Deep venous thrombosis revealed during ultrasound-guided femoral nerve block.

Ultrasound imaging used to facilitate performance of a femoral nerve block also affords imaging of adjacent anatomical structures. Following a fracture of the femur, an ultrasound guided femoral nerve block (UGFNB) was performed to provide analgesia; this led to the incidental finding of a previously undiagnosed femoral vein thrombosis (DVT), resulting in a change in patient management before surgery. An inferior vena cava (IVC) filter was placed before intramedullary nailing of the fracture.

Ultrasound-guided infraclavicular brachial plexus block.

BACKGROUND: Peripheral nerve blocks are almost always performed as blind procedures. The purpose of this study was to test the feasibility of seeing individual nerves of the brachial plexus and directing the block needle to these nerves with real time imaging. METHODS: Using ultrasound guidance, infraclavicular brachial plexus block was performed in 126 patients. Important aspects of this standardized technique included (i) imaging the axillary artery and the three cords of the brachial plexus posterior to the pectoralis minor muscle, (ii) marking the position of the ultrasound probe before introducing a Tuohy needle, (iii) maintaining the image of the entire length of the needle at all times during its advancement, (iv) depositing local anaesthetic around each of the three cords and (v) placing a catheter anterior to the posterior cord when indicated. RESULTS: In 114 (90.4%) patients, an excellent block permitted surgery without a need for any supplemental anaesthetic or conversion to general anaesthesia. In nine (7.2%) patients local or perineural administration of local anaesthetic, and in three (2.4%) conversion to general anaesthesia, was required. Mean times to administer the block, onset of block and complete block were 10.0 (SD 4.4), 3.0 (1.3) and 6.7 (3.2) min, respectively. Mean lidocaine dose was 695 (107) mg. In one patient, vascular puncture occurred. In 53 (42.6%) patients, an indwelling catheter was placed, but only three required repeat injections, which successfully prolonged the block. CONCLUSION: The use of ultrasound appears to permit accurate deposition of the local anaesthetic perineurally, and has the potential to improve the success and decrease the complications of infraclavicular brachial plexus block.

Monitoring for suspected pulmonary embolism.

It is fortunate that serious embolic phenomena are uncommon because, with the exception of neurosurgery in the sitting position and cardiac surgery, thoracic echocardiography and the precordial Doppler device, the most sensitive indicators of embolism, are seldom used. Vigilance is required of the anesthesiologist to recognize the rapid fall in end-tidal PCO2, the usual first indicator of a clinically significant PE. Any sudden deterioration in the patient's vital signs should include embolism in the differential diagnosis, particularly during procedures that carry a high risk of the complication.

Guidelines for the treatment of acidaemia with THAM.

THAM (trometamol; tris-hydroxymethyl aminomethane) is a biologically inert amino alcohol of low toxicity, which buffers carbon dioxide and acids in vitro and in vivo. At 37 degrees C, the pK (the pH at which the weak conjugate acid or base in the solution is 50% ionised) of THAM is 7.8, making it a more effective buffer than bicarbonate in the physiological range of blood pH. THAM is a proton acceptor with a stoichiometric equivalence of titrating 1 proton per molecule. In vivo, THAM supplements the buffering capacity of the blood bicarbonate system, accepting a proton, generating bicarbonate and decreasing the partial pressure of carbon dioxide in arterial blood (paCO2). It rapidly distributes through the extracellular space and slowly penetrates the intracellular space, except for erythrocytes and hepatocytes, and it is excreted by the kidney in its protonated form at a rate that slightly exceeds creatinine clearance. Unlike bicarbonate, which requires an open system for carbon dioxide elimination in order to exert its buffering effect, THAM is effective in a closed or semiclosed system, and maintains its buffering power in the presence of hypothermia. THAM rapidly restores pH and acid-base regulation in acidaemia caused by carbon dioxide retention or metabolic acid accumulation, which have the potential to impair organ function. Tissue irritation and venous thrombosis at the site of administration occurs with THAM base (pH 10.4) administered through a peripheral or umbilical vein: THAM acetate 0.3 mol/L (pH 8.6) is well tolerated, does not cause tissue or venous irritation and is the only formulation available in the US. In large doses, THAM may induce respiratory depression and hypoglycaemia, which will require ventilatory assistance and glucose administration. The initial loading dose of THAM acetate 0.3 mol/L in the treatment of acidaemia may be estimated as follows: THAM (ml of 0.3 mol/L solution) = lean body-weight (kg) x base deficit (mmol/L). The maximum daily dose is 15 mmol/kg for an adult (3.5L of a 0.3 mol/L solution in a 70kg patient). When disturbances result in severe hypercapnic or metabolic acidaemia, which overwhelms the capacity of normal pH homeostatic mechanisms (pH < or = 7.20), the use of THAM within a 'therapeutic window' is an effective therapy. It may restore the pH of the internal milieu, thus permitting the homeostatic mechanisms of acid-base regulation to assume their normal function. In the treatment of respiratory failure, THAM has been used in conjunction with hypothermia and controlled hypercapnia. Other indications are diabetic or renal acidosis, salicylate or barbiturate intoxication, and increased intracranial pressure associated with cerebral trauma. THAM is also used in cardioplegic solutions, during liver transplantation and for chemolysis of renal calculi. THAM administration must follow established guidelines, along with concurrent monitoring of acid-base status (blood gas analysis), ventilation, and plasma electrolytes and glucose.

Prolongation of lidocaine spinal anesthesia with phenylephrine.

The effect of added phenylephrine on the duration of sensory analgesia during lidocaine spinal anesthesia was determined in 65 ASA class I-III patients randomly divided into three groups. Group 1 (n = 25) received 62.5 mg lidocaine in 7.5% glucose; group 2 (n = 21) received lidocaine with 2 mg phenylephrine; and group 3 (n = 19) received lidocaine with 5 mg phenylephrine. The level of analgesia to pin prick was assessed by an anesthesiologist unaware of the drug combination used. The mean +/- SD cephalad level of analgesia did not differ among the groups. In group 1, the times for two- and for four-segment regression of the level of analgesia, and the time for regression of analgesia to the T-12 dermatome, were 77 +/- 19 (1 SD), 99 +/- 24, and 109 +/- 26 min, respectively. The corresponding values were 98 +/- 25, 118 +/- 27, and 130 +/- 36 min in group 2 and 124 +/- 32, 142 +/- 31, and 162 +/- 35 min in group 3. All the regression times in group 2 were significantly longer than those in group 1 (P less than 0.05). All the regression times in group 3 were significantly longer than those in group 2 (P less than 0.02). It is concluded that clinically useful prolongation of sensory analgesia may be obtained by addition of phenylephrine to lidocaine during spinal anesthesia.

Arterial to end-tidal CO2 gradients during spontaneous breathing, intermittent positive-pressure ventilation and jet ventilation.

Arterial to end-tidal CO2 tension gradients were measured in 18 dogs during spontaneous breathing (SB), intermittent positive-pressure ventilation (IPPV), and both low-frequency and high-frequency jet ventilation (LFJV and HFJV). The dogs were anesthetized with nembutal and permitted to breathe spontaneously through an 8-mm internal diameter endotracheal tube; blood gas tensions, cardiac output, and end-tidal CO2 partial pressure (PetCO2) were measured. IPPV, LFJV, and HFJV were then instituted in a random sequence and measurements repeated. PaO2, PaCO2 and cardiac output were similar during all four ventilatory modes. The mean PaCO2 differed significantly (p less than .001) from PetCO2 during IPPV, LFJV, and HFJV but not during SB. The mean PaCO2-PetCO2 gradient was 3.7 +/- 1 (SD), 12.6 +/- 5.0, and 24.3 +/- 8 torr during IPPV, LFJV and HFJV, respectively. The large gradients during LFJV and HFJV were not produced by dilution of tracheal CO2 by entrained air or by oxygen delivered by the jet. These results suggest that both LFJV and HFJV may be associated with a large PaCO2-PetCO2 gradient.

Antidepressants do not increase the lethality of ketamine in mice.

Swiss-Webster mice were allocated to 35 groups of 20 each, including controls, to evaluate the effect of pretreatment with antidepressant drugs on the LD50 of ketamine i.p. Deaths occurred only in groups given ketamine 400 or 600 mg kg-1. Within these groups, there were no consistent differences among untreated mice and those given one of three daily doses of either a tricyclic (amitriptyline) or monoamine oxidase inhibitor (tranylcypromine) antidepressant in their drinking water for 19 days before the ketamine injections. The ketamine LD50 values for the three major pretreatment groups were: controls 400 mg kg-1; amitriptyline 478 mg kg-1; tranylcypromine 483 mg kg-1. Although non-fatal additive toxicity is not ruled out by these findings, mortality from ketamine was not increased by pretreatment with either type of antidepressant.