ABSTRACT
Although percutaneous dilatational tracheostomy (PDT) is fast becoming the method of choice for securing an airway in chronic ventilated patients in an intensive care unit (ICU). Subcutaneous emphysema is an unusual and sometimes lethal complication which may extend the length of stay in the ICU. We report a case of massive subcutaneous emphysema without tracheal wall laceration that occurred in the ICU after PDT. An 81-year-old woman was admitted to our ICU due to infective exacerbation of chronic obstructive airways disease. Her medical therapy included nebulized bronchodilators, steroids and empirical antibiotics. Within thirty-six hours of initial endotracheal intubation PDT was performed. Several hours following the procedure, the patient developed massive subcutaneous emphysema encompassing her entire body. No pneumothorax was identified on subsequent chest X-ray. Laryngoscopic and bronchoscopic examination showed no evidence of tracheal wall laceration. We discuss the etiology and management plan for this rare complication.
Subject(s)
Postoperative Complications , Subcutaneous Emphysema , Tracheostomy , Aged, 80 and over , Chronic Disease , Fatal Outcome , Female , Humans , Postoperative Complications/etiology , Postoperative Complications/therapy , Pulmonary Disease, Chronic Obstructive/surgery , Subcutaneous Emphysema/etiology , Subcutaneous Emphysema/therapy , Tracheostomy/methodsABSTRACT
UNLABELLED: Previously, we reported that propofol hyperpolarizes vascular smooth muscle (VSM) cells of small arteries and veins. The current study was designed to determine whether propofol-mediated hyperpolarization is the result of specific effects on potassium channels known to exist in VSM and on steps in the intracellular nitric oxide (NO), cyclic guanosine monophosphate (cGMP), and cyclic adenosine monophosphate (cAMP) second messenger pathways. VSM transmembrane potentials (E(m)) were measured in situ in sympathetically denervated, small mesenteric arteries and veins of Sprague-Dawley rats. Effects of propofol on VSM E(m) were determined before and during superfusion with specific inhibitors of VSM calcium-activated (K(Ca)), adenosine triphosphate-sensitive (K(ATP)), voltage-dependent (K(v)), and inward rectifying (K(IR)) potassium channels and with endogenous mediators of vasodilation. Propofol significantly hyperpolarized VSM in small mesenteric vessels. This hyperpolarization was abolished on inhibition of K(Ca) and K(ATP) channel activity and on inhibition of NO and cGMP (but not cAMP). Assuming a close inverse correlation between the magnitude of VSM E(m) and contractile force, these results suggest that propofol induces hyperpolarization and relaxation in denervated, small mesenteric vessels by activation of K(Ca) and K(ATP) channels. Such channel activation may be mediated by activation of NO and cGMP, but not cAMP, second messenger pathways. IMPLICATIONS: The results of this study indicate that propofol-mediated hyperpolarization in vascular smooth muscle can be attributed to the activation of calcium-activated, adenosine triphosphate-sensitive potassium channels, the nitric oxide, and cyclic guanosine monophosphate pathways.
Subject(s)
Anesthetics, Intravenous/pharmacology , Mesenteric Arteries/drug effects , Mesenteric Veins/drug effects , Muscle, Smooth, Vascular/drug effects , Propofol/pharmacology , Animals , Blood Pressure/drug effects , Cyclic AMP/antagonists & inhibitors , Cyclic AMP/physiology , Cyclic GMP/antagonists & inhibitors , Cyclic GMP/physiology , Enzyme Inhibitors/pharmacology , In Vitro Techniques , Injections, Intravenous , Male , Membrane Potentials/drug effects , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide/physiology , Nitric Oxide Synthase/antagonists & inhibitors , Nitric Oxide Synthase Type III , Potassium Channels/drug effects , Rats , Rats, Sprague-Dawley , Second Messenger Systems/drug effects , Sympathectomy , Sympathetic Nervous System/physiologyABSTRACT
UNLABELLED: We indirectly assessed the in vivo effect of propofol on sympathetic neural and endothelial control of vascular smooth muscle (VSM) tone in Sprague-Dawley rats by measurement of in situ responses of VSM transmembrane potential (E(m)) in intact, small mesenteric arteries and veins superfused with physiologic salt solution. Measurements were made before, during, and after propofol infusion (10 and 30 mg x kg(-1) x h(-1)) in sympathetically innervated and locally denervated vessels. Propofol's effect on E(m) response to superfusion with acetylcholine (ACh), in physiologic salt solution also containing NG-nitro-L-arginine-methyl-ester and indomethacin, was determined in innervated vessels. At 30 mg x kg(-1) x h(-1), propofol caused greater arterial VSM hyperpolarization in innervated compared with denervated vessels (4.8 +/- 2.0 mV versus 2.8 +/- 1.5 mV, respectively). ACh hyperpolarized arterial, but not venous, VSM (e.g., 11.7 +/- 2.4 mV at 10(-4) M). ACh-induced hyperpolarization was eliminated by 30 mg x kg(-1) x h(-1) propofol. Assuming a close inverse correlation between magnitude of VSM E(m) and contractile force, these results suggest that propofol attenuates both sympathetic neural and nonneural regulation of VSM tone. They also suggest that propofol and ACh may act competitively in the second messenger cascade regulating VSM K+ channel activity in mesenteric resistance arteries. IMPLICATIONS: Vascular smooth muscle (VSM) contractile force responses to the IV anesthetic, propofol, were indirectly assessed by VSM membrane potential changes to clarify the mechanisms underlying attenuation of peripheral vascular control of arterial blood pressure. Results indicate that propofol-induced VSM membrane hyperpolarization and coupled reduction of VSM contractile force underlie such attenuation.
