Portal vein thrombosis after second Pfizer/BioNTech coronavirus disease 2019 vaccine.

We have reviewed a case of portomesenteric venous thrombosis that occurred shortly after the administration of the second Pfizer/BioNTech coronavirus disease 2019 (COVID-19) vaccine and discussed the literature surrounding the subject. Our report was generated after reviewing the patient's medical records and clinical images with his written informed consent. The literature review was conducted using PubMed and Google Scholar. Portomesenteric venous thrombosis after the Pfizer/BioNTech COVID-19 vaccine has previously been reported, although infrequently. We did not find enough information, given the paucity of the reported data, to assert a causative relationship between the Pfizer/BioNTech COVID-19 vaccine and the occurrence of portomesenteric thrombosis.

Tortuous ulnar artery presenting as left distal forearm mass.

Knowledge of anatomic variation in vasculature is critical to safe medical intervention as conduits vary in morphology, architecture, and course. Tortuosity is a common anatomic variant in certain arterial beds; however, its prevalence in ulnar arteries is not well documented in the literature. Here we report two cases of tortuous ulnar arteries in patients being evaluated for upper extremity hemodialysis access.

Right carotid-cutaneous fistula and right carotid pseudoaneurysm formation secondary to a chronically infected polyethylene terephthalate patch.

Carotid endarterectomy (CEA) remains the treatment for significant carotid stenosis and stroke prevention. Approximately 100,000 CEAs are performed in the United States every year. Randomized trials have demonstrated an advantage of patch carotid angioplasty over primary closure. Complications from patches include thrombosis, transient ischemic attack, stroke, restenosis, pseudoaneurysm (PA), and infection. PA after CEA is rare, with a reported average of 0.37% of cases. We describe an unusual case of PA after polyethylene terephthalate (PTFE) patching for CEA. An 88-year-old female with Alzheimer's disease living in a nursing facility with a history of skin cancer on her right chest developed a new area of intermittent brisk bleeding on her right neck which was initially believed to be related to her skin cancer. She had a remote history of right CEA with a PTFE patch approximately a decade ago. A computed tomography angiograph-head-and-neck with showed a partially thrombosed PA in the region of her right common carotid artery bifurcation with a tract containing gas and fluid extending to the skin surface suspicious for a partially thrombosed, leaking PA. She was taken urgently to the operating room on broad-spectrum antibiotics where we performed a right neck exploration, ligation of a bleeding carotid PA by ligation of the right common, internal, and external carotid arteries, explantation of a chronically infected polyethylene terephthalate patch, and closure with a sternocleidomastoid advanced flap with multilayered closure. She was discharged to her nursing facility with 6 weeks of ceftriaxone intravenous (IV) and metronidazole IV through a peripherally inserted central catheter (PICC) line with no neurological sequelae.

Mesenteric vein thrombosis can be safely treated with anticoagulation but is associated with significant sequelae of portal hypertension.

BACKGROUND: Mesenteric venous thrombosis (MVT) is a relatively uncommon but potentially lethal condition associated with bowel ischemia and infarction. The natural history and long-term outcomes are poorly understood and under-reported. METHODS: A single-institution retrospective review of noncirrhotic patients diagnosed with MVT from 1999 to 2015 was performed using International Classification of Diseases, Ninth Revision and radiology codes. Patients were excluded if no radiographic imaging was available for review. Eighty patients were identified for analysis. Demographic, clinical, and radiographic data on presentation and at long-term follow-up were collected. Long-term sequelae of portal venous hypertension were defined as esophageal varices, portal vein cavernous transformation, splenomegaly, or hepatic atrophy, as seen on follow-up imaging. RESULTS: There were 80 patients (57.5% male; mean age, 57.9 ± 15.6 years) identified; 83.3% were symptomatic, and 80% presented with abdominal pain. Median follow-up was 480 days (range, 1-6183 days). Follow-up radiographic and clinical data were available for 50 patients (62.5%). The underlying causes of MVT included cancer (41.5%), an inflammatory process (25.9%), the postoperative state (20.7%), and idiopathic cases (18.8%). Pancreatic cancer was the most common associated malignant neoplasm (53%), followed by colon cancer (15%). Twenty patients (26%) had prior or concurrent lower extremity deep venous thromboses. Most patients (68.4%) were treated with anticoagulation; the rest were treated expectantly. Ten (12.5%) had bleeding complications related to anticoagulation, including one death from intracranial hemorrhage. Four patients underwent intervention (three pharmacomechanical thrombolysis and one thrombectomy). One patient died of intestinal ischemia. Two patients had recurrent MVT, both on discontinuing anticoagulation. Long-term imaging sequelae of portal hypertension were noted in 25 of 50 patients (50%) who had follow-up imaging available. Patients with long-term sequelae had lower recanalization rates (36.8% vs 65%; P = .079) and significantly higher rates of complete as opposed to partial thrombosis at the initial event (73% vs 43.3%; P < .005). Long-term sequelae were unrelated to the initial cause or treatment with anticoagulation (P = NS). CONCLUSIONS: Most cases of MVT are associated with malignant disease or an inflammatory process, such as pancreatitis. A diagnosis of malignant disease in the setting of MVT has poor prognosis, with a 5-year survival of only 25%. MVT can be effectively treated with anticoagulation in the majority of cases. Operative or endovascular intervention is rarely needed but important to consider in patients with signs of severe ischemia or impending bowel infarction. There is a significant incidence of radiographically noted long-term sequelae from MVT related to portal venous hypertension, especially in cases of initial complete thrombosis of the mesenteric vein.

Endovascular treatment of acute renal failure secondary to caval thrombosis and suprarenal filter migration.

Although inferior vena cava filter placement is a safe and effective method of reducing the risk of pulmonary embolism, devastating complications can result from thrombosis and migration. Here we present a case of acute renal failure as a result of suprarenal inferior vena cava filter migration and caval thrombosis. We discuss a novel endovascular approach for its management by mechanical aspirational thrombectomy.

Intraluminal nonbacterial intestinal components control gut and lung injury after trauma hemorrhagic shock.

OBJECTIVE: To test whether the mucus layer, luminal digestive enzymes, and intestinal mast cells are critical components in the pathogenesis of trauma shock-induced gut and lung injury. BACKGROUND: Gut origin sepsis studies have highlighted the importance of the systemic component (ischemia-reperfusion) of gut injury, whereas the intraluminal component is less well studied. METHODS: In rats subjected to trauma hemorrhagic shock (T/HS) or sham shock, the role of pancreatic enzymes in gut injury was tested by diversion of pancreatic enzymes via pancreatic duct exteriorization whereas the role of the mucus layer was tested via the enteral administration of a mucus surrogate. In addition, the role of mast cells was assessed by measuring mast cell activation and the ability of pharmacologic inhibition of mast cells to abrogate gut and lung injury. Gut and mucus injury was characterized functionally, morphologically, and chemically. RESULTS: Pancreatic duct exteriorization abrogated T/HS-induced gut barrier loss and limited chemical mucus changes. The mucus surrogate prevented T/HS-induced gut and lung injury. Finally, pancreatic enzyme-induced gut and lung injury seems to involve mast cell activation because T/HS activates mast cells and pharmacologic inhibition of intestinal mast cells prevented T/HS-induced gut and lung injury. CONCLUSIONS: These results indicate that gut and gut-induced lung injury after T/HS involves a complex process consisting of intraluminal digestive enzymes, the unstirred mucus layer, and a systemic ischemic-reperfusion injury. This suggests the possibility of intraluminal therapeutic strategies.

Testosterone depletion or blockade in male rats protects against trauma hemorrhagic shock-induced distant organ injury by limiting gut injury and subsequent production of biologically active mesenteric lymph.

BACKGROUND: We tested the hypothesis that testosterone depletion or blockade in male rats protects against trauma hemorrhagic shock-induced distant organ injury by limiting gut injury and subsequent production of biologically active mesenteric lymph. METHODS: Male, castrated male, or flutamide-treated rats (25 mg/kg subcutaneously after resuscitation) were subjected to a laparotomy (trauma), mesenteric lymph duct cannulation, and 90 minutes of shock (35 mm Hg) or trauma sham-shock. Mesenteric lymph was collected preshock, during shock, and postshock. Gut injury was determined at 6 hours postshock using ex vivo ileal permeability with fluorescein dextran. Postshock mesenteric lymph was assayed for biological activity in vivo by injection into mice and measuring lung permeability, neutrophil activation, and red blood cell deformability. In vitro neutrophil priming capacity of the lymph was also tested. RESULTS: Castrated and flutamide-treated male rats were significantly protected against trauma hemorrhagic shock (T/HS)-induced gut injury when compared with hormonally intact males. Postshock mesenteric lymph from male rats had a higher capacity to induce lung injury, Neutrophil (PMN) activation, and loss of red blood cell deformability when injected into naïve mice when compared with castrated and flutamide-treated males. The increase in gut injury after T/HS in males directly correlated with the in vitro biological activity of mesenteric lymph to prime neutrophils for an increased respiratory burst. CONCLUSIONS: After T/HS, gut protective effects can be observed in males after testosterone blockade or depletion. This reduced gut injury contributes to decreased biological activity of mesenteric lymph leading to attenuated systemic inflammation and distant organ injury.

Trauma hemorrhagic shock-induced lung injury involves a gut-lymph-induced TLR4 pathway in mice.

BACKGROUND: Injurious non-microbial factors released from the stressed gut during shocked states contribute to the development of acute lung injury (ALI) and multiple organ dysfunction syndrome (MODS). Since Toll-like receptors (TLR) act as sensors of tissue injury as well as microbial invasion and TLR4 signaling occurs in both sepsis and noninfectious models of ischemia/reperfusion (I/R) injury, we hypothesized that factors in the intestinal mesenteric lymph after trauma hemorrhagic shock (T/HS) mediate gut-induced lung injury via TLR4 activation. METHODS/PRINCIPAL FINDINGS: The concept that factors in T/HS lymph exiting the gut recreates ALI is evidenced by our findings that the infusion of porcine lymph, collected from animals subjected to global T/HS injury, into naïve wildtype (WT) mice induced lung injury. Using C3H/HeJ mice that harbor a TLR4 mutation, we found that TLR4 activation was necessary for the development of T/HS porcine lymph-induced lung injury as determined by Evan's blue dye (EBD) lung permeability and myeloperoxidase (MPO) levels as well as the induction of the injurious pulmonary iNOS response. TRIF and Myd88 deficiency fully and partially attenuated T/HS lymph-induced increases in lung permeability respectively. Additional studies in TLR2 deficient mice showed that TLR2 activation was not involved in the pathology of T/HS lymph-induced lung injury. Lastly, the lymph samples were devoid of bacteria, endotoxin and bacterial DNA and passage of lymph through an endotoxin removal column did not abrogate the ability of T/HS lymph to cause lung injury in naïve mice. CONCLUSIONS/SIGNIFICANCE: Our findings suggest that non-microbial factors in the intestinal mesenteric lymph after T/HS are capable of recreating T/HS-induced lung injury via TLR4 activation.

HIF-1 mediates pathogenic inflammatory responses to intestinal ischemia-reperfusion injury.

Acute lung injury (ALI) and the development of the multiple organ dysfunction syndrome (MODS) are major causes of death in trauma patients. Gut inflammation and loss of gut barrier function as a consequence of splanchnic ischemia-reperfusion (I/R) have been implicated as the initial triggering events that contribute to the development of the systemic inflammatory response, ALI, and MODS. Since hypoxia-inducible factor (HIF-1) is a key regulator of the physiological and pathophysiological response to hypoxia, we asked whether HIF-1 plays a proximal role in the induction of gut injury and subsequent lung injury. Utilizing partially HIF-1α-deficient mice in a global trauma hemorrhagic shock (T/HS) model, we found that HIF-1 activation was necessary for the development of gut injury and that the prevention of gut injury was associated with an abrogation of lung injury. Specifically, in vivo studies demonstrated that partial HIF-1α deficiency ameliorated T/HS-induced increases in intestinal permeability, bacterial translocation, and caspase-3 activation. Lastly, partial HIF-1α deficiency reduced TNF-α, IL-1ß, cyclooxygenase-2, and inducible nitric oxide synthase levels in the ileal mucosa after T/HS whereas IL-1ß mRNA levels were reduced in the lung after T/HS. This study indicates that prolonged intestinal HIF-1 activation is a proximal regulator of I/R-induced gut mucosal injury and gut-induced lung injury. Consequently, these results provide unique information on the initiating events in trauma-hemorrhagic shock-induced ALI and MODS as well as potential therapeutic insights.

Loss of the intestinal mucus layer in the normal rat causes gut injury but not toxic mesenteric lymph nor lung injury.

There is substantial evidence that gut barrier failure is associated with distant organ injury and systemic inflammation. After major trauma or stress, the factors and mechanisms involved in gut injury are unknown. Our primary hypothesis is that loss of the intestinal mucus layer will result in injury of the normal gut that is exacerbated by the presence of luminal pancreatic proteases. Our secondary hypothesis is that the injury produced in the gut will result in the production of biologically active mesenteric lymph and consequently distant organ (i.e., lung) injury. To test this hypothesis, five groups of rats were studied: 1) uninstrumented naive rats; 2) control rats in which a ligated segment of distal ileum was filled with saline; 3) rats with pancreatic proteases placed in their distal ileal segments; 4) rats with the mucolytic N-acetylcysteine (NAC) placed in their distal ileal segments; and 5) rats exposed to NAC and pancreatic proteases in their ileal segments. The potential systemic consequences of gut injury induced by NAC and proteases were assessed by measuring the biological activity of mesenteric lymph as well as gut-induced lung injury. Exposure of the normal intestine to NAC, but not saline or proteases, led to increased gut permeability, loss of mucus hydrophobicity, a decrease in the mucus layer, as well as morphological evidence of villous injury. Although proteases themselves did not cause gut injury, the combination of pancreatic proteases with NAC caused more severe injury than NAC alone, suggesting that once the mucus barrier is impaired, luminal proteases can injure the now vulnerable gut. Because comparable levels of gut injury caused by systemic insults are associated with gut-induced lung injury, which is mediated by biologically active factors in mesenteric lymph, we next tested whether this local model of gut injury would produce active mesenteric lymph or lead to lung injury. It did not, suggesting that gut injury by itself may not be sufficient to induce distant organ dysfunction. Therefore, loss of the intestinal mucus layer, especially in the presence of intraluminal pancreatic proteases, is sufficient to lead to injury and barrier dysfunction of the otherwise normal intestine but not to produce gut-induced distant organ dysfunction.