Polymicrobial odontogenic periorbital and orbital necrotizing fasciitis (PONF): A case report.

PURPOSE: To present a case of periorbital and orbital necrotizing fasciitis (PONF) from an odontogenic source with a distinct microbiologic profile and highlight the need for emergent multidisciplinary management. OBSERVATIONS: A 39-year-old man presented with periorbital swelling, pain, and erythema following facial trauma. Imaging revealed peri-dental collections, accompanying maxillary sinusitis, and pre- and post-septal involvement. Immediate surgical debridement of necrotic tissue along with broad-spectrum antibiotics were pursued for management. Cultures grew multiple organisms, most notably Streptococcus milleri group and Staphylococcus lugdunensis. CONCLUSIONS AND IMPORTANCE: PONF is a rare yet potentially fatal disease. Streptococcus milleri group and a fulminant course are to be suspected when the source is odontogenic. Timely multidisciplinary surgical debridement and medical management with intravenous antibiotics is critical for best outcomes.

Delayed periorbital hemorrhage in oculoplastic surgery patients on oral anticoagulants.

Periorbital hemorrhage is a potentially sight threatening surgical complication. The effect of new oral anticoagulants (NOACs) on hemorrhagic events after periorbital surgery has not been investigated. We describe four cases of severe delayed postoperative hemorrhage associated with NOACs, in addition to three cases in patients on traditional antithrombotic agents. Time of delayed hemorrhage ranged from postoperative day 2 to 6. Six patients required surgical intervention to achieve control of bleeding, and two patients required transfusion of blood products. Risk factors and management of this rare complication are discussed.

Factors Associated With Increased Risk of Serious Ocular Injury in the Setting of Orbital Fracture.

Importance: Orbital fractures are common in ocular trauma, and there is a need to develop predictive tools to estimate risk of concurrent ocular injury. Objective: To identify clinical and radiographic features that are associated with increased risk of substantial ocular injury in the setting of orbital fracture. Design, Setting, and Participants: Retrospective consecutive case series of patients who sustained orbital fractures between 2012 and 2018. Examinations were done at 1 of 2 level 1 trauma centers in the emergency or inpatient setting. A total of 430 consecutive patients (500 eyes) between 2012 and 2017 met inclusion criteria for the training sample. After building a predictive model, 88 additional consecutive patients (97 eyes) between 2017 and 2018 who met inclusion criteria were collected as a test sample. Main Outcomes and Measures: The primary outcome measure was substantial ocular injury distinct from orbital fracture. Results: The mean age of our patient population was 53.5 years (range, 16-100 years). The overall rate of substantial ocular injury was 20.4%, and the rate of injury requiring immediate ophthalmic attention was 14.4%. Five variables were found to be associated with increased risk of substantial ocular injury: blunt trauma with a foreign object (odds ratio [OR], 19.4; 95% CI, 6.3-64.1; P < .001), inability to count fingers (OR, 10.1; 95% CI, 2.8-41.1; P = .002), roof fracture (OR, 9.1; 95% CI, 2.8-30.0; P = .002), diplopia on primary gaze (OR, 6.7; 95% CI, 1.7-25.1; P = .003), and conjunctival hemorrhage or chemosis (OR, 4.2; 95% CI, 2.2-8.5; P < .001). The results were translated into a bedside tool that was tested in an independent group of eyes (n = 97) and found to be associated with substantial ocular injury with a 95% sensitivity (95% CI, 77.2-99.9), 40% specificity (95% CI, 28.9-52.0), 31.8% positive predictive value (95% CI, 27.5-36.5), and 96.8% negative predictive value (95% CI, 81.3-99.5). Conclusions and Relevance: A minority of patients with an orbital fracture had a substantial ocular injury. Certain radiographic and clinical findings were associated with substantial ocular injury. Testing of the algorithm in prospective longitudinal settings appears warranted.

Role of connexin40 in the autoregulatory response of the afferent arteriole.

Connexins in renal arterioles affect autoregulation of arteriolar tonus and renal blood flow and are believed to be involved in the transmission of the tubuloglomerular feedback (TGF) response across the cells of the juxtaglomerular apparatus. Connexin40 (Cx40) also plays a significant role in the regulation of renin secretion. We investigated the effect of deleting the Cx40 gene on autoregulation of afferent arteriolar diameter in response to acute changes in renal perfusion pressure. The experiments were performed using the isolated blood perfused juxtamedullary nephron preparation in kidneys obtained from wild-type or Cx40 knockout mice. Renal perfusion pressure was increased in steps from 75 to 155 mmHg, and the response in afferent arteriolar diameter was measured. Hereafter, a papillectomy was performed to inhibit TGF, and the pressure steps were repeated. Conduction of intercellular Ca(2+) changes in response to local electrical stimulation was examined in isolated interlobular arteries and afferent arterioles from wild-type or Cx40 knockout mice. Cx40 knockout mice had an impaired autoregulatory response to acute changes in renal perfusion pressure compared with wild-type mice. Inhibition of TGF by papillectomy significantly reduced autoregulation of afferent arteriolar diameter in wild-type mice. In Cx40 knockout mice, papillectomy did not affect the autoregulatory response, indicating that these mice have no functional TGF. Also, Cx40 knockout mice showed no conduction of intercellular Ca(2+) changes in response to local electrical stimulation of interlobular arteries, whereas the Ca(2+) response to norepinephrine was unaffected. These results suggest that Cx40 plays a significant role in the renal autoregulatory response of preglomerular resistance vessels.

Closure of multiple types of K+ channels is necessary to induce changes in renal vascular resistance in vivo in rats.

Inhibition of K(+) channels might mediate renal vasoconstriction. As inhibition of a single type of K(+) channel caused minor or no renal vasoconstriction in vivo in rats, we hypothesized that several classes of K(+) channels must be blocked to elicit renal vasoconstriction. We measured renal blood flow (RBF) in vivo in anesthetized Sprague-Dawley rats. Test agents were infused directly into the renal artery to avoid systemic effects. Inhibition of BK(Ca) and K(ir) channels (with TEA and Ba(2+), respectively) caused small and transient reductions in RBF (to 93 ± 2% and 95 ± 1% of baseline, respectively). K(ATP), SK(Ca) or K(v) channel blockade (with glibenclamide, apamin and 4-aminopyridine, respectively) was without effect. However, a cocktail of all blockers caused a massive reduction of RBF (to 15 ± 10% of baseline). Nifedipine and mibefradil abolished and reduced, respectively, this RBF reduction. The effect of the cocktail of K(+) channel blockers was confirmed in mice using the isolated blood-perfused juxtamedullary nephron preparation. A cocktail of K(+) channel openers (K(+), NS309, NS1619 and pinacidil) had only a minor effect on baseline RBF in vivo in rats, but reduced the vasoconstriction induced by bolus injections of norepinephrine or angiotensin II (by 33 ± 5% and 60 ± 5%, respectively). Our results indicate that closure of numerous types of K(+) channels could participate in the mediation of agonist-induced renal vasoconstriction. Our results also suggest that renal vasoconstriction elicited by K(+) channel blockade is mediated by nifedipine-sensitive Ca(2+) channels and partly by mibefradil-sensitive Ca(2+) channels.