste of The Wild

Vet Pharma Distribution

Veteco

Boehringer Ingelheim

 

Because of them we will enjoy our meeting full of knowledge.

 

Soon we will come with more information

Ear tip vasculitis in a Bull Terrier dog – case report

giuliaDr Giulia Nadasan-Cozma

Giu The Vet- veterinary clinic

Arad, Romania

Pacient data and history:

Name: Connor

Breed: Bull Terrier

Age: 2 years

 

Patient presented for a dermatological consult after a few days of bleeding from the auricular pinnae.

The owner noted that the onset was acute, the lesions appeared “ overnight” and the animal was bothered by them, and started scratching and bleeding.

 

Dermatological findings:

Vasculitis lesions are noted bilaterally on the apex of the pinnae consisting of  alopecia, ulceration, crusting in different stages and necrosis that led to loss of tissue and altered the shape of the pinnal apex.

The crust comes off very easily and hemorrhage starts.

Lesions begin at the apical margins of the pinnae and spread along the concave surface.

 

Diagnosis:

 

A sample was performed by the impression smear technique and sent to the lab for cytology. The result was consistent with neutrophilic acute inflammation. In correlation with the clinical aspect, we had a strong suspicion of vascular damage, which may be caused by inflammatory or noninflammatory diseases, and often are idiopathic. The diagnosis is normally confirmed by histopathology but unfortunately the owner did not agree with the medical procedure.

Diferential diagnosis:

Proliferative thrombovascular necrosis of the pinnae is the dermatological diagnosis but to confirm this diagnosis, a biopsy and a histopathology exam is needed.

Ear tip ulcerative dermatitis can be another dermatological diagnosis.

Vaccine associated vasculitis can be another cause.

Vasculitis can be associated with coexisting disease like hypersensitivity disorders, food allergies, insect bites and many drugs administration, even dexamethasone or prednisone.

Given the note that Connor is an atopic dog, atopy itself can be the reason these lesions appeared because he was treated with prednisolone over an year because of his atopic syndrome and owner’s budget restraints.

 

Treatment and outcome:

After a long talk the owner chose surgery but in the end we managed to convince him to try medication for at least 14 days.

The following treatment options were offered:

1: Oclacitinib

Dosage: 0.5-0.6 mg/kg/12 h

1 tablet of 16 mg to be given BID 30-90 days according to the studies

 

2.

  • Local topical Tacrolimus 0,1%
  • Pentoxifylline tablets, dosage 15mg/kg BID
  • Doxicycline tablets, 5 mg/kg BID
  • Niacinamide tablets 500 mg/dog TID, for 30-90 days, may not work.

Treatment with oclacitinib (Apoquel 16 mg) was started despite budget restraints and Connor started to get better by day 7.

The treatment lasted 7 weeks ( 49 days) until complete remission of lesions.

He continued with Apoquel 16 mg 1×1/24 h to control his atopic syndrome.

pic 1 pic 2 pic 3 pic 4 pic 5 pic 6

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Conclusion:

Oclacitinib it is not typically used to treat vasculitis in dogs but should be included

among the therapeutic options for ear tip vasculitis if there are no signs of infection. Oclacitinib has immune modulatory effects on numerous cytokine-mediated inflammatory, autoimmune or immune-mediated diseases in dogs. This type of vascular damage of the pinna is sometimes idiopathic and is hard to find a definitive diagnosis without a histopathology exam.

 

References:

 

  1. Silvia Colombo, Luisa Cornegliani, Antonella Vercelli, Alessandra Fondati – Ear tip ulcerative dermatitis treated with oclacitinib in 25 dogs: a retrospective case series (2021) – Veterinary Dermatology
  2. Thelma Lee Gross, P. J. Ihrke, E.J. Walder, V.K.Affolter – Skin diseases of the dog and cat, 2nd Edition, 2020, Blackwell
  3. Rosanna Marsella, Katherine Doerr, Andrea Gonzales,Wayne Rosenkrantz – Oclacitinib 10 years later: lessons learned and directions for the future

(2023) –  J Am Vet Med Assoc.

  1. William H. Miller Jr., Craig E. Griffin, Karen L. Campbell  – Muller and Kirk’s  Small animal dermatology, 7nd Edition, 2012, Elsevier

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

mihai

Michel (Mihai) GUZU, DVM, Dipl EVDC, ADVETIA Small Animal Hospital, Vélizy-Villacoublay, France
Dr Mihai Guzu

Dr Elena-Nenciulescu

Dr Elena Nenciulescu

 

 

 

 

 

 

 

 

 

 

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).

Figure 1: Initial clinical presentation, with appearance of the rostral intermandibular region before (a) and after shearing of the area of the swelling

Figure 1: Initial clinical presentation, with appearance of the rostral intermandibular region before (a) and after shearing of the area of the swelling

1b

 

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).

 

2a 2b 2c

 

 

 

 

 

 

 

 

 

 

 

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.

 

fig 3

fig 3

3b

Figure 3: Surgical debridement (a) and immediate postoperative aspect of the advancement flap with passive drain in place (b). Followed: Histological analysis reports ulcerative gingivitis with severe chronic suppurative osteomyelitis and inclusion of intralesional bacterial colonies. During the control on day 5 after surgery dehiscence of several skin points is noted after removal of the drain. Open wound management with iterative hydrocolloid dressings was undertaken for an additional 14 days. Skin point removal was performed 27 days after the initial presentation (Figure 4).

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.

Figure 4: Clinical aspect of the operating site during the control at 3 months after the procedure.

Figure 4: Clinical aspect of the operating site during the control at 3 months after the procedure.

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.

Figure 5: Stages of tooth resorption

Figure 5: Stages of tooth resorption

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)

types

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

Dr Mila Kisyova

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.

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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.

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

 

 

Duplex kidney formation: developmental mechanisms and genetic predisposition Vladimir M. Kozlov, Andreas Schedl, iBV, Institut de Biologie Valrose, Equipe Labellisée Ligue Contre le Cancer, Université Cote d’Azur, Centre de Biochimie, UFR Sciences, Parc Valrose, Nice Cedex 2, 06108, France

Duplex kidney formation: developmental mechanisms and genetic predisposition
Vladimir M. Kozlov, Andreas Schedl, iBV, Institut de Biologie Valrose, Equipe Labellisée Ligue Contre le Cancer, Université Cote d’Azur, Centre de Biochimie, UFR Sciences, Parc Valrose, Nice Cedex 2, 06108, France

 

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).

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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:
1A

1A

2-B

2-B

 

3-C

3-C

 

 

 

 

 

 

 

4-D

4-D

 

 

 

5-E

5-E

 

 

 

 

 

6-F

6-F

 

 

 

 

 

 

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)