Histopathological changes in the lungs from dogs with tick paralysis: 25 cases (2010-2012).

OBJECTIVE: To determine the prevalence and nature of histological lung lesions in dogs with tick paralysis. METHODS: A prospective study of 25 client-owned dogs that died during treatment for tick paralysis or were euthanased because of either the severity of the disease process or financial constraints was conducted at a veterinary emergency hospital in Queensland, Australia. Lung specimens were collected postmortem for histopathological examination. RESULTS: All 25 dogs had significant pulmonary changes: 9 exhibited congestion and alveolar oedema, with no obvious inflammatory cell infiltrate; 1 exhibited a mild increase in the number of alveolar macrophages in addition to congestion and alveolar oedema; the remaining 15 dogs had moderate or severe bronchopneumonia, with 2 showing evidence of aspiration pneumonia. CONCLUSION: Dogs with clinically severe tick paralysis are likely to have pulmonary parenchymal disease. Bronchopneumonia may be present in a significant proportion of cases and may reflect aspiration.

Management of respiratory failure from tick paralysis.

OBJECTIVE: The primary objective of this review is to improve the recognition and management of respiratory failure in dogs and cats treated for tick paralysis in veterinary practice. OUTLINE: We review the definitions of respiratory failure in dogs and cats, differentiating hypoxaemic lung failure and hypercapnic ventilation failure. We also identify unsustainable breathing effort, despite normal blood gas values, as a form of respiratory failure. We analyse the research into possible mechanisms of respiratory failure in dogs and cats with tick paralysis and propose strategies that may aid in identification and management of respiratory failure when it develops in small animal patients affected by tick paralysis. CONCLUSIONS: Dogs and cats with tick paralysis may develop respiratory failure despite management with tick antiserum. Prompt recognition and effective support strategies should improve the survival of these patients.

Novel pressurized solvent extraction vessels for the analysis of polychlorinated biphenyl congeners in avian whole blood.

Persistent organic pollutants remain a serious threat to many food-chain systems. New pollutants continue to emerge. The present study has created novel extraction vessels which are compatible with readily available commercial instrumentation to validate the analysis of one class of persistent organic pollutants, polychlorinated biphenyls (PCBs), in avian blood. The volumes used can be reasonably sampled without sacrificing individuals, or comprising breeding or migratorial success. The procedure consists of the pressurized solvent extraction (PSE) of analytes in a novel PSE extraction vessel. The new extraction cell contains a 38-cm long, coiled, re-packable, in situ clean-up column. Lipid elimination, using Florisil, occurs within the coiled region of the extraction vessel, eliminating the requirement for post extraction clean-up. For development, 0.2 g samples of chicken whole blood have been used. Extract volumes are reduced from (30 to 10) cm(3), compared to unmodified systems. The new PSE vessel with its integrated clean-up method showed satisfactory performance for the analysis of ten environmentally relevant PCB congeners in chicken whole blood samples with recoveries in the range of (70-130)%. Detection limits using gas chromatography coupled with large volume injection ion-trap mass spectrometry (GC-LVI-ITMS-MS) were in the range of (0.05-0.5) ng g(-1). The relative standard deviations for all congeners investigated were better than 5%. This is the first PSE validation to have been conducted on unaltered whole blood samples.

The effect of hetastarch (670/0.75) on urine specific gravity and osmolality in the dog.

BACKGROUND: Urine specific gravity (USG) is used clinically to estimate urine osmolality (UOsm). Although USG has been shown to have a linear correlation with UOsm in dogs, the relationship is altered when there are significant numbers of high molecular weight (MW) molecules in the urine. HYPOTHESIS: USG would no longer predict UOsm in dogs given intravenous hetastarch (670/0.75)(HES). ANIMALS: Eight healthy employee-owned adult dogs. METHODS: Prospective, controlled experimental study. USG and UOsm were measured every 30 minutes from t=0 minutes to t=360 minutes. Dogs were administered 20 mL/kg of either NaCl 0.9% (control group, n=4) or HES (treatment group, n=8) IV over 1 hour starting at t=90 minutes. RESULTS: There was a decrease in UOsm in both groups starting at t=120 minutes and continuing for the study duration, and there was no significant difference in UOsm between treatment and control groups across all time points. There was an appropriate decrease in USG from t=120 minutes for the control group. In the treatment group, USG increased significantly at t=120 minutes (P= .0006), t=150 minutes (P= .0002), and t=180 minutes (P= .0044). The largest increase in USG occurred at t=150 minutes with a mean USG of 1.070 +/- 0.021 (range 1.038-1.104). CONCLUSIONS AND CLINICAL IMPORTANCE: Urine specific gravity should not be used to estimate urine solute concentration in dogs following the administration of 20 mL/kg of HES. In a clinical setting, the evaluation of USG following this dose of HES may lead to an overestimation of urine concentration.

Weaning from mechanical ventilation.

Patients that require positive pressure ventilation to maintain sufficient alveolar ventilation or pulmonary gas exchange may eventually reach a point in the course of their care wherein mechanical ventilation is no longer necessary. This process of transferring the work of breathing from the ventilator back to the patient is referred to as ventilator weaning. The term "ventilator weaning" may be used to refer to all methods by which this transfer of workload may be accomplished. In many patients, particularly those with short-lasting or readily correctable causes of respiratory insufficiency (e.g., general anesthesia), the discontinuation of positive pressure ventilation may be easily achieved. Indeed, in patients awakening from general anesthesia, the axiom "awake enough to blink, awake enough to breath" may prove to be a sufficient guideline. However, in those patients requiring long-term mechanical ventilatory support, the process can prove to be both frustrating and exceptionally challenging. It is of crucial importance to identify those patients that may be successfully weaned because of both the financial impact of prolonged intensive care unit hospitalization and the risks imposed on the patient by the process of positive pressure ventilation. To be able to predict which patients may be ready to be weaned from the ventilator requires an understanding of the balance between the work of breathing (ventilatory load) and the ability of the patient's respiratory pump to meet those needs (ventilatory capacity). The management of patients experiencing difficulty during the weaning process requires that the clinician recognize imbalances between ventilatory load and capacity and to correct these imbalances once identified.

Haemodynamic effects of ATP in dogs during hypoxia-induced pulmonary hypertension.

Pulmonary hypertension may result from an increase in vascular resistance caused by persistent hypoxia. We have investigated the effects of adenosine triphosphate (ATP), administered into the pulmonary artery, on haemodynamic changes occurring in anaesthetized adult dogs subjected to acute hypoxic pulmonary vasoconstriction. Hypoxia alone (ventilation with 10% O2/90% N2) caused significant increases in mean pulmonary arterial blood pressure (PAP), central venous pressure (CVP), and cardiac index (CI) by 71, 102 and 38%, respectively. ATP (0.03-3.0 micromol/kg/min approximately 0.02-1.65 mg/kg/min), when infused under hypoxic conditions, significantly reduced both mean PAP and systemic arterial blood pressure (ABP) in a dose-dependent manner. The maximum decrease in mean PAP amounted to 20%; mean ABP, on the other hand, was decreased by up to 52% (P<0.01). Heart rate, CI, CVP and pulmonary occlusion pressure were not dose-dependently affected by ATP. Our data indicate that while pulmonary arterial administration of ATP in mature dogs during hypoxic pulmonary hypertension causes dilation in the pulmonary vascular bed, it is even more effective in dilating the systemic vasculature. This result suggests a need for further evaluation and warrants cautious use of ATP in the treatment of hypoxic pulmonary hypertension in adult dogs.

Deep sedation and mechanical ventilation without paralysis for 3 weeks in normal beagles: exaggerated resistance to metocurine in gastrocnemius muscle.

BACKGROUND: Patients in the intensive care unit may have muscle weakness in the recovery phase, and disuse atrophy may play a role in this weakness. To assess this problem, the authors measured changes in the potency of the nondepolarizing neuromuscular blocking agent metocurine in a canine model that involved 3 weeks of intensive care, nonparalyzing anesthesia with pentobarbital, and positive-pressure ventilation. METHODS: Six dogs were anesthetized with pentobarbital to a sufficient depth that spontaneous and reflex muscle movements were absent. Their tracheas were intubated, their lungs were mechanically ventilated, and they received round-the-clock intensive medical and nursing care for 3 weeks. Transduced gastrocnemius muscle responses to metocurine were determined weekly. A 4- to 15-min infusion of 148-4,300 microg/min (longer durations and greater concentrations on progressive weeks) yielded more than 80% paralysis. Serial metocurine plasma concentrations during the onset of the block and recovery provided data to determine pharmacokinetics using NONMEM. Metocurine plasma concentrations and the degree of paralysis were used to model the effect compartment equilibration constant, and the Hill equation was used to yield the slope factor and potency within the effect compartment. RESULTS: The metocurine effect compartment concentration associated with a 50% diminution of twitch height after 3 weeks was 1,716+/-1,208 ng/ml (mean +/- SD), which was significantly different from 257+/-34 ng/ml, the value on day 0. There were no pharmacokinetic differences. CONCLUSION: The absence of muscle tone and reflex responsiveness for 3 weeks was associated with exaggerated resistance to the neuromuscular blocker metocurine.

Plasma electrolyte and metabolite concentrations associated with pentobarbital or pentobarbital-propofol anesthesia during three weeks' mechanical ventilation and intensive care in dogs.

Propofol and pentobarbital were used for deep sedation during prolonged mechanical ventilation (3 weeks) and nutritional supplementation in 17 clinically normal dogs in an intensive care setting. Tolerance developed to both drugs. Propofol, in combination with pentobarbital, at an infusion rate of 75 micrograms/kg of body weight per minute was preferred. Pentobarbital infusion alone, begun at the rate of 5 to 6 mg.kg-1.h-1, was satisfactory. The combination of both drugs provided smooth, stable anesthesia and required minimal interventions by intensive care unit personnel. Blood gas tensions and electrolyte, parathyroid hormone (PTH), and metabolite concentrations were generally stable throughout, unless condition of the dog deteriorated (e.g., infection, pneumothorax). Hematocrit and red blood cell count decreased with time, likely attributable principally to multiple blood sample collections. White blood cell count, alkaline phosphatase, phosphate, fibrinogen, cholesterol, and triglyceride values increased with time, in association with pentobarbital and the combination of pentobarbital and propofol. Some of these changes appear to have been related to generic responses to stress and inflammation, some to altered metabolism, and some to the lipid solvent of propofol. The increase in triglyceride concentration was greater when propofol was used. Mortality was 47%, with death occurring between days 2 and 18.

Posttransplantation lymphoproliferative disorders in bone marrow transplant recipients are aggressive diseases with a high incidence of adverse histologic and immunobiologic features.

Posttransplantation lymphoproliferative disorders (PT-LPDs) occurring in T-cell depleted (TCD) allogeneic bone marrow transplant recipients seem to be different from those that arise in solid organ recipients in their early development, the high incidence of extensive dissemination at presentation, and their aggressive course and high fatality rate. We report a series of 10 patients with PT-LPDs after TCD allogeneic bone marrow transplant. We studied the correlation between the morphology of the lesions; their clonality based on immunoglobulin (Ig) heavy chain gene rearrangement analysis and immunohistochemistry; their proliferative activity as measured by immunoperoxidase staining for the proliferating cell nuclear antigen (PCNA) and the presence of p53 gene product overexpression. Histologically, our cases corresponded to the two morphologic categories of polymorphic B-cell lymphoma (PBCL, seven cases) and malignant lymphoma immunoblastic (ML-IB, three cases). Ig light-chain staining showed monoclonality in a minority of the cases, whereas Ig gene rearrangement analysis by polymerase chain reaction revealed B-cell clonality in three of seven cases of PBCL and in all three cases of ML-IB. The Epstein-Barr virus (EBV) genome, the expression of EBV latent membrane protein or both were found in all 10 specimens. High proliferative activity (PCNA > or = 66%) was found in all cases, with a mean PCNA value of 56% in PBCL and 84% in ML-IB. Five specimens were p53+ (two of seven PBCL and three of three ML-IB). Two of four PBCL cases resolved with the administration of donor leukocytes. All of the remaining patients died of the PT-LPD within a short time from admission. Our results show that the PT-LPDs after TCD bone marrow transplantation are characterized by a high frequency of high-grade histologic subtypes, frequent monoclonality, high proliferative activity, frequent overexpression of p53 gene product, and poor prognosis. These characteristics observed in only a minority of cases of PT-LPDs occurring after solid organ transplantation may account for the less aggressive clinical behavior observed in those diseases.

Hypoplastic myelodysplastic syndromes can be distinguished from acquired aplastic anemia by CD34 and PCNA immunostaining of bone marrow biopsy specimens.

Hypoplastic myelodysplastic syndromes (h-MDSs) are difficult to distinguish from acquired aplastic anemia (AA) because of the considerable clinical, cytologic, and histologic similarities between these two disorders. Recent studies have suggested that the bone marrow (BM) in AA is characterized by a decreased number of CD34+ cells and reduced expression of proliferating cell nuclear antigen (PCNA), features that have not been associated with MDS. To determine the potential importance of these markers in the differential diagnosis of hypoplastic BM disorders, we immunostained 50 BM biopsy specimens of cytogenetically characterized cases of AA (27) and h-MDS (23). Immunohistochemical staining for CD34 was performed with QBEND10 (Vector, Burlingame, Calif), a monoclonal antibody (MoAb) reactive in routinely processed specimens, while PCNA was assessed by the PC10 MoAb (Dako, Carpinteria, Calif) using a microwave over-based antigen retrieval technique. Bone marrow specimens of h-MDS cases showed statistically higher values of PCNA and CD34 than did those of the AA cases: mean values (+/- SD) of CD34-positive cells in h-MDS, 0.94% +/- 1.1; AA, 0.04% +/- 0.1 (P = .0002); PCNA-positive cells in h-MDS, 43.59% +/- 13.3; AA, 14.80% +/- 6.4 (P < .0001). Our study confirms that AA is characterized by low expression of PCNA in BM and reduced CD34 frequency compared with h-MDS and supports the concept of an early deficiency of stem cells in the former disorder. The results also illustrate how immunostaining permits a simple distinction of these conditions in routinely processed BM biopsy specimens.

Clinical applications of quantitative acid-base chemistry.

Stewart used physicochemical principles of aqueous solutions to develop an understanding of variables that control hydrogen ion concentration (H+) in body fluids. He proposed that H+ concentration in body fluids was determined by PCO2, strong ion difference (SID = sum of strong positive ion concentrations minus the sum of the strong anion concentrations) and the total concentration of nonvolatile weak acid (Atot) under normal circumstances. Albumin is the major weak acid in plasma and represents the majority of Atot. These 3 variables were defined as independent variables, which determined the values of all other relevant variables (dependent) in plasma, including H+. The major strong ions in plasma are sodium and chloride. The difference between Na+ and Cl- may be used as an estimation of SID. A decrease in SID below normal results in acidosis (increase in H+) and an increase in SID above normal results in alkalosis (decrease in H+). Unidentified strong anions such as lactate will decrease the SID, if present. Equations developed by Fencl allow Stewart's work to be easily applied clinically for evaluating the metabolic (nonrespiratory) contribution to acid-base balance. This approach separates the net metabolic abnormality into components, and allows one to easily detect mixed metabolic acid-base abnormalities. The Fencl approach provides insight into the nature and severity of the disturbances that exist in the patient. Sodium, chloride, protein, and unidentified anion derangements may contribute to the observed metabolic acid-base imbalance.

The cardiovascular sparing effect of fentanyl and atropine, administered to enflurane anesthetized dogs.

Cardiovascular effects of high dose opioid together with low dose inhalant were compared with inhalant alone to determine whether opioid/inhalant techniques were less depressant on the cardiovascular system. The effects of positive pressure ventilation and increasing heart rate to a more physiological level were also studied. Cardiovascular measurements recorded during administration of enflurane at 1.3 minimum alveolar concentration (MAC; 2.89 +/- 0.02%) to spontaneously breathing dogs (time 1) and during controlled ventilation [arterial carbon dioxide tension at 40 +/- 3 mmHg (time 2)] were similar. At time 2, mixed venous oxygen tension and arterial and mixed venous carbon dioxide tensions were significantly decreased, while arterial and mixed venous pH were significantly increased compared to measurements at time 1. After administration of fentanyl to achieve plasma fentanyl concentration of 71.7 +/- 14.4 ng/mL and reduction of enflurane concentration to yield 1.3 MAC multiple (0.99 +/- 0.01%), heart rate significantly decreased, while mean arterial pressure, central venous pressure, stroke index, and systemic vascular resistance index increased compared to measurements taken at times 1 and 2. Pulmonary arterial occlusion pressure was significantly increased compared to measurements taken at time 2. After administration of atropine until heart rate was 93 +/- 5 beats/min (plasma fentanyl concentration 64.5 +/- 13.5 ng/mL) heart rate, mean arterial pressure, cardiac index, oxygen delivery index, and venous admixture increased significantly compared to values obtained at all other times.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary effects of halothane in hypovolemic dogs.

Cardiopulmonary effects of halothane administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. Halothane was delivered by face mask, dogs were intubated, then halothane end-tidal concentration of 1.13 +/- 0.02% was maintained, and cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to halothane administration, systemic vascular resistance index, oxygen extraction, and base deficit increased. Compared with baseline values, these variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, oxygen delivery index, oxygen consumption index, mixed venous oxygen tension, mixed venous oxygen content, venous admixture, arterial bicarbonate concentration, and mixed venous pH. At all times after intubation, arterial and venous oxygen tensions and mixed venous carbon dioxide tensions were increased. Three minutes after intubation, base deficit and mixed venous carbon dioxide tension increased, and mean arterial pressure and arterial and venous pH decreased, compared with values measured immediately prior to halothane administration. Fifteen minutes after intubation, systemic vascular resistance index decreased and, at 15 and 30 minutes, mean arterial pressure and arterial and venous pH remained decreased. At 60 minutes, mean pulmonary arterial pressure and pulmonary arterial occlusion pressure were increased and mixed venous pH was decreased, compared with values measured before halothane administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular and respiratory effects of propofol administration in hypovolemic dogs.

Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 6 mg of propofol/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to propofol administration, oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after propofol administration, mean pulmonary arterial pressure, pulmonary vascular resistance, oxygen utilization ratio, venous admixture, and arterial and mixed venous carbon dioxide tensions increased, whereas mean arterial pressure, arterial oxygen tension, mixed venous oxygen content, arterial and mixed venous pH decreased from values measured prior to propofol administration. Fifteen minutes after propofol administration, mixed venous carbon dioxide tension was still increased; however by 30 minutes after propofol administration, all measurements had returned to values similar to those measured prior to propofol administration.

Cardiopulmonary effects of etomidate in hypovolemic dogs.

Cardiopulmonary effects of etomidate administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. One milligram of etomidate/kg of body weight was then administered IV to 7 dogs, and the cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to etomidate administration, heart rate, arterial oxygen tension, and oxygen utilization ratio increased. Compared with baseline values, the following variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, mixed venous oxygen content, and arterial carbon dioxide tension. Three minutes after etomidate administration, central venous pressure, mixed venous and arterial carbon dioxide tension, and venous admixture increased, and heart rate, arterial and venous pH, and arterial oxygen tension decreased, compared with values measured immediately prior to etomidate administration. Fifteen minutes after etomidate injection, arterial pH and heart rate remained decreased. At 30 minutes, only heart rate was decreased, and at 60 minutes, mean arterial pressure was increased, compared with values measured before etomidate administration. Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.

Cardiovascular and pulmonary effects of atropine reversal of oxymorphone-induced bradycardia in dogs.

Oxymorphone was administered intravenously (IV) to 10 dogs (0.4 mg/kg initial dose followed by 0.2 mg/kg three times at 20-minute intervals). Four hours after the last dose of oxymorphone, heart rates were less than 60 bpm in six dogs. After atropine (0.01 mg/kg IV) was administered, heart rate decreased in five dogs and sinus arrhythmia or second degree heart block occurred in four of them. A second injection of atropine (0.01 mg/kg IV) was administered 5 minutes after the first and the heart rates increased to more than 100 bpm in all six dogs. Ten minutes after the second dose of atropine, heart rate, cardiac output, left ventricular minute work, venous admixture, and oxygen transport were significantly increased, whereas stroke volume, central venous pressure, systemic vascular resistance, and oxygen extraction ratio were significantly decreased from pre-atropine values. The PaCO2 increased and the PaO2 decreased but not significantly. The oxymorphone-induced bradycardia did not produce any overtly detrimental effects in these healthy dogs. Atropine reversed the bradycardia and improved measured cardiovascular parameters.

Hemostatic defects associated with two infusion rates of dextran 70 in dogs.

We investigated changes in hemostatic function after infusion of 6% dextran 70 (high molecular weight dextran) at 2 rates. Six healthy dogs underwent 3 regimens: 20 ml of dextran/kg of body weight administered in 1 hour (trial A), 20 ml of dextran/kg administered in 30 minutes (trial B), and 0.9% sodium chloride solution as a control administered over 1 hour to achieve hemodilution equivalent to that for 20 ml of dextran/kg (trial C). Before and at 2, 4, 8, and 24 hours after the start of trials A and B, we measured PCV, total solids (TS) concentration, amount of von Willebrand factor antigen (vWf:Ag), factor VIII coagulant activity (VIII:C), prothrombin time, activated partial thromboplastin time (APTT), platelet retention in a glass bead column, and buccal mucosa bleeding time (BMBT). Values were not obtained at 8 and 24 hours for trial C. Saline-induced changes in hemostasis were significant (P less than 0.05) from baseline throughout the sample collection period. Significant differences (P less than 0.05) between trial A and control were observed for vWf:Ag, VIII:C, BMBT, APTT, TS, and PCV values at 2 hours, and for VIII:C at 4 hours. Significant differences (P less than 0.05) between trial B and control were observed for APTT, TS, and PCV values at 2 hours, and for vWf:Ag, VIII:C, BMBT, APTT, TS, and PCV values at 4 hours. During trials A and B, mean values of analytes infrequently deviated from reference intervals, and clinical signs of bleeding were not observed in any dog.(ABSTRACT TRUNCATED AT 250 WORDS)