Dexmedetomidine as an adjuvant to 0.5% ropivacaine in ultrasound-guided axillary brachial plexus block.

WHAT IS KNOWN AND OBJECTIVE: The aim of this study was to elucidate the effect of dexmedetomidine added to ropivacaine on the onset and duration of sensory and motor block and duration of analgesia of ultrasound-guided axillary brachial plexus block. METHODS: Thirty-seven ASA physical status I-II patients with elective forearm and hand surgery under ultrasound-guided axillary brachial plexus block were randomly divided into 2 groups. Patients in ropivacaine-dexmedetomidine group (group RD, n = 19) received 15 mL of 0.5% ropivacaine with 100 µg (1 mL) dexmedetomidine, and patients in ropivacaine group (group R, n = 18) received 15 mL of 0.5% ropivacaine with 1 mL of normal saline. Onset time and duration of sensory and motor block and duration of analgesia were assessed. RESULTS AND DISCUSSION: Duration of sensory block (U-value = 35, P < .001), duration of motor block (P = .001) and duration of analgesia (P < .001) were extended in group RD compared to group R. Onset time of sensory block in group RD was significantly faster than in group R (U-value = 65.5, P = .001). Onset time of motor block showed no significant difference between the 2 groups (U-value = 116.5, P = .096). Adverse reactions were reported only in group RD (bradycardia in 2 and hypotension in 3 patients). WHAT IS NEW AND CONCLUSION: Our study indicated that dexmedetomidine 100 µg as adjuvant on ultrasound-guided axillary plexus block significantly prolonged the duration of sensory block and analgesia, as well as accelerated the time to onset of sensory block. These results should be weighed against the increased risks of motor block prolongation, transient bradycardia and hypotension and allow for attentive optimism, only if prolonged clinical trials provide a definitive answer.

Gigantic hepatic amebic abscess presenting as acute abdomen: a case report.

INTRODUCTION: Amebiasis is a parasitic disease caused by Entamoeba histolytica. It most commonly results in asymptomatic colonization of the gastrointestinal tract, but some patients develop intestinal invasive or extra-intestinal diseases. Liver abscess is the most common extra-intestinal manifestation. The large number of clinical presentations of amebic liver abscess makes the diagnosis very challenging in non-endemic countries. Late diagnosis of the amebic abscess may lead to perforation and amebic peritonitis, resulting in high mortality rates. CASE PRESENTATION: This report describes a 37-year-old white man, suffering from hepatitis B, with a gigantic amebic liver abscess presenting as an acute abdomen due to its rupture. Rapid deterioration of the patient's condition and acute abdomen led to an emergency operation. A large volume of free fluid together with debris was found at the moment of entry into the peritoneal cavity because of a rupture of the hepatic abscess at the position of the segment VIII. Surgical drainage of the hepatic abscess was performed; two wide drains were placed in the remaining hepatic cavities and one on the right hemithorax. The patient was hospitalized in the ICU for 14 days and for another 14 days in our department. The diagnosis of amebic abscess was made by the pathologists who identified E. histolytica in the debris. CONCLUSION: Acute abdomen due to a ruptured amebic liver abscess is extremely rare in western countries where the parasite is not endemic. Prompt diagnosis and treatment are fundamental to preserving the patient's life since the mortality rates remain extremely high when untreated, even nowadays.