Acute noncardiogenic pulmonary edema in an anesthetized Nubian goat kid

ObservationsA 1-month-old Nubian goat presented for sialocyst resection. Physical examination and bloodwork were unremarkable. While pre-oxygenating, the goat was sedated with midazolam and morphine (0.1 mg kg^?1 each) intravenously (IV). General anesthesia was induced 5 minutes later with 1.7 mg kg^?1 propofol. Sevoflurane was administered in oxygen without assisted ventilation via a cuffed orotracheal tube. Throughout the first 85 minutes of anesthesia, the goat was well-oxygenated (SpO₂, ≥97%), ventilating adequately (Pe′CO₂, 36–48 mmHg), and had normal mean arterial blood pressure (MAP, 60–85 mmHg). Blood-gas values at 45 minutes were consistent with adequate ventilation on oxygen. At 75 minutes, the goat moved in response to surgical stimulation, requiring additional propofol (0.4 mg kg^?1). After 10 minutes, MAP dropped precipitously to 40 mmHg and frequent multiform premature ventricular contractions (PVCs) were observed. Crystalloids, hetastarch, and dopamine (5 μg kg^?1 minute^?1) were administered to correct the hypotension. Arterial blood-gas analysis revealed that the goat had become hypoxemic (PaO₂, 50 mmHg). Intermittent positive pressure ventilation (IPPV) was initiated. Subsequent blood-gas analysis did not show significant improvement in PaO₂ (53 and 56 mmHg, respectively). Occasional PVCs were observed thereafter. Surgery ended, and sevoflurane and IPPV were discontinued. The goat was extubated within 7 minutes and received 100% oxygen by mask. Diffuse crackles were ausculted over both hemithoraces. Suspecting pulmonary edema, furosemide (1 mg kg^?1) was administered IV. Radiographs taken immediately post-operatively revealed a severe, caudodorsal airspace (alveolar) pattern, confirming the diagnosis. Respiration improved considerably within an hour with nasal oxygen and two additional doses of furosemide.ConclusionsThe goat developed acute, drug-induced, noncardiogenic pulmonary edema in response to the second dose of propofol.     

Post‐anesthetic pulmonary edema in two horses

Case 1 A two‐year old, 462 kg Standard bred horse was anesthetized for arthroscopy and castration. During anesthesia, hyperemia of the mucosal membranes and urticaria were noticed. During 5 hours of anesthesia subcutaneous edema of the eyelids and neck region developed. In the recovery box, the orotracheal (OT) tube was left in situ and secured in place with tape. Following initial attempts to stand, the horse became highly agitated and signs consistent with pulmonary edema developed subsequently. Arterial hypoxemia (PaO₂: 3.7 kPa [28 mmHg]) and hypocapnia (PaCO₂: 3.1 kPa [23 mmHg]) were confirmed. Oxygen and furosemide were administered. The horse was assisted to standing with a sling. Therapy continued with bilateral intra‐nasal oxygen insufflation. Ancillary medical therapy included flunixin meglumine, penicillin, gentamycin and dimethylsulfoxide. Following 7 hours of treatment the arterial oxygen tensions began to increase towards normal values. Case 2 An 11‐year old, 528 kg Paint horse was anesthetized for surgery of a submandibular mass. The 4‐hour anesthetic period was unremarkable. The OT tube was left in situ for the recovery. During recovery, the horse was slightly agitated and stood after three attempts. Clinical signs consistent with pulmonary edema and arterial hypoxemia (PaO₂: 5 kPa [37.5 mmHg]) subsequently developed following extubation. Respiratory signs resolved with medical therapy, including unilateral nasal oxygen insufflation, furosemide, flunixin meglumine and dimethylsulfoxide. The diagnosis of pulmonary edema in these horses was made by clinical signs and arterial blood‐gas analysis. While pulmonary radiographs were not taken to confirm the diagnosis, the clinical signs following anesthesia support the diagnosis in both cases. The etiology of pulmonary edema was most likely multifactorial.     

The cardiopulmonary effects of anesthetic induction with isoflurane,ketamine‐diazepam or propofol‐diazepam in the hypovolemic dog

ObjectiveTo evaluate and compare the cardiopulmonary effects of induction of anesthesia with isoflurane (Iso), ketamine–diazepam (KD), or propofol–diazepam (PD) in hypovolemic dogs.Study designProspective randomized cross–over trial.AnimalsSix healthy intact, mixed breed, female dogs weighing 20.7 ± 4.2 kg and aged 22 ± 2 months.MethodsDogs had 30 mL kg^?1 of blood removed at a rate of 1.5 mL kg^?1 minute^?1 under isoflurane anesthesia. Following a 30–minute recovery period, anesthesia was reinduced. Dogs were assigned to one of three treatments: isoflurane via facemask using 0.5% incremental increases in the delivered concentration every 30 seconds, 1.25 mg kg^?1 ketamine and 0.0625 mg kg^?1 diazepam intravenously (IV) with doses repeated every 30 seconds as required, and 2 mg kg^?1 propofol and 0.2 mg kg^?1 diazepam IV followed by 1 mg kg^?1 propofol increments IV every 30 seconds as required. Following endotracheal intubation all dogs received 1.7% end–tidal isoflurane in oxygen. Cardiopulmonary variables were recorded at baseline (before induction) and at 5 or 10 minute intervals following endotracheal intubation.ResultsInduction time was longer in Iso (4.98 ± 0.47 minutes) compared to KD (3.10 ± 0.47 minutes) or PD (3.22 ± 0.45 minutes). To produce anesthesia, KD received 4.9 ± 2.3 mg kg^?1 ketamine and 0.24 ± 0.1 mg kg^?1 diazepam, while PD received 2.2 ± 0.4 mg kg^?1 propofol and 0.2 mg kg^?1 diazepam. End–tidal isoflurane concentration immediately following intubation was 1.7 ± 0.4% in Iso. Arterial blood pressure and heart rate were significantly higher in KD and PD compared to Iso and in KD compared to PD. Arterial carbon dioxide partial pressure was significantly higher in PD compared to KD and Iso immediately after induction.Conclusions and clinical relevanceIn hypovolemic dogs, KD or PD, as used in this study to induce anesthesia, resulted in less hemodynamic depression compared to isoflurane.     

Acute pulmonary edema in a dog with severe pulmonary valve stenosis: A rare complication after balloon valvuloplasty

Pulmonic stenosis is a frequent congenital heart disease in dogs, and the treatment of choice is balloon valvuloplasty which is usually safe and successful. The authors describe for the first time a severe complication after balloon valvuloplasty in a five-month-old dog. After effective treatment, with a considerable drop in right ventricular pressures, the dog developed hypoxemia and dyspnea due to pulmonary edema. The dog underwent intensive care and symptoms improved after a few hours of oxygen therapy, continuous positive airway pressure, and furosemide. Although this event is rare, it could have a large impact on patient survival and should be considered in the treatment of severe pulmonary valve stenosis in the future.     

Effect of propofol and ketamine-diazepam on intraocular pressure in healthy premedicated dogs

Objective

To compare the effect of propofol and ketamine/diazepam for induction following premedication on intraocular pressure (IOP) in healthy dogs.

Suspected air embolism associated with post-anesthetic pulmonary edema and neurologic sequelae in a horse

A 523 kg Quarter Horse was anesthetized for unilateral eye enucleation. The anesthetic period was unremarkable. During anesthetic recovery the cap on the jugular venous catheter became dislodged. Clinical signs of pulmonary edema associated with moderate arterial hypoxemia subsequently developed. Although pulmonary edema resolved with medical therapy, the day following anesthetic recovery, clinical signs of vestibular disease and blindness developed. Treatment included nasal oxygen insufflation, flunixin meglumine, furosemide, dexamethasone, thiamine, dimethylsulfoxide, antimicrobials, and phenylbutazone. The horse recovered and was discharged from the hospital after 7 days of treatment and was neurologically normal at 6 weeks. While venous air embolism was not confirmed in this case, the catheter cap complication followed by signs of pulmonary edema and neurologic sequelae support the presumptive pathogenesis of this horse's complications. Diagnostic confirmation of air embolism in horses with compatible acute clinical signs should be documented with echocardiography.     

Fatal acute lung injury after balloon valvuloplasty in a dog with pulmonary stenosis

A one-year-old French Bulldog was referred for the management of a severe form of pulmonary valve stenosis (PS) complicated by right-sided congestive heart failure.Echocardiography showed severe valvular PS with right ventricular concentric hypertrophy, dilatation and severe right atrial enlargement. A pulmonary balloon valvuloplasty (PBV) was performed with a balloon-to-pulmonary annulus ratio of 1.36. Echocardiography immediately after PBV showed a significant reduction in right atrial and ventricular size, improved opening and mobility of the pulmonary valve leaflets, and a 75% reduction in the pulmonary pressure gradient from 158 mmHg pre-operative to 40 mmHg post-operative. The dog recovered well from anesthesia, but 2 h later, it suddenly showed severe respiratory distress. Focus cardiac ultrasound showed increased left cardiac size with echocardiographic signs of high left ventricular filling pressure. Bedside lung ultrasound showed diffuse numerous-to-confluent B lines, compatible with a severe alveolar-interstitial syndrome. The dog was treated with furosemide, helmet continuous positive airway pressure, and then mechanical ventilation but without success.At post-mortem evaluation, histological examination of the lung showed diffuse, severe broncho-alveolar edema with mixed leukocyte, fibrin, and red blood cell infiltrate. Moreover, severe congestion and multifocal alveolar hemorrhages were evident. All findings were compatible with fatal acute lung injury after PBV secondary to pulmonary reperfusion-ischemia injury and increased pulmonary capillary hydrostatic pressure. Based on the present case, acute lung injury should be considered as a rare but serious complication of PBV.     

Suspected fatal venous air embolism during anaesthesia in a Pomeranian dog with pulmonary calcification

CASE HISTORY: Death occurred in a 1.25 kg, 9-month-old female Pomeranian dog undergoing anaesthesia for surgical repair of partially healed fractures of the radius and ulna.

CLINICAL FINDINGS: Following sedation, anaesthesia was induced using thiopentone and maintained with halothane in oxygen. An acute decrease in the dog's end-tidal carbon dioxide (EtCO₂) measurements was noted approximately 50 min after induction, immediately following delivery of a 5-ml bolus of lactated Ringer's solution (LRS) administered to flush a small (0.06 ml) volume of fentanyl via a pre-placed intravenous (I/V) catheter. Venous air embolism (VAE) was suspected and the dog died despite interventive therapy. On post-mortem examination, several air bubbles were noted when the right ventricle was opened under water. Histologically, the kidneys appeared abnormal with immature glomeruli, and the lungs appeared diffusely mineralised. The origin of the air was probably small bubbles and microbubbles that may have been present in the extension set and 20 ml syringe used for the administration of fentanyl and I/V fluids to the dog.

DIAGNOSIS: Renal dysplasia and diffuse pulmonary calcification, with VAE as the probable cause of death.

CLINICAL RELEVANCE: In this case of VAE-associated anaesthetic death, it is further speculated that underlying pulmonary disease, in the form of pulmonary calcification, may have contributed to an increased sensitivity to the adverse effects of VAE.     

The effects of ketamine hydrochloride and diazepam on the intraocular pressure and pupil diameter of the dog’s eye

Objective To determine the effects of 10% ketamine hydrochloride and 0.5% diazepam on intraocular pressure (IOP) and horizontal pupil diameter (HPD) in the canine eye. Procedures Ten healthy dogs for each treatment group were used in this study. In the first group, 20 mg/kg ketamine hydrochloride was injected intravenously; in the second, 0.5 mg/kg diazepam was similarly injected; and in the third, a control group, 0.9% saline was used. In all groups, IOP and HPD were measured every 5 min for 35 min in the first group, and 60 min in the second and third group. Results A maximum increase in IOP was obtained 5 min after ketamine injection, with IOP of 23.2 ± 5.8 mmHg (a 45.0% increase compared to baseline) in the right eye and 22.9 ± 5.9 mmHg (a 43.5% increase) in the left eye (both significant at P < 0.01). A significant IOP increase was observed throughout the research period of 35 min. Statistically significant increases in HPD (P < 0.05) were observed only at 5 and 25 min after ketamine injection. A significant increase in IOP was obtained 10 min after diazepam injection, showing a maximum IOP 20 ± 5.0 mmHg in the right eye (9.3% increase) and 19.9 ± 5.1 mmHg (8.7% increase) in the left eye (both significant at P < 0.05). HPD decreased during the study period, reaching the lowest level 30 min post‐treatment. Conclusions This study showed a substantial increase in IOP after ketamine injection and a less substantial, but still significant increase after diazepam injection. These findings should be taken into consideration when using these drugs in dogs with fragile corneas, or in dogs predisposed or affected by glaucoma.     

Acute onset of pulmonary necrotising arteritis in a dog with a left-to-right patent ductus arteriosus

A 12-week-old, clinically normal Chihuahua was referred for investigation for a continuous heart murmur. Cardiac evaluation revealed an anatomically and haemodynamically typical left-to-right shunting patent ductus arteriosus. The continuous wave Doppler measurement of peak ductal jet velocity of 5.6 m/s was suggestive of a normal pulmonary to systemic arterial pressure ratio. The dog returned 16 days later with right heart failure and severe pulmonary hypertension. Marked reduction in left-to-right shunting was demonstrated and the ductal jet velocity had decreased to 2.5 m/s. Immediate ductus ligation, oxygen therapy before and after the operation, and administration of hydralazine failed to reduce pulmonary hypertension, and the dog was euthanased. Histopathological examination of the lung showed pulmonary necrotising arteritis with acute and chronic arterial lesions. Chronic pulmonary vascular changes related to high flow have been associated with altered nitric oxide and endothelin responses. These changes may be responsible for the acute onset of pulmonary hypertension due to relatively minor vascular insults in some human and veterinary patients with left-to-right shunts. The potential for acute progression supports the recommendations for early ductus ligation and the prognostic importance of detecting pulmonary hypertension presurgically in patent ductus arteriosus patients.     

Acute tumour lysis syndrome in a dog with B-Cell multicentric lymphoma

A 5-year-old, spayed female German Shepherd dog was admitted to hospital with marked generalised lymphadenomegaly and splenomegaly. A stage Va B-cell multicentric lymphoma was diagnosed on clinical, cytological (lymph node, bone marrow), histological-immunohistochemical (lymph node excision) and imaging grounds. Since no satisfactory remission was achieved using a multi-drug chemotherapy protocol that included cyclophosphamide, vincristine, cytosine arabinoside, prednisolone, and subsequently supplemented by L-asparaginase, it was replaced by another protocol combining vincristine, L-asparaginase, prednisolone, cyclophosphamide and doxorubicin. Soon after the third weekly session of the second protocol, the clinical status of the animal deteriorated suddenly and severely, with a bleeding tendency, jaundice, hyperuricaemia, hyperphosphataemia, azotaemia, hyperbilirubinaemia and, presumptive disseminated intravascular coagulation. There was also complete regression of lymphadenomegaly. This report emphasises the clinicopathological features and the diagnostic peculiarities of the acute tumour lysis syndrome, which occurs uncommonly in dogs.     

Hypoxaemia and suspected pulmonary oedema in a Dorper ewe after diazepam-ketamine induction of anaesthesia

Anaesthesia was required in an 18-month-old Dorper ewe scheduled for surgical repair of an abdominal hernia. Anaesthesia was induced with diazepam (0.15 mg/kg) and ketamine (6 mg/kg), and maintained with halothane in oxygen on a circle anaesthetic machine. Hypotension, hypoxaemia, cyanosis and pulmonary oedema were observed from the start of surgery, but the symptoms improved towards the completion of the procedure. The aetiology of this condition could not be established. It is suggested that propylene glycol, the organic solvent in the diazepam formulation, may have stimulated the release of vasoactive substances that resulted in pulmonary oedema.     

Acute blindness in a dog caused by an explosive blast

A 3-year-old, intact male, mixed breed dog was presented with a complaint of acute blindness. Ten days previously, the area where the dog was walking came under a rocket attack, and a rocket landed and exploded 300 meters away from the dog. Physical examination was unremarkable. Ophthalmoscopic examination revealed posterior segment fibrin clots and extensive vitreal hemorrhage in the right eye. A total retinal detachment (360 degrees retinal dialysis) with no evidence of hemorrhage was noted in the left eye. There was no sign of any penetrating ocular trauma, and it was assumed that the posterior segment findings were primary injuries caused by the blast wave itself. Following anti-inflammatory treatment, partial vision was restored in the right eye. Surgical re-attachment of the retina was discussed and declined by the owner. This report describes, for the first time, vitreal hemorrhage and retinal detachment as the sole injuries caused by an explosive blast wave.     

Acute necrotising pulmonary vasculitis and pulmonary hypertension in a juvenile dog

A five-month-old female Jack Russell terrier was presented for investigation of acute lethargy, anorexia, coughing, respiratory distress and weakness. Examination findings included cyanosis, a grade 3 of 6 systolic heart murmur and prolonged capillary refill time. Radiography and echocardiography revealed severe pulmonary hypertension, cor pulmonale and right-sided heart failure. Indirect measurement of the systolic pulmonary artery pressure estimated pressures over 100 mmHg. Despite treatment the patient died. Post-mortem examination did not identify a congenital cardiovascular anomaly. Histopathology confirmed acute necrotising pulmonary arteritis and immunohistochemistry failed to identify any immune complex or complement deposition.     

The effect of four anesthetic protocols on splenic size in dogs

Objective To characterize the effects of four anesthetic protocols on the size of the spleen during surgery in dogs. Study design Prospective experimental trial. Animals Twenty‐four beagle dogs, 1.1 ± 0.3 years of age and weighing 10.9 ± 2.7 kg. Methods Dogs were allocated to receive one of four anesthetic protocols: 1 – pre‐medication with acepromazine and butorphanol, induction with thiopental; 2 – pre‐medication with acepromazine and butorphanol, induction with propofol; 3 – pre‐medication with medetomidine and butorphanol, induction with propofol; and 4 – pre‐medication with medetomidine and butorphanol, induction with ketamine and diazepam. Anesthesia was then maintained with halothane. At laparotomy, the spleen length, width, and height were measured, these were measured again just prior to closure of the abdomen. Splenic area and volume were calculated. Hematocrit and total serum protein (TSP) were measured before and after induction and during laparotomy. Results Splenic volume was greatest after protocol 4 (161.2 ± 40.2 cm³; p < 0.05) and was least after protocol 2. The differences in volume were because of differences in length, width, and height between groups. There was no significant change in area, length, or width over the study period. Hematocrit decreased significantly in all dogs but at different times. The decrease occurred after pre‐medication if acepromazine was administered, at induction following protocol 3 and during surgery following protocol 4. Conclusions If splenic volume is to be minimized during surgery, then acepromazine and propofol should be used in the anesthetic protocol. The administration of medetomidine, diazepam, and ketamine will produce a greater splenic volume. Lack of correlation between hematocrit and spleen size following the anesthetic protocols studied suggests sequestration of red blood cells in nonsplenic sites.     

Polycythemia in dogs with chronic hypoxic pulmonary disease

BackgroundProlonged tissue hypoxia caused by chronic pulmonary disease is commonly regarded as an important mechanism in the development of secondary polycythemia, but little clinical data are available to support this hypothesis.ObjectiveTo study the prevalence and severity of erythrocytosis accompanying chronic hypoxic pulmonary disease in dogs.AnimalsForty‐seven dogs with hypoxic chronic pulmonary disease, 27 dogs with nonhypoxic chronic pulmonary disease, and 60 healthy controls.MethodsDogs with chronic pulmonary disease and chronic hypoxemia (partial pressure of arterial oxygen [PaO₂] < 80 mm Hg on at least 2 arterial blood gas measurements a minimum of 1 month apart) were identified retrospectively from patient records. Association between arterial oxygen and red blood cell parameters was analyzed using Pearson''s correlation coefficients and multivariable linear regression analysis.ResultsRed blood cell parameters measured at the end of the hypoxemia period were within the laboratory reference range in most dogs. In chronically hypoxemic dogs, hematocrit (Hct) was increased in 4/47 (8.5%; 95% confidence interval [CI], 0‐17) dogs, erythrocyte count (Erytr) was increased in 12/47 (26%; 95%CI, 13‐38) dogs and hemoglobin concentration (Hb) was increased in 3/47 (6.4%; 95%CI, 0‐14) dogs. No marked polycythemia (Hct ≥65%) was noted in any of the dogs. Red blood cell parameters were not associated with the severity of hypoxemia (correlation to PaO₂: Erytr, r = −.14; Hb, r = −.21; Hct, r = −.14; P > .05 for all).Conclusions and Clinical ImportancePolycythemia is uncommon, and usually mild if present, in dogs with chronic hypoxia caused by pulmonary disease.