[show abstract][hide abstract] ABSTRACT: Marking of surgical instruments is essential to ensure their proper identification after sterile processing. The National Quality Forum defines unintentionally retained foreign objects in a surgical patient as a serious reportable event also called "never event."
We hypothesize that established practices of surgical instrument identification using unkempt tape labels and plastic tags may expose patients to "never events" from retained disintegrating labels.Testing of the hypothesis: We demonstrate the near miss of a "never event" during a surgical case in which the breakage of an instrument label remained initially unwitnessed. A fragment of the plastic label was accidentally found in the wound upon closing. Further clinical testing of the occurrence of this "never event" appears not feasible. As the name implies a patient should never be exposed to the risk of fragmenting labels.Implication of the hypothesis: Current practice does not mandate verifying intact instrument markers as part of the instrument count. The clinical confirmation of our hypothesis mandates a change in perioperative practice: Mechanical labels need to undergo routine inspection and maintenance. The perioperative count must not only verify the quantity of surgical instruments but also the intactness of labels to ensure that no part of an instrument is left behind. Proactive maintenance of taped and dipped labels should be performed routinely. The implementation of newer labeling technologies - such as laser engraved codes - appears to eliminate risks seen in traditional mechanical labels.This article reviews current instrument marking technologies, highlights shortcomings and recommends safe instrument handling and marking practices implementing newer available technologies.
[show abstract][hide abstract] ABSTRACT: Penetrating injuries to the hand can compromise important anatomic structures, and persisting foreign objects may become a source of infection. Foreign body intrusions into the hand are among the most common injuries to the upper extremity seen in the Emergency Department. Radiolucent organic objects, as well as a few higher density inorganic materials such as plastic, present a diagnostic challenge and are routinely missed using standard radiography. While the literature describes the use of high-frequency ultrasound as an adjunct to conventional diagnostics, to our knowledge, no formal algorithm has been published.
We describe a case of incomplete wooden splinter removal, presenting as a late midpalmar abscess five months after the initial injury, and requiring two subsequent surgical explorations for definitive treatment. This case has led us to implement a formal diagnostic pathway including high-frequency ultrasound at our institution. We contrast this presentation with a subsequent case involving a much smaller wooden palmar foreign body that was easily identified under ultrasound and removed without sequelae.
Many hand injuries are caused by low density, radiolucent foreign bodies. These objects can easily escape traditional evaluation in the emergency room including standard radiography. We present an algorithm implementing high frequency ultrasound to minimize the risk of missing radiolucent penetrating foreign objects in the hand.
[show abstract][hide abstract] ABSTRACT: Sweeping injuries of the elbow characterized by traumatic loss of medial or lateral epicondyles, collateral ligaments, and surrounding soft tissue result in loss of joint stability. Reconstruction of medial or lateral collateral ligaments is challenging due to loss of the cortical bone and the resultant difficulty in identifying the isometric attachment point. We describe a unique injury pattern and a surgical technique to restore joint stability using a bone tendon (Achilles) allograft. The technique was applied to 4 consecutive patients with a mean age of 35 (22-57) years and a mean follow-up of 20 months. Three patients with the lateral sweep injury had losses of the lateral epicondyle, lateral collateral ligament along with radial nerve palsy in 2. One patient with the medial sweep injury lost the medial epicondyle, medial collateral ligament, and had ulnar nerve palsy. All patients had an unstable ulnohumeral joint and underwent bone-tendon allograft (Achilles) reconstruction. The elbow joint was covered with a rotational radial forearm flap in 1 patient: myofasciocutaneous-free gracilis flap in 1 and rotational fasciomyocutaneous latissimus dorsi flap in 2 patients. One patient had an open reduction and internal fixation of distal third humerus shaft fracture, intercalary nerve grafting to the ulnar nerve, and repair of the brachial artery. At the final follow-up, average elbow motion was 115 degrees. Radiographic bone-to-bone healing was achieved in all patients. According to the American Shoulder and Elbow Surgeon's Assessment; average patient rated pain, function, and satisfaction scores were 3.4, 2.3, and 5, respectively. The average Disabilities of the Arm, Shoulder and Hand questionnaire score was 25. The use of bone-tendon allograft to reconstruct collateral ligaments of the elbow restored the elbow stability with a satisfactory functional outcome (evidence: level 4).
Journal of orthopaedic trauma 04/2012; · 1.78 Impact Factor
[show abstract][hide abstract] ABSTRACT: Sepsis continues to be a poorly understood syndrome with a high mortality rate. While we are beginning to decipher the intricate interplay of the inflammatory response during sepsis, the precise regulation of the hypothalamic-pituitary-adrenal (HPA) axis and its impact on electrolyte homeostasis during sepsis remains incompletely understood.
Sepsis was induced in adult male Sprague-Dawley rats by cecal ligation and puncture (CLP). Plasma samples were obtained as a function of time (6-48 hrs) after CLP and compared with healthy animals (neg ctrl). Samples were analyzed for adrenocorticotropin (ACTH), corticosterone, and aldosterone levels, as well as concentrations of sodium (Na+), potassium (K+), chloride (Cl-), and magnesium (Mg2+).
ACTH levels were found to be significantly reduced 6-24 hrs after CLP in comparison to baseline levels and displayed gradual recovery during the later course (24-48 hrs) of sepsis. Plasma corticosterone concentrations exhibited a bell-shaped response, peaking between 6 and 12 hrs followed by rapid decline and concentrations below negative control levels 48 hrs after injury. Aldosterone levels in septic animals were continuously elevated between 6 and 48 hrs. Whereas plasma Na+ levels were found to be persistently elevated following CLP, levels of K+, Cl- and Mg2+ were significantly reduced as a function of time and gradually recovered during the later course of sepsis.
CLP-induced sepsis resulted in dynamic changes of ACTH, corticosterone, and aldosterone levels. In addition, electrolyte levels showed significant disturbances after CLP. These electrolyte perturbations might be evoked by a downstream effect or a dysfunctional HPA-axis response during sepsis and contribute to severe complications during sepsis.
[show abstract][hide abstract] ABSTRACT: Two cohorts of patients who had corrective osteotomies and volar platings for malunited fractures of the distal radius were compared retrospectively to determine whether the time to union and the outcome were affected by bone allograft.
Patients in the first group (n = 14) did not receive any bone graft; patients in the second group (n = 14) had allograft bone chips following volar plating. Indications for surgery, surgical technique, and postoperative rehabilitation were the same in both groups. Volar cortical contact was maintained using a volar locking plate in all patients. Radiographic parameters of deformity correction, time to union, wrist and forearm range of motion, grip strength, patient-rated wrist evaluation and Disabilities of the Arm, Shoulder, and Hand questionnaire were used to evaluate the outcome before and after the surgery. Average follow-up time was 36 weeks. Patients who had diabetes, who smoked, who had a body mass index of more than 35, and who required lengthening for deformity correction were excluded from the study.
Osteotomies in both groups healed without loss of surgical correction. Final outcome and time to union revealed no significant differences, clinically or statistically, between the 2 groups. The Disabilities of the Arm, Shoulder, and Hand score was improved in both groups.
When volar cortical contact was maintained using a volar locked plate, bone allograft at the osteotomy site did not improve the final outcome.
The Journal of hand surgery 11/2011; 36(11):1804-9. · 1.33 Impact Factor
[show abstract][hide abstract] ABSTRACT: Burn injury is frequently complicated by bacterial infection. Following burn injury, exposure to endotoxin produces a measurable decrease in cardiomyocyte sarcomere contractile function. Lipopolysaccharide-binding protein (LBP) is an acute phase protein that potentiates the recognition of lipopolysaccharide (LPS) by binding to the lipid A moiety of LPS. In this study, we sought to determine the effect of recombinant rat LBP (rLBP) on cardiomyocyte sarcomere function after burn or sham injury in the presence or absence of bacterial endotoxin.
Rats underwent a full-thickness 30% total body surface area scald or sham burn. At 24 h post-injury, cardiomyocytes were isolated, plated at 50,000 cells/well, and incubated with 50 μg/mL LPS and rLBP or chloramphenicol acetyltransferase (BVCat, an irrelevant control protein produced using the same expression system as rLBP) at concentrations by volume of 1%, 5%, 10%, and 30%. Subsets of cardiomyocytes were incubated with 5% rat serum or 30% rLBP and blocking experiments were conducted using an LBP-like synthetic peptide (LBPK95A). In vitro sarcomere function was measured using a variable rate video camera system with length detection software.
Co-culture of burn and sham injury derived cardiomyocytes with high-dose rLBP in the presence of LPS resulted in a significant reduction to the functional impairment observed in peak sarcomere shortening following exposure to LPS alone. LBP-like peptide LBPK95A at a concentration of 20 μg/mL, in the presence of LPS, abolished the ability of 30% rLBP and 5% rat serum to restore peak sarcomere shortening of cardiomyocytes isolated following burn injury to levels of function exhibited in the absence of endotoxin exposure.
In the setting of LPS challenge following burn injury, rLBP at high concentrations restores cardiomyocyte sarcomere contractile function in vitro. Rather than potentiating the recognition of LPS by the cellular LPS receptor complex, rLBP at high concentrations likely results in an inhibitory binding effect that minimizes the impact of endotoxin exposure on cardiomyocyte function following thermal injury.
Journal of Surgical Research 01/2011; 165(1):128-35. · 2.02 Impact Factor
[show abstract][hide abstract] ABSTRACT: An alcoholic 50-year-old male patient with a history of schizophrenia sustained stab wounds into both ventricles and left lung, and survived following an emergency department thoracotomy. The EDT wound, however became infected requiring serial debridements of soft tissue, rib cartilage and sternum. Regional flap options such as pectoralis major and latissimus dorsi muscle flaps could not be employed due to inadequate reach of these flaps. Additionally, bilateral transection of the internal mammary arteries during emergency thoracotomy eliminated the use of rectus abdominis muscles as pedicled flaps based on the superior epigastric vasculature. Therefore, the EDT wound was reconstructed by using the right rectus abdominis muscle as a free flap. The deep inferior epigastric vessels of the flap were anastomosed to the right internal mammary vessels proximal to their transection level in the third-forth intercostal space. The flap healed with no further wound complications.
World Journal of Emergency Surgery 01/2010; 5:12. · 0.92 Impact Factor
[show abstract][hide abstract] ABSTRACT: Introduction: Many studies have demonstrated the existence of an anti-inflammatory, parasympathetic pathway, termed as the inflammatory reflex. Burn-induced heart failure has been investigated in many previous studies. Proinflammatory cytokines, such as TNF-alpha, IL-1beta, and IL-6, have been shown to play a key pathogenetic role and vagus nerve stimulation attenuates proinflammatory cytokine production. This study was designed to evaluate postburn alterations of cardiac functional parameters after vagal electrostimulation. Material and Methods: A 30% total body surface area standardized, full-thickness rat burn model was used. Electric stimulation of the vagus nerve was performed. The following functional cardiac parameters were measured by ventricular microcatheterization: Maximal and minimal left ventricular pressure, mean left ventricular pressure, end-diastolic pressure (EDP), positive and negative pressure rise and fall (+/-dP/dt), cardiac contractility index, and assessment of the heart rate. Results: Vagus nerve stimulation improved maximal and minimal left ventricular pressure values compared with burn-only animals. End-diastolic pressure was elevated significantly in stimulated animals; however, EDP values were comparable with those in sham-injured animals. Analyzing positive and negative pressure development, +/-dP/dt was restored to levels measured in sham-injured animals but not to control animal levels. No variations in heart rate were found. Conclusion: We as well as others have shown that inflammation after burn injury is a key pathogenetic element, and this study provides new evidence that cardiac function is also improved by vagus nerve stimulation. These results lead us to consider novel therapeutic options for the treatment of postburn cardiac dysfunction.
[show abstract][hide abstract] ABSTRACT: Topical inhibition of activated p38 MAPK within burn wounds attenuates the local and systemic inflammatory response. In this study, we investigated the effects of local activated p38 MAPK inhibition on burn-induced cardiac dysfunction.
Using a standardized rat model of scald burn injury, rats were given a 30% total body surface area partial thickness burn or sham injury, and the wounds were treated with an activated p38 MAPK inhibitor (SB) or vehicle. Systemic blood pressure measurements were recorded in vivo followed by in vitro assessment of sarcomere contraction in single-cell suspensions of isolated cardiomyocytes.
Systolic blood pressure or maximum left ventricular pressures in vivo and peak cardiomyocyte sarcomere contractility in vitro were significantly reduced after burn injury. These functional deficits were abolished 24 h after burn injury following local p38 MAPK inhibition. In vitro incubation of normal cardiomyocytes with homogenate from burned skin or burn serum resulted in a similar pattern of impaired cardiomyocyte contractility. These effects were reversed in normal cardiomyocytes exposed to burn skin homogenates treated topically with a p38 MAPK inhibitor. A Western blot analysis showed that cardiac p38 MAPK activation was not affected by dermal blockade of activated p38 MAPK, arguing against systemic absorption of the inhibitor and indicating the involvement of systemic cytokine signaling.
Topical activated p38 MAPK inhibition within burned skin attenuates the release of proinflammatory mediators and prevents burn-induced cardiac dysfunction after thermal injury. These results support the inhibition of burn-wound inflammatory signaling as a new therapeutic approach to prevent potential postthermal injury multiorgan dysfunction syndrome.
Surgery 10/2009; 146(4):775-85; discussion 785-6. · 3.37 Impact Factor
[show abstract][hide abstract] ABSTRACT: The clinical appearance of septic disorders is characterized by an enormous dynamic. The sepsis-induced dysbalance of the immune system necessitates immediate and aggressive therapeutic interventions to prevent further damage progression of the disease to septic shock and multiple organ failure. This includes supportive therapy to normalize and maintain organ and tissue perfusion as well as the identification of the infection focus. In cases where an infectious focus is identified, surgical source control frequently is a key element of the treatment strategy besides pharmacologic and supportive measures. The integrative approach of the management of septic patients requires rapid communication between the involved medical disciplines and the nursing personnel. Therefore, this article outlines current therapeutic concepts of septic diseases as well as central nursing aspects.
Der Chirurg 09/2009; 80(10):934-46. · 0.52 Impact Factor
[show abstract][hide abstract] ABSTRACT: The interaction of the CNS and the immune system is well known. A parasympathetic anti-inflammatory pathway has recently been described. Both electrical and pharmacological parasympathetic stimulation attenuate proinflammatory mediator generation. Burn induces abacterial cytokine generation and we sought to evaluate whether parasympathetic stimulation after experimental burn decreases cardiodepressive mediator generation.
A 30% TBSA full-thickness rat burn model was used. After microsurgical preparation of the cervical portion of the vagus nerve, we performed electric vagus nerve stimulation. Serum was harvested and organ samples of heart and liver were homogenized. Samples were subjected to sandwich-ELISA specific for TNF-alpha, IL-1beta and IL-6. Heart rate measurements were done using left ventricular microcatheterization. Statistical analysis was done using Student's t-tests and analysis of variance (ANOVA).
Burn induced a significant rise of TNF-alpha, IL-1beta and IL-6 in organ homogenates and serum. After cervical vagal electrostimulation, serum and organ homogenate levels of proinflammatory cytokines were markedly reduced compared to burn controls. Left ventricular microcatheter assessment demonstrated no cardiodepressive effect of the vagal stimulation itself.
Our results encourage further research regarding the neuroimmunologic background of burn, possibly leading to the development of a novel therapeutic approach to burn-induced organ dysfunction and immunodysregulation.
Burns: journal of the International Society for Burn Injuries 06/2009; 35(6):783-9. · 1.95 Impact Factor
[show abstract][hide abstract] ABSTRACT: Despite significant advances in burn surgery and critical care, severe burn trauma defined as injuries covering more than 25% of the total body surface area, is still associated with high mortality and morbidity. Burn trauma is a whole body injury where peripheral dermal injury rapidly results in systemic inflammation and inflammatory core organ damage. The severe disturbance of internal homeostasis involves all vital organ systems and obligates early referral to specialized burn centers. Treatment of severely burned patients is a multifaceted challenge directed by pathophysiologic events which progress from local skin destruction, disruption of physicochemical and microvascular barriers to breakdown of peripheral and central circulation, organ failure and ultimately death. While early intensive care focuses on maintenance of tissue oxygenation and perfusion, surgical treatment deals with management of the burn wounds as a source of inflammation and infection. Here wound debridement and coverage is essential to abrogate systemic effects of inflammation and limit pathogen invasion. While control of early burn stages minimizes mortality due to burn shock, subsequent burn sepsis continues to be a formidable challenge for physicians and the main cause of burn mortality.
Der Unfallchirurg 06/2009; 112(5):472-8. · 0.64 Impact Factor
[show abstract][hide abstract] ABSTRACT: Septic encephalopathy secondary to a breakdown of the blood-brain barrier (BBB) is a known complication of sepsis. However, its pathophysiology remains unclear. The present study investigated the effect of complement C5a blockade in preventing BBB damage and pituitary dysfunction during experimental sepsis.
Using the standardised caecal ligation and puncture (CLP) model, Sprague-Dawley rats were treated with either neutralising anti-C5a antibody or pre-immune immunoglobulin (Ig) G as a placebo. Sham-operated animals served as internal controls.
Placebo-treated septic rats showed severe BBB dysfunction within 24 hours, accompanied by a significant upregulation of pituitary C5a receptor and pro-inflammatory cytokine expression, although gene levels of growth hormone were significantly attenuated. The pathophysiological changes in placebo-treated septic rats were restored by administration of neutralising anti-C5a antibody to the normal levels of BBB and pituitary function seen in the sham-operated group.
Collectively, the neutralisation of C5a greatly ameliorated pathophysiological changes associated with septic encephalopathy, implying a further rationale for the concept of pharmacological C5a inhibition in sepsis.
Critical care (London, England) 03/2009; 13(1):R12. · 4.72 Impact Factor
[show abstract][hide abstract] ABSTRACT: Severe burn injury remains a major burden on patients and healthcare systems. Following severe burns, the injured tissues mount a local inflammatory response aiming to restore homeostasis. With excessive burn load, the immune response becomes disproportionate and patients may develop an overshooting systemic inflammatory response, compromising multiple physiological barriers in the lung, kidney, liver, and brain. If the blood-brain barrier is breached, systemic inflammatory molecules and phagocytes readily enter the brain and activate sessile cells of the central nervous system. Copious amounts of reactive oxygen species, reactive nitrogen species, proteases, cytokines/chemokines, and complement proteins are being released by these inflammatory cells, resulting in additional neuronal damage and life-threatening cerebral edema. Despite the correlation between cerebral complications in severe burn victims with mortality, burn-induced neuroinflammation continues to fly under the radar as an underestimated entity in the critically ill burn patient. In this paper, we illustrate the molecular events leading to blood-brain barrier breakdown, with a focus on the subsequent neuroinflammatory changes leading to cerebral edema in patients with severe burns.
Critical care (London, England) 02/2009; 13(3):215. · 4.72 Impact Factor
[show abstract][hide abstract] ABSTRACT: Complications arising from accidental intraarterial drug injections have been described in the past. However, given the multitude of injected substances and complex pathophysiology, guidelines regarding diagnosis and management of patients with intraarterial injections remain vague. As such it remains unclear, when to expect limb ischemia and whether and for how long to monitor patients after intraarterial injections.
We present the case of a "near miss event" in an i.v. drug abuser presenting to the emergency department 3 hours after injection of water dissolved zolpidem (Ambientrade mark) tablets into the right ulnar artery. Chief complaint was forearm pain. Clinical examination at the time revealed no concern for limb ischemia and patient was discharged. The patient returned unplanned 18 hours after injection with an ischemic right hand. Angiography revealed no flow in the distal ulnar artery and minimal flow in the palmar arch. Emergent intraarterial thrombolysis with Urokinase was performed and restored hand perfusion. Clinical follow-up 3 months after injury showed full recovery with regular recapillarisation and normal Allen test.
This case report highlights the need to rigorously monitor patients with suspected intraarterial injections for potential delayed onset of limb ischemia. This is to our knowledge the first described case report of a successful revascularization after prolonged ischemia with delayed onset after zolpidem injection. We recommend close monitoring of these patients for at least 24 hours in addition to starting prophylactic anticoagulation.
[show abstract][hide abstract] ABSTRACT: Trotz erheblicher Fortschritte der chirurgischen und intensivmedizinischen Therapie besitzt das schwere Verbrennungstrauma
(>25% Körperoberfläche) eine weiterhin hohe Mortalität und Morbidität. Periphere Brandwunden lösen beim Schwerbrandverletzten
eine systemische Entzündungsreaktion aus, die rasch den Gesamtorganismus und die Vitalfunktionen erfasst. Die umgehende Patientenüberweisung
in ein Schwerbrandverletztenzentrum ist obligat. Nach thermischer Schädigung der physikochemischen Hautbarriere kommt es in
der Verbrennungswunde zur Aktivierung inflammatorischer Mediatoren, die den Zusammenbruch mikrovaskulärer Endothelbarrieren
mit Ödembildung sowie eine inflammatorische Organschädigung begünstigen. Die Primärbehandlung beinhaltet die Aufrechterhaltung
zellulärer Oxygenierung durch zielorientierte Volumensubstitution und die Stabilisierung des pulmonalen Gasaustauschs. Ein
frühes chirurgisches Débridement und die Deckung der Verbrennungswunde minimieren die Wundinfektion und bakterielle Invasion
und stabilisieren Flüssigkeits- wie Hitzeverluste. Inflammation und verbrennungsassoziierte Immunsuppression begünstigen die
Keiminvasion und Entwicklung der Verbrennungssepsis – ein Krankheitsbild, das trotz moderner Therapie Haupttodesursache auf
Despite significant advances in burn surgery and critical care, severe burn trauma defined as injuries covering more than
25% of the total body surface area, is still associated with high mortality and morbidity. Burn trauma is a whole body injury
where peripheral dermal injury rapidly results in systemic inflammation and inflammatory core organ damage. The severe disturbance
of internal homeostasis involves all vital organ systems and obligates early referral to specialized burn centers. Treatment
of severely burned patients is a multifaceted challenge directed by pathophysiologic events which progress from local skin
destruction, disruption of physicochemical and microvascular barriers to breakdown of peripheral and central circulation,
organ failure and ultimately death. While early intensive care focuses on maintenance of tissue oxygenation and perfusion,
surgical treatment deals with management of the burn wounds as a source of inflammation and infection. Here wound debridement
and coverage is essential to abrogate systemic effects of inflammation and limit pathogen invasion. While control of early
burn stages minimizes mortality due to burn shock, subsequent burn sepsis continues to be a formidable challenge for physicians
and the main cause of burn mortality.
Der Unfallchirurg 01/2009; 112(5):472-478. · 0.64 Impact Factor