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Notes: Objective: To discuss a new clinical presentation of organophosphate toxicity called the intermediate syndrome in a dog.Case summary: A mixed breed dog presented with generalized weakness, hypoventilation and hypoxemia. The weakness was most marked in the thoracic limbs, cervical and respiratory muscles. The history revealed a likely exposure to an organophosphate compound. The other dog in the household demonstrated mild clinical signs of organophosphate toxicity. A blood cholinesterase level was markedly reduced. Therapy included placement of a tracheostomy tube and mechanical ventilation. The dog gradually improved over the following 8 days but had persistent cervical ventroflexion for a total of 4 weeks.New or unique information provided: Organophosphate toxicity can present as a paralysis following the acute cholinergic crisis. The muscular weakness predominantly affects the thoracic limb and neck muscles but cranial nerve deficits can also occur. Dogs can die from the associated respiratory depression. Oxime therapy is indicated in the treatment of this syndrome.

Notes: Objective: To determine the continuous changes in blood volume in response to fluid administration using an in-line hematocrit monitor.Design: Prospective study.Setting: Research laboratory.Animals: Four healthy dogs.Interventions: Each dog received intravenous boluses of 80 mL/kg of 0.9% saline (S), 4 mL/kg of 7.5% saline (HS), 20 mL/kg of dextran 70 (D), 20 mL/kg of hetastarch (HES), or no fluids (control, C) on separate occasions. Fluids were administered at 150 mL/min in the S, D, and HES groups, and at 1 mL/kg/min in the HS group.Measurements and main results: Blood volume changes were measured every 20 seconds for 240 minutes using an in-line hematocrit monitor. There was a rapid rise in blood volume during all infusions. Immediately after the administration of crystalloid fluids, the rapid rise in blood volume ceased. Subsequently, there was a steep decline in blood volume for 10 minutes, and a slower decline thereafter. In contrast, the rise in blood volume continued for at least 10 minutes after the infusion of the colloids was complete, and a plateau was observed for the remainder of the experiment. The blood volume effect, as measured by area under the curve, was significantly greater in the saline group than the other groups during the infusion time and for the 0–240 minutes time period. The areas under the curve for the two colloid solutions were not significantly different from each other during any time periods. The percent increase in blood volume immediately following the infusions was 76.4±10.0 in the S group, 17.1±3.2 in the HS group, 23.0±10.5 in the D group, and 27.2±6.4 in the HES group. At 30 minutes from the start of the infusion, the mean percent increases in blood volumes were 35.2±9.3 in the S group, 12.3±0.9 in the HS group, 35.9±7.3 in the D group, and 36.8±6.5 in the HES group. At 240 h post-infusion, the mean percent increases in blood volume were 18.0±9.7 in the S group, 2.9±6.1 in the HS group, 25.6±16.1 in the D group, and 26.6±8.6 in the HES group. The C group had a mean percent change in blood volume of −3.7±3.4 at the end of the experiment.Conclusions: This study indicates that the rapid administration of saline at clinically relevant doses leads to the largest immediate increase in blood volume, although this change is transient because of rapid redistribution of the fluid. Despite a brief increase in blood volume that was almost 3 times the volume administered, hypertonic saline led to the smallest increase in blood volume post-infusion. The synthetic colloid solutions increased the blood volume by an amount greater than that infused and the effect was sustained for a longer period of time than seen following crystalloid administration, but the maximum increase in blood volume was significantly less than saline. The measurement of continuous changes in blood volume, using an in-line hematocrit monitor, was a useful means of assessing the dynamic effects of fluid administration in dogs in a research setting.

Notes: Objective: To collate canine cardiopulmonary measurements from previously published and unpublished studies in instrumented, unsedated, normovolemic and moderately hypovolemic dogs.Design: Collation of data obtained from original investigations in our research laboratory.Setting: Research laboratory, School of Veterinary Medicine.Subjects: Sixty-eight dogs.Interventions: Subjects were percutaneously instrumented with an arterial catheter and a thermodilution cardiac output catheter. A femoral artery catheter was percutaneously placed for blood removal.Measurements and main results: Body weight, arterial and mixed-venous pH and blood gases, arterial, pulmonary arterial, pulmonary artery occlusion, and central venous blood pressure, cardiac output, and core body temperature were measured. Body surface area, bicarbonate concentration, standard base excess, cardiac index (CI), stroke volume, systemic and pulmonary vascular resistance, left and right ventricular work and stroke work indices, left and right rate-pressure product, alveolar PO2, alveolar–arterial PO2 gradient, arterial and mixed-venous and pulmonary capillary oxygen content, oxygen delivery, oxygen consumption, oxygen extraction, venous admixture, arterial and venous blood carbon dioxide content, arterial–venous carbon dioxide gradient, carbon dioxide production were calculated.In 68 dogs, hypovolemia sufficient to decrease mean arterial blood pressure (ABPm) to an average of 62 mmHg, was associated with the following changes: arterial partial pressure of carbon dioxide (PaCO2) decreased from 40.0 to 32.9 mmHg; arterial base deficit (BDa) increased from −2.2 to −6.3 mEq/L; lactate increased from 0.85 to 10.7 mm/L, and arterial pH (pHa) did not change. Arterial partial pressure of oxygen (PaO2) increased from 100.5 to 108.3 mmHg while mixed-venous PO2 (PmvO2) decreased from 49.1 to 34.1 mmHg. Arterial and mixed-venous oxygen content (CaO2 and CmvO2) decreased from 17.5 to 16.5 and 13.8 to 9.6 mL/dL, respectively. The alveolar–arterial PO2 gradient (A-a PO2) increased from 5.5 to 8.9 mmHg while venous admixture decreased from 2.9% to 1.4%. The ABPm decreased from 100 to 62 mmHg; pulmonary arterial pressure (PAPm) decreased from 13.6 to 6.4 mmHg; and pulmonary arterial occlusion pressure (PAOP) decreased from 4.9 to 0.1 mmHg. CI decreased from 4.31 to 2.02 L/min/m2. Systemic and pulmonary vascular resistance (SVRI and PVRI) increased from 1962 to 2753 and 189 to 269 dyn s/cm5, respectively. Oxygen delivery (DO2) decreased from 787 to 340 mL/min/m2 while oxygen consumption (VO2) decreased from 172 to 141 mL/min/m2. Oxygen extraction increased from 20.9% to 42.3%.Conclusions: Moderate hypovolemia caused CI and oxygen delivery to decrease to 47% and 42% of baseline. Oxygen extraction, however, doubled and, therefore, oxygen consumption decreased only to 82% of baseline.

Notes: Dogs and cats receiving cardiopulmonary resuscitation (CPR) were evaluated for factors leading to cardiac arrest and for survival following the procedure. One-hundred-thirty-five canine and forty-three feline patients seen at the University of California, Davis Veterinary Medical Teaching Hospital that received CPR between August 1987 and December 1991 were studied. Initial resuscitation attempts were unsuccessful in 72% of dogs and 58% of cats. Five dogs and one cat were still alive 3 days after CPR. Ultimately only four dogs and one cat were discharged from the hospital alive. These five patients with uniquely longer survival all had cardiac arrests associated with drug and/or anesthetic reactions.

Notes: Blood was withdrawn from 15 dogs over the course of about 1 hour until the mean arterial blood pressure was reduced to 60 mm Hg. Small aliquots of additional blood were withdrawn in order to maintain the mean arterial blood pressure near 60 mm Hg for an additional hour. Oxymorphone (0.4 mg/kg) was then administered intravenously to ten dogs, and all measurements were repeated in 5, 15, 30, and 60 minutes. Five dogs served as controls.Heart rate, tidal volume, arterial oxygen, oxygen extraction, and pH significantly decreased after oxymorphone administration, while systemic and pulmonary arterial blood pressures, systemic vascular resistance (transiently), breathing rate, minute ventilation, physiologic dead space, venous admixture, venous oxygen, arterial and venous carbon dioxide, and bicarbonate concentration increased significantly. Cardiac output was also increased, but the change was not statistically significant. Oxymorphone was associated with significantly lower heart rate, tidal volume, arterial oxygen, and pH, and higher systemic and pulmonary arterial pressure, cardiac output, venous oxygen, and arterial and venous carbon dioxide, compared to the control group, which did not receive oxymorphone.Oxymorphone significantly improved cardiovascular performance and tissue perfusion in these hypovolemic dogs. Oxymorphone did cause a significant increase in arterial carbon dioxide and a decrease in arterial oxygenation. Oxymorphone is an opioid agonist that may represent a reasonable alternative for the induction of anesthesia in patients who are candidates for induction hypotension.

Notes: Eleven awake dogs and two cats received high-frequency jet ventilation (HFJV) via a transtracheal catheter for 6 hours to evaluate their clinical tolerance to the technique. A bronchoscopic examination was performed in all animals prior to and the morning of the day after the procedure to determine the gross effects of the technique on the tracheal epithelium.All animals tolerated the technique well, exhibiting no discomfort and only a minimal amount of coughing. Only one dog exhibited coughing on the day following the procedure. No bronchoscopic changes were noted after HFJV in one dog. In one dog and one cat, the only observed change was an increase in the prominence of the vascularity compared to that observed prior to HFJV. The remaining animals exhibited more severe tracheal changes that included: an accumulation of mucus (seven dogs, one cat), focal spots of hemorrhage (two dogs), linear stretches of epithelial denuding (two dogs), and diffuse reddening and epithelial denuding (four dogs).High-frequency jet ventilation by a transtracheal intravenous catheter is well tolerated for short-term ventilatory support in dogs and cats, but the magnitude of the tracheal damage observed in the present report may preclude long-term ventilatory support by this tecnique.

Notes: Veterinary patients are treated with colloid solutions for plasma volume expansion and maintenance of plasma colloid oncotic pressure (COP). In practice COP is usually extrapolated from measurement of albumin, total protein, or refractometric total solids (TS) as an estimate of total protein. The objective of this study was to determine if refractometer readings accurately reflect levels of synthetic colloid in the blood. Serial dilutions of synthetic colloids Dextran 70 and hetastarch into 2.5% and 5% human serum albumin (HSA) were prepared, and COP and TS measurements were performed. Synthetic colloids were found to produce a significant increase in measured COP, without a significant change in refractometric TS readings. Measured COP correlated well with concentration of synthetic colloid. In clinical patients, treatment of decreased COP with synthetic colloids should be monitored by direct measurement of COP or by observing resolution of clinical signs of hypovolemia or edema. (Vet Emerg & Crit Care, 1998; 8: 21–26)

Notes: The incidence and clinical progression of oral lesions in a cohort of critically ill patients administered mechanical ventilation via orotracheal intubation were observed prospectively in the Intensive Care Unit (ICU) of the University of California, Davis Veterinary Medical Teaching Hospital. Oral cavities of these patients were examined within 24 hours of being placed on the ventilator and at least daily thereafter during ventilator therapy. As part of the study protocol, any lesion noted was treated. Twenty-one critically ill canine patients (median age of 7 yrs; range 〈1 to 19 yrs) were observed from 1 January 1995 through 31 August 1995. Over ninety percent (90.5%) of the observed patients developed oral lesions subsequent to being mechanically ventilated. Erosive and ulcerative mucosal lesions were the most frequently observed (15/43) with the tongue being the most frequently involved oral structure. Most of the observed soft tissue oral lesions appeared secondary to persistently applied pressure from teeth, mouth gags, endotracheal tubes, and other monitoring devices. Efforts taken to prevent persistently applied trauma, such as periodic positional changes of equipment and padding of susceptible structures, apeared effective in preventing oral lesions. There were indications of gastric reflux in 6 patients (28.6%), as evidenced by secretions in the oral cavity with a pH of 〈6 and containing digested blood. Ulcerative lesions in the subset of patients with gastric reflux seemed to worsen in severity with exposure to the low pH secretions. Over the course of the study, the ICU nursing staff developed an effective protocol for the care of the oral cavity: treating mucosal erosions and ulcers topically8 with a dilute chlorhexidine solution (0.05%), removing oral secretions via suction as needed, and padding persistently traumatized tissues with glycerin moistened gauze. Oral lesions in orotrachealy intubated and mechanically ventilated patients are predictable, preventable, and treatable. Most lesions are pressure induced, associated with monitoring/therapeutic equipment, and appear to be preventable with appropriate nursing protocls. Most observed oral lesions clinically improved with routine, periodic dilute chlorhexidine rinses and relief of applied pressure.

Notes: Gastric dilatation-volvulus (GDV) was surgiclly induced in 10 dogs. Five of the dogs were pretreated with 50 mg/kg PO of allopurinol to determine the effect of xanthine oxidase inhibition on the pathophysiology of GDV. After 150 minutes, the GDV was corrected, and lactated Ringer's solution was administered intravenoulsy (resuscitation). Two hundred forty minutes after relief fo GDV, the dogs were euthanatized without recovery from anesthesia. Administration of allopurinol was associated with a reduced (P〈0.01) incidence of hepatic necrosis and a lower (P〈0.045) serum phosphorus level than observed in the control group at the end of the experiment. The increase in base deficit in the allopurinol-treated group after resuscitation was also less(P〈0.045) than the control group. In conclusion, this study suggests that inhibition of xanthine oxidase-derived oxygen free radicals protects against hepatic necrosis in dogs with GDV. Resuscitation appears to be a time of profound physiologic stress for dogs with GDV.

Notes: The ability of the SAV 6 high-frequency jet ventilator to effectively ventilate three anesthetized, paralyzed cats (3.2–4.2 kg), two small dogs (7.2 and 10.0 kg), six medium-sized dogs (20.5–25.0 kg), and three large dogs (36.0–43.0 kg) via a 14-gauge (dogs) or a 16-gauge (cats) catheter placed percutaneously into the trachea via the cricothyroid membrane or into a preplaced endotracheal tube was evaluated. The lowest driving pressure within the range of 0.25 to 2.0 kg/cm2 (1 kg/cm2= 14.2 psi) and the highest cycle rate within the range of 60 to 240 per minute that would generate a PaCO2 of 30 ± 3 mm Hg were determined.All animals could be ventilated to a PaC02 of 30 ± 3 mm Hg by the endotracheal tube and transtracheal route, except the largest dogs, which couid be ventilated to an average PaC02 of 36 mm Hg by the transtracheal route. The transtracheal route consistently required higher driving pressures and lower cycle rates than did the endotracheal tube route. Cats could be ventilated with a driving pressure of 0.25 kg/cm2; small dogs could be ventilated with 0.5 to 1.0 kg/cm2; medium-sized dogs with 1.0 to 1.5 kg/cm2; and large dogs with 1.5 to 2.0 kg/cm2.The SAV 6 high-frequency jet ventilator can effectively ventilate cats and dogs (7.2–43.0 kg) via a transtracheal catheter and an endotracheal tube.