What is the best treatment for hypotension in healthy dogs during anaesthesia maintained with isoflurane?

Hypotension is a common and potentially life-threatening complication of general anaesthesia in dogs. Due to the combination of cardiovascular side effects of many anaesthetic, sedative and analgesic drugs used peri-operatively hypotension is frequently reported even in healthy dogs undergoing elective procedures. Several treatment options for hypotension have been advocated. Potential treatments include rapid administration of either crystalloid or colloid fluids; pharmacological treatments to increase cardiac output and/or systemic vascular resistance; or reduction in the delivery of the volatile anaesthetic agents. This critical appraisal considers the current evidence for which treatment is the best option for treating hypotension in healthy euvolemic dogs undergoing general anaesthesia maintained with isoflurane. Fourteen relevant studies were appraised, including 12 laboratory studies and two small clinical trials. One study demonstrated that reduction in the delivery of isoflurane may correct hypotension, but this treatment may not always be feasible. In general, rapid administration of fluids did not increase blood pressure and failed to correct hypotension. Synthetic colloids demonstrated some efficacy, but results were inconsistent between studies and large volumes may be required. Infusion of dopamine appears to be the most reliable pharmacological option consistently increasing blood pressure, cardiac output and correcting hypotension.

Respiratory Support for Pharmacologically Induced Hypoxia in Neonatal Calves.

Practical methods to provide respiratory support to bovine neonates in a field setting are poorly characterised. This study evaluated the response of healthy neonatal calves with pharmacologically induced respiratory suppression to nasal oxygen insufflation and to continuous positive airway pressure (CPAP) delivered via an off-the-shelf device. Ten calves were randomised to receive either nasal oxygen insufflation (Group 1, n = 5) or CPAP (Group 2, n = 5) as a first treatment after induction of respiratory depression by intravenous administration of xylazine, fentanyl, and diazepam. Calves received the alternate treatment after 10 minutes of breathing ambient air. Arterial blood gas samples were obtained prior to sedation, following sedation, following the first and second treatment, and after breathing ambient air before and after the second treatment. Oxygen insufflation significantly increased arterial oxygen partial pressure (PaO2) but was also associated with significant hypercapnia. When used as the first treatment, CPAP was associated with significantly decreased arterial partial pressure of carbon dioxide but did not increase PaO2. These results suggest that the use of CPAP may represent a practical method for correction of hypercapnia associated with inadequate ventilation in a field setting, and further research is required to characterise the use of CPAP with increased inspired oxygen concentrations.

Quality of life in thalassemia: a comparison of SF-36 results from the thalassemia longitudinal cohort to reported literature and the US norms.

Thalassemia is a chronic, inherited blood disorder, which, in its most severe form, causes life-threatening anemia. Advances in treatment have led to increased life expectancy however the need for chronic blood transfusions and chelation therapy remains a significant burden for patients. Our study compared health related quality of life (HRQOL) from the Thalassemia Clinical Research Network's (TCRNs) Thalassemia Longitudinal Cohort (TLC) study to US norms and assessed association with clinical variables. There were 264 patients over age 14 who completed the Medical Outcomes Study 36-Item Short Form Health Survey version 2 (SF36v2) baseline assessment. When compared to US norms, TLC patients had statistically significant (P < 0.05) worse HRQOL on five of the eight subscales (physical functioning, role-physical, general health, social functioning, and role-emotional) and on both summary scales (physical component summary and mental component summary). Women, older patients, and those with more disease complications and side effects from chelation reported lower HRQOL. In general, adolescents and adults with thalassemia report worse HRQOL than the US population, despite contemporary therapy. The SF-36 should become a standard instrument for assessing HRQOL in thalassemia to determine predictors of low HRQOL which may be better addressed by a multidisciplinary team.

Catheter-related deep venous thrombosis in children with hemophilia.

Central venous catheters (CVCs) are a common adjunct to hemophilia therapy, but the risk of CVC-related deep venous thrombosis (DVT) in hemophiliacs is not well defined. In a previous study, 13 patients with CVCs had no radiographic evidence of DVT. However, recent abstracts and case studies demonstrate that DVT does occur. Therefore, this study sought to determine the frequency of DVT in children with hemophilia and long-term CVCs and to correlate venographic findings with clinical features. All hemophilia patients with tunneled subclavian CVCs in place for 12 months or more were candidates for evaluation. Patients were examined for physical signs of DVT and questioned about catheter dysfunction. Contrast venograms were obtained to identify DVT. Fifteen boys with severe hemophilia were evaluated, including 9 from the initially studied group of 13. Eight patients had evidence of DVT, 5 of whom previously had normal venograms. Five of 15 patients had clinical problems related to the CVC, all of whom had DVT. Four of 15 patients had suggestive physical signs; 3 had DVT. The mean duration of catheter placement for all patients was 57.5 months (range, 12-102 months). For patients with DVT, the mean duration was 66.6 +/- 7.5 months, compared to 49.5 +/- 7.2 months for patients without DVT (P =.06). No patient whose CVC was in place fewer than 48 months had an abnormal venogram. Many hemophilia patients with CVCs develop DVT of the upper venous system, and the risk increases with duration of catheter placement.

Acute lymphoblastic leukemia complicated by choroid plexus carcinoma.

A 14-year-old boy with acute lymphoblastic leukemia in remission developed headaches characteristic of migraines. His neurologic examination was normal, serial studies of cerebrospinal fluid were unremarkable, and the headaches responded promptly to antimigraine therapy. Ultimately, radiographic and pathologic examinations demonstrated a choroid plexus carcinoma.

Beneficial effect of intravenous dexamethasone in children with mild to moderately severe acute chest syndrome complicating sickle cell disease.

Acute chest syndrome (ACS) in patients with sickle cell disease (SCD) has historically been managed with oxygen, antibiotics, and blood transfusions. Recently high-dose corticosteroid therapy was shown to reduce the duration of hospitalization in children with SCD and vaso-occlusive crisis. Therefore, we chose to assess the use of glucocorticoids in ACS. We conducted a randomized, double-blind placebo-controlled trial to evaluate the efficacy and toxicity of intravenous dexamethasone (0.3 mg/kg every 12 hours x 4 doses) in children with SCD hospitalized with mild to moderately severe ACS. Forty-three evaluable episodes of ACS occurred in 38 children (median age, 6.7 years). Twenty-two patients received dexamethasone and 21 patients received placebo. There were no statistically significant differences in demographic, clinical, or laboratory characteristics between the two groups. Mean hospital stay was shorter in the dexamethasone-treated group (47 hours v 80 hours; P = .005). Dexamethasone therapy prevented clinical deterioration and reduced the need for blood transfusions (P < .001 and = .013, respectively). Mean duration of oxygen and analgesic therapy, number of opioid doses, and the duration of fever was also significantly reduced in the dexamethasone-treated patients. Of seven patients readmitted within 72 hours after discharge (six after dexamethasone; P = .095), only one had respiratory complications (P = 1.00). No side effects clearly related to dexamethasone were observed. In a stepwise multiple linear regression analysis, gender and previous episodes of ACS were the only variables that appeared to predict response to dexamethasone, as measured by lengh of hospital stay. Intravenous dexamethasone has a beneficial effect in children with SCD hospitalized with mild to moderately severe acute chest syndrome. Further study of this therapeutic modality is indicated.

Elevation of homocysteine and excitatory amino acid neurotransmitters in the CSF of children who receive methotrexate for the treatment of cancer.

PURPOSE: Folate deficiency, either by diet or drug, increases plasma homocysteine (Hcy). Hcy damages cerebrovascular endothelium, and hyperhomocysteinemia is a risk factor for stroke. Hcy is metabolized to excitatory amino acid (EAA) neurotransmitters, such as homocysteic acid (HCA) and cysteine sulfinic acid (CSA), which may cause seizures and excitotoxic neuronal death. We postulated that excess Hcy and EAA neurotransmitters may partly mediate methotrexate (MTX)-associated neurotoxicity. PATIENTS AND METHODS: In this retrospective analysis, we used high-performance liquid chromatography (HPLC) to measure Hcy, HCA, and CSA in CSF from two groups of children: (1) a control group of patients with no MTX exposure, and (2) a treatment group of patients who had received MTX no more than 7 days before a scheduled lumbar puncture. RESULTS: The treatment group had a significantly (P = .0255) greater concentration of Hcy in CSF (0.814 micromol/L +/- 0.215 [mean +/- SEM], n = 23) than the control group (0.210 micromol/L +/- 0.028, n = 34). HCA and CSA were not detected in CSF from control patients (n = 29); however, MTX caused marked accumulation of CSF HCA (119.1 micromol/L +/- 32.0, n = 16) and CSA (28.4 micromol/L +/- 7.7, n = 16) in the treatment group. Patients with neurologic toxicity at the time of lumbar puncture had many of the highest concentrations of Hcy, HCA, and CSA. CONCLUSION: These data support our hypothesis that MTX-associated neurotoxicity may be mediated by Hcy and excitotoxic neurotransmitters.