Evaluation of midazolam-ketamine with dexmedetomidine and fentanyl for injectable anaesthesia in dogs

dexmedetomidine and fentanyl for injectable anaesthesia in dogs. Vet. arhiv 83, 509

Usporedna analiza učinkovitosti kombinacije ropivakaina, bupivakaina i ksilazin-ketamina za epiduralnu analgeziju u koza.

The study was conducted on eighteen healthy non-descript male goats divided into 3 groups: A, B and C, having 6 animals in each. Lumbosacral epidural ropivacaine (0.6 mg/kg), bupivacaine (0.5 mg/kg) and xylazine and ketamine (0.025 mg/kg and 2.5 mg/kg) were administered in groups A, B and C, respectively. The treatments were compared using clinical, physiological, haematological, biochemical and acid base/blood gas parameters. The earliest onset of analgesia was produced by epidural xylazine and ketamine combination. Xylazine and ketamine, bupivacaine and ropivacaine produced complete analgesia of the tail, perineum, inguinal region and thighs for variable intervals. The xylazine and ketamine combination produced analgesia of a greater extent and longer duration, followed by bupivacaine and ropivacaine. Mild sedation was produced by the xylazine and ketamine combination alone. Recovery was faster with ropivacaine, followed by bupivacaine and the xylazine and ketamine combination. The xylazine and ketamine combination produced a non-significant decrease in the heart rate and respiratory rate of the animals. There were insignificant fluctuations in pCO2, pO2, SO2, pH and HCO-3 values from base line at different intervals in all the groups. The changes in haematobiochemical and blood electrolyte values were transient, and hence of little significance in all the groups. The results of this study suggest that all these drugs could be considered safe for epidural analgesia in the administered doses for healthy goats.Istraživanje je provedeno na 18 zdravih jaraca podijeljenih u tri skupine (A, B i C). U svakoj skupini bilo je po 6 jaraca. U svrhu lumbosakralne epiduralne analgezije, skupini A bio je primijenjen ropivakain (0,6 mg/kg), skupini B bupivakain (0,5 mg/kg), a skupini C ksilazin i ketamin (0,025 mg/kg i 2,5 mg/kg). Učinci su bili uspoređeni na osnovi kliničkih, fizioloških, hematoloških, biokemijskih i acidobaznih pokazatelja te statusa plinova u krvi. Najbrži početak analgezije postignut je epiduralnom primjenom kombinacije ksilazina i ketamina. Ksilazin i ketamin, bupivakain te ropivakain izazvali su potpunu analgeziju repa, perineuma, ingvinalnog i bedrenog područja u različitim vremenskim razmacima. Najjača i najduža analgezija postignuta je kombinacijom ksilazina i ketamina. Zatim je po jačini i dužini slijedila analgezija bupivakainom pa ropivakainom. Srednje jaka sedacija postignuta je zasebnom primjenom ksilazina i ketamina. Oporavak nakon analgezije bio je najbrži pri uporabi ropivakaina, zatim bupivakaina te na posljetku kombinacije ksilazinketamina. Kombinacija ksilazina i ketamina izazvala je nesignifi kantan pad frekvencije bila i disanja. Kod svih skupina jaraca, u različitim vremeskim razmacima, opažena su i nesignifikantna odstupanja od početnih vrijednosti za pCO2, pO2, SO2, pH i HCO–3. Promjene hematoloških i biokemijskih pokazatelja kao i elektrolita u krvi bile su kratkotrajne i od malog značenja u svim promatranim skupinama. Rezultati pokazuju da se svi istraženi analgetici, u upotrijebljenim dozama, mogu smatrati sigurnima za epiduralnu analgeziju zdravih koza

Prosudba učinkovitosti celomske tekućine kišne gujavice na cijeljenje rana u punoj debljini kože kunića.

The present study was conducted on 16 New Zealand White rabbits of 10-12 months of age, to evaluate the healing potential of earthworm coelomic fluid in full thickness skin wounds. Under xylazine-ketamine anaesthesia, four rectangular full thickness excisional skin wounds, measuring 2×2 cm2 were created on the dorsum of each animal and designated as groups I, II, III and IV. Wounds were treated by topical coelomic fluid (I), 0.5 % povidone-iodine and coelomic fluid (II), 0.5 % povidone-iodine (III) and normal saline (IV). Healing was evaluated on the basis of gross and histomorphological parameters. The mean wound area was significantly lesser (P<0.05) in the wounds of groups I and II as compared to groups III and IV, up to 21 days. Out of 16 wounds, nine wounds in group I (56.25 %) and 11 wounds in group II (68.75 %) healed completely by day 21, but none in groups III and IV. Histomorphological studies showed more mature and densely placed collagen and better epithelialization in groups I and II as compared to groups III and IV. It was concluded that coelomic fluid of the earthworm Eisenia foetida can accelerate healing of full-thickness skin wounds in rabbits.Istraživanje je provedeno na 16 novozelandskih bijelih kunića u dobi od 10 do 12 mjeseci s ciljem da se prosudi mogući učinak celomske tekućine kišne gujavice na cijeljenje rana u punoj debljini kože u kunića. Kunići su bili podijeljeni u četiri skupine označene I, II, III i IV. Četiri pravokutne ekscizijske kožne rane u punoj debljini veličine 2x2 cm načinjene su na leđima svake životinje pod anestezijom ksilazin-ketaminom. Rane su bile obrađene celomskom tekućinom (skupina I), 0,5 %-tnim povidon-jodom i celomskom tekućinom (skupina II), 0,5 %-tnim povidon-jodom (skupina III) i fiziološkom otopinom (skupina IV). Cijeljenje rana bilo je prosuđivano na osnovi patoanatomskih i patohistoloških nalaza. Prosječna površina rana 21 dan nakon ekscizije bila je značajno manja (P<0,05) u skupinama I i II u usporedbi s površinom skupina III i IV. Devet od 16 rana u skupini I (56,25 %) i 11 u skupini II (68,75 %) u potpunosti su zacijelile 21 dan nakon ekscizije, dok nijedna nije zacijelila u skupini III i IV. Patohistološki nalaz pokazao je više zrelog i gušće raspoređenog kolagena te bolju epitelizaciju u skupinama I i II u usporedbi sa skupinama III i IV. Može se zaključiti da celomska tekućina kišne gujavice Eisenia foetida može ubrzati cijeljenje rana u punoj debljini kože u kunića

Prosudba učinka midazolam-ketamina s deksmedetomidinom i fentanilom za injekcijsku anesteziju u pasa.

A prospective randomized blinded study was conducted on 12 clinically healthy adult dogs of both sexes (mean weight of 18.34 ± 0.78 kg) divided into three groups (n = 4). The animals received 0.4 mg/kg midazolam and 10 μg/kg dexmedetomidine (group A), 0.4 mg/kg midazolam and 20 μg/kg dexmedetomidine (group B) and 0.4 mg/kg midazolam + 20 μg/kg dexmedetomidine + 4 μg/kg fentanyl (group C) intramuscularly, using separate syringes. Ten minutes later Ketamine was administered intravenously in all the groups. A significantly (P<0.05) shorter weak time (onset of sedation) and down time (onset of recumbency) were recorded in animals in group C as compared to the animals of groups A and B. Muscle relaxation was excellent in group C. The pedal reflex was abolished up to 30 min in groups A and B and up to 60 min in group C. Intubation was only possible in groups B and C. The anaesthetic induction dose of ketamine was minimal in group C. Standing recovery time was shortest in the animals of group C. Respiratory rate (RR) decreased significantly (P<0.05) throughout the observation period, but rectal temperature (RT) decreased significantly (P<0.05) towards the end of the observation period in all the groups. Heart rate decreased significantly (P<0.05) in the animals of group B. Mean arterial pressure (MAP) was maintained within the physiological range in all the groups. It was concluded that dexmedetomidine (10 μg/kg)-midazolam-ketamine can produce anaesthesia for about 20 min in dogs. Increasing the dose of dexmedetomidine did not enhance the duration of anaesthesia, but the further addition of fentanyl not only reduced the induction dose of ketamine but also increased the duration of anaesthesia up to 50 min. Dexmedetomidine-midazolam-fentanyl-ketamine can be used for prolonged duration of injectable anaesthesia in dogs.Poduzeto je prospektivno istraživanje na 12 slučajno odabranih klinički zdravih pasa i kuja (prosječne tjelesne mase 18,34 ± 0,78 kg) podijeljenih u tri skupine (n = 4). Životinjama skupine A bio je intramuskularno primijenjen midazolam u dozi od 0,4 mg/kg i deksmedetomidin u dozi od 10 μg/kg. Životinjama skupine B bio je i/m primijenjen midazolam u dozi od 0,4 mg/kg i deksmedetomidin 20 μg/kg, a životinje skupine C primile su i/m 0,4 mg/kg midazolama, 20 μg/kg deksmedetomidina i 4 μg/kg fentanila. Deset minuta nakon toga svim je životinjama intravenski bio ubrizgan ketamin. Značajno (P<0,05) kraće vrijeme smirivanja (nastup sedacije) i vrijeme lijeganja ustanovljeno je u životinja skupine C u usporedbi sa skupinama A i B. Opuštanje mišićja bilo je izvrsno u skupini C. Nožni refleks nestao je nakon 30 minuta u skupinama A i B, a nakon 60 minuta u skupini C. Intubacija je bila moguća samo u životinja skupine B i C. Doza ketamina potrebna za početak anestezije bila je najmanja u životinja skupine C. Vrijeme potrebno za ponovno ustajanje bilo je najkraće u životinja skupine C. Frekvencija disanja značajno se smanjila (P<0,05) u čitavom razdoblju promatranja, dok se rektalna temperatura u svih životinja značajno smanjila (P<0,05) na kraju razdoblja promatranja. Frekvencija bila znatno se smanjila (P<0,05) u životinja skupine B. Srednji arterijski tlak bio je u fiziološkim granicama u svih životinja. Može se zaključiti da kombinacija deksmedetomidin (10 μg/kg)-midazolam-ketamin može u pasa dovesti do anestezije za oko 20 minuta. Povećanje doze deksmedetomidina nije povećalo trajanje anestezije. Ipak, daljnja primjena fentanila ne samo da je smanjila početnu dozu ketamina već je povećala trajanje anestezije na 50 minuta. Deksmedetomidin-midazolam-fentanil-ketamin mogu se rabiti za produženo trajanje injekcijske anestezije u pasa

Clinicophysiological and haemodynamic effects of fentanyl with xylazine, medetomidine and dexmedetomidine in isoflurane-anaesthetised water buffaloes (<i>Bubalus bubalis</i>)

The present study was undertaken to investigate the sedative, analgesic and clinical effects of xylazine, medetomidine and dexmedetomidine with fentanyl as pre-anaesthetics in water buffaloes and to compare the dose-sparing effect of xylazine, medetomidine and dexmedetomidine on thiopental for induction and isoflurane for maintenance of anaesthesia in water buffaloes. Six male water buffaloes randomly received intravenous fentanyl (5.0 µg/kg body weight) and xylazine (0.05 mg/kg body weight), fentanyl (5.0 µg/kg body weight) and medetomidine (2.5 µg/kg body weight), fentanyl (5.0 µg/kg body weight) and dexmedetomidine (5.0 µg/kg body weight) at weekly intervals in groups I1, I2 and I3, respectively. After 15 min, the animals were restrained in right lateral recumbency and anaesthesia was induced by 5% thiopental sodium administered intravenously. The intubated animal was connected to the large animal anaesthesia machine and isoflurane in 100% oxygen (5 L/min) was insufflated for 60 min. The treatments were compared by clinicophysiological, haematobiochemical and haemodynamic parameters. Fentanyl-medetomidine and fentanyl-dexmedetomidine produced more cardiovascular depression during the pre-anaesthetic period but less depression of cardio-respiratory dynamics in the post induction and maintenance period. Quicker recovery was recorded in I2 and I3 groups. A lower dose of thiopental was required in group I3 (4.33 mg/kg ± 0.66 mg/kg) than in groups I2 (4.41 mg/kg ± 0.98 mg/kg) and I1 (4.83 mg/kg ± 0.79 mg/kg). The dose of isoflurane was less in group I3 (45.50 mL ± 5.45 mL) than in group I1 and I2 (48.66 mL ± 5.10 mL and 48.00 mL ± 6.38 mL). Better anaesthesia was recorded with fentanyl-dexmedetomidine-thiopental-isoflurane (group I3) than with fentanyl-medetomidine-thiopental-isoflurane (group I2) and fentanyl-xylazine-thiopental-isoflurane (group I1). Fentanyl-medetomidine and fentanyl-dexmedetomidine were better pre-anaesthetic agents in comparison to fentanyl-xylazine for thiopental and isoflurane anaesthesia. Fentanyl-dexmedetomidine-thiopental-isoflurane and fentanyl-medetomidine-thiopental-isoflurane produced effective surgical anaesthesia and were found to be safe, as cardio-pulmonary functions were well preserved during maintenance anaesthesia with no deleterious effect on vital organ functions in water buffaloes

Non-alcoholic fatty liver disease: Not time for an obituary just yet!

There has been a concerted effort to change the nomenclature of non-alcoholic fatty liver disease (NAFLD) to metabolic dysfunction-associated fatty liver disease (MAFLD), and one wonders if it is appropriate and timely to bid adieu to the good old term. Numerous reasons have been put forth to justify this, as outlined in a recently published statement proposing the change. However, there are considerable flaws in the proposal, and changing NAFLD to MAFLD is unlikely to move the field forward.We have serious misgivings on this matter.o begin with, the statement by the MAFLD consensus group that the term NAFLD was coined by Ludwig and colleagues is factually incorrect. Although the histological features of NAFLD were first described decades ago, Klatskin and his colleagues, in 1979, were the first to use the term \u2018non-alcoholic liver disease\u2019.Later, while reporting similar findings, Ludwig and colleagues coined the term \u201cnon-alcoholic steatohepatitis (NASH)\u201d.Although an association between metabolic syndrome (MS) and NAFLD has been established and NAFLD termed the hepatic manifestation of MS, this generalisation has since been questioned, since the complex heterogeneity of this entity precludes any single postulation to explain its pathogenesis. Besides, individuals with normal BMI also develop NAFLD, and studies in non-Caucasian populations have shown that a significant proportion of patients with NAFLD do not have insulin resistance (IR).Further, even with elevated hepatic triacylglycerol and diacylglycerol content, hepatic IR has not been observed in murine models,and dissociation of hepatic steatosis from IR has also been noted in a subset of individuals. Importantly, in subjects with PNPLA3 polymorphisms,steatosis occurs independently of IR and serum lipid concentration. Further, increased serum bile acid levels also seem to be independently associated with NASH in non-diabetics.NAFLD is also associated with gut dysbiosis independent of BMI and IR. Finally, \u201csoft\u201d drink consumption has also been linked to the development of fatty liver independent of obesity, diabetes and hyperlipidemia.and last but not least, cigarette smoking too has been found to be an independent risk factor in NAFLD progression. Thus it is clear that pathogenesis of NAFLD is multifactorial and complex, involving multiple and divergent pathways.In Medicine, a change of name of any disease has significant implications for both medical professionals and patients.The term \u2018NAFLD\u2019 aptly describes individuals who have fatty liver but neither consume significant amounts of alcohol nor had any other reason for fatty liver. Research in NAFLD to date has failed to pinpoint any factor as the sole cause for hepatic steatosis and NAFLD still encompasses a spectrum of disorders, metabolic syndrome being a part \u2013 maybe a major part \u2013 of that spectrum with a relatively barren treatment armamentarium. Will changing nomenclature address these concerns? We fear it might paradoxically misdirect therapeutics in the direction of MS alone which may ultimately turn out to be a red herring. The consensus group found multiple faults with the term NAFLD; these include: i) NAFLD is a disease of exclusion instead of being defined by inclusion, ii) NAFLD is a vastly heterogeneous entity and cannot be managed as one single condition and iii) patients with NAFLD do consume alcohol and the impact of alcohol, albeit in non-significant amounts, is under scrutiny. In Medicine, naming a disease through exclusion has been acceptable since time immemorial. Non-Hodgkin lymphoma encompasses vastly diverse malignancies and yet the terminology very effectively delineates those disorders from Hodgkin lymphoma. Regarding heterogeneity, it is not clear how a mere change of name would make the entity more homogeneous. If the word \u201cmetabolic\u201d in MAFLD is meant as a reference to MS, it would be a rejection of much of the scientific evidence gathered on NAFLD pathogenesis. In contrast to the assertion of the proponents of MAFLD, who after splitting \u201cnonalcoholic\u201d into - \u2018non\u2019 and \u2018alcoholic\u2019, suggest that the word \u201cnon\u201d trivializes the problem while the word \u201calcoholic\u201d demeans the patient, we believe that the word \u2018nonalcoholic\u2019 does go a long way in destigmatizing the patient. The European Liver Patients Association (ELPA) is believed to have expressed displeasure with the term NAFLD to the European Commission in 2018, and suggested that a change in nomenclature was required. The degree of assertion and the rationale for such a suggestion are unclear; it is also unclear whether the diverse pathogenesis of NAFLD \u2013 especially in non-Caucasians \u2013 was considered in the decision. Further, an opinion on the impact of non-significant alcohol intake on hepatic steatosis is also unclear as acknowledged in the consensus statement. Notably, metabolic abnormalities and BMI are well described risk factors for alcoholic liver disease too,but it is unclear why both conditions more or less related to alcohol should be brought under the umbrella of MAFLD. The change of nomenclature has also been argued against since NAFLD is treated by cardiologists, diabetologists and primary care providers in addition to hepatologists; a name change could create unnecessary clinical confusion and coding issues. The heterogeneity of NAFLD and presence of multiple pathophysiological pathways inherent to its progression implies that the time is ripe to classify NAFLD in a novel way that takes into account the various pathophysiological processes. We wish to propose the \u2018MEGA-D\u2019 classification emphasising the \u2018mega diversity\u2019 or heterogeneity in NAFLD where NAFLD remains the umbrella entity with different subgroups under it (NAFLD-M: Metabolic syndrome associated NAFLD, NAFLD-E: Environmental Stressor Related NAFLD, NAFLD-G: Genetic Factor Associated NAFLD, NAFLD-A: Bile Acid Dysregulation Related NAFLD, NAFLD-D: Gut Dysbiosis Related NAFLD) representing separate pathways culminating in hepatic steatosis. We feel, instead of semantic juggling, collaborative efforts should be launched worldwide to better understand the vast heterogeneity in NAFLD across populations and ethnicities and explore its different pathophysiologic mechanisms, with the sole purpose of modifying disease progression, bolstering the treatment arsenal and curbing this epidemic