Unrecognized hand ischemia after intraarterial drug injection: successful management of a "near miss" event

<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Case report</p> <p>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 (Ambien™) 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.</p> <p>Conclusion</p> <p>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.</p

Reconstruction of an emergency thoracotomy wound with free rectus abdominis flap: Anatomic and radiologic basis for the surgical technique

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

Vascular injuries after minor blunt upper extremity trauma: pitfalls in the recognition and diagnosis of potential "near miss" injuries

<p>Abstract</p> <p>Background</p> <p>Low energy trauma to the upper extremity is rarely associated with a significant vascular injury. Due to the low incidence, a high level of suspicion combined with appropriate diagnostic algorithms are mandatory for early recognition and timely management of these potentially detrimental injuries.</p> <p>Methods</p> <p>Review of the pertinent literature, supported by the presentation of two representative "near miss" case examples.</p> <p>Results</p> <p>A major diagnostic pitfall is represented by the insidious presentation of significant upper extremity arterial injuries with intact pulses and normal capillary refill distal to the injury site, due to collateral perfusion. Thus, severe vascular injuries may easily be missed or neglected at the upper extremity, leading to a long-term adverse outcome with the potential need for a surgical amputation.</p> <p>Conclusion</p> <p>The present review article provides an outline of the diagnostic challenges related to these rare vascular injuries and emphasizes the necessity for a high level of suspicion, even in the absence of a significant penetrating or high-velocity trauma mechanism.</p

Inhibition of complement C5a prevents breakdown of the blood-brain barrier and pituitary dysfunction in experimental sepsis

INTRODUCTION: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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

An essential role for complement C5a in the pathogenesis of septic cardiac dysfunction

Defective cardiac function during sepsis has been referred to as “cardiomyopathy of sepsis.” It is known that sepsis leads to intensive activation of the complement system. In the current study, cardiac function and cardiomyocyte contractility have been evaluated in rats after cecal ligation and puncture (CLP). Significant reductions in left ventricular pressures occurred in vivo and in cardiomyocyte contractility in vitro. These defects were prevented in CLP rats given blocking antibody to C5a. Both mRNA and protein for the C5a receptor (C5aR) were constitutively expressed on cardiomyocytes; both increased as a function of time after CLP. In vitro addition of recombinant rat C5a induced dramatic contractile dysfunction in both sham and CLP cardiomyocytes, but to a consistently greater degree in cells from CLP animals. These data suggest that CLP induces C5aR on cardiomyocytes and that in vivo generation of C5a causes C5a–C5aR interaction, causing dysfunction of cardiomyocytes, resulting in compromise of cardiac performance