Delayed cerebral ischemia (DCI) is one of the main complications of spontaneous subarachnoid haemorrhage and one of its causes is the cortical spreading depolarizations (CSDs). Cortical spreading depolarizations are waves of neuronal and glial depolarizations in which there is loss of neuronal ionic homeostasis with potassium efflux and sodium and calcium influx. In damaged brain areas and brain areas at risk, such as those adjacent to subarachnoid haemorrhage (SAH), CSDs induce microvascular vasoconstriction and, therefore, hypoperfusion and spread of ischemia. Several studies have been devoted to minimize secondary injuries that occur hours to days after an acute insult. Ketamine, a drug until recently contraindicated in the neurosurgical population for potentially causing intracranial hypertension, has re-emerged as a potential neuroprotective agent due to its pharmacodynamic effects at the cellular level. These effects include anti-inflammatory mechanisms, and those of microthrombosis and cell apoptosis controls, and of modulation of brain excitotoxicity and CSDs. A literature review was performed at PubMed covering the period from 2002 to 2019. Retrospective studies confirmed the effects of ketamine on the control of CSDs and, consequently, of DCI in patients with SAH, but did not show improvement in clinical outcome. The influence of ketamine on the occurrence/development of DCI needs to be further confirmed in prospective randomized studies

Background: Heparin-induced thrombocytopenia/thrombosis (HIT/T) is characterized by a fall in platelet count 5-10days after starting heparin therapy and is diagnosed with specific 4-T clinical features and laboratory tests. This complication is relatively common in Cardiothoracic surgery patients. Objective: To evaluate the positive and negative predictive value of various HIT laboratory tests and assess any correlation between HIT, the underlying diagnosis, underlying procedure, and mechanical cardiac devices. Patients and methods: The patient’s medical records were correlated with two laboratories HIT diagnostic tests, the pan-specific screening test with IgG, IgA, and IgM antibodies, followed by HIT specific IgG ELISA. Results: Total n = 80 patients were assessed, 48% (n = 38) were HIT screen pan-specific negative and 50% (n = 40) were HIT pan-specific positive and 2 cases were inconclusive. 17% (n = 14) were both pan-specific and specific HIT IgG ELISA positive. There were 5 atypical cases. One patient had Eosinophilic myocarditis and was HIT ELISA IgG neg. Argatroban was given on clinical grounds with successful recovery. One patient with Sarcoidosis had an aggressive course and received IV Immunoglobulin (IVIG) but succumbed secondary to liver failure. One patient progressed to gut ischemia and had surgical intervention but succumbed. Two patients with mechanical heart valves were on Argatroban but relapsed and responded to IVIG therapy. Conclusion: Our study indicates that 9/16 (> 50%) HIT-positive patients had valve replacement or cardiac devices suggesting that like knee arthroplasty there is a high incidence of HIT in patients with mechanical heart valves and cardiac devices and this warrants further prospective study. 

Aim: To examine the relationship between the levels of HbA1c and hospital admission rates.Methods: We recorded HbA1c levels of all diabetic patients in Tripoli University Hospital over one year.Results: The mean HbA1c was 8.03%, with no difference between males and females. Over half of patients (56.5%) were admitted through their diabetes was well-controlled. Over half of the patients with type 1 diabetes (57/102, 55.9%) had a high HbA1c at admission compared to 42.1% of patients with type 2, who were mainly admitted with HbA1c level within the acceptable range set for this study. The HbA1c level was positively and significantly correlated with the length of hospital stay (R = 0.93, p = 0.000), and was significantly associated with hyperglycemia, diabetic ketoacidosis, coronary artery disease, limb ischemia, cataract, osteomyelitis, and non-alcoholic steatohepatitis.Conclusion: HbA1c is correlated significantly with hospitalization in type 1 diabetes but not in type 2.

Percutaneous coronary angioplasty is a minimally invasive procedure aimed at unclogging a coronary artery with a low complication rate (with a serious complication rate of 3% to 7% and a mortality rate of 1.2%). Device entrapment during PCI is a rare but life-threatening complication that occurs in < 1% of PCIs and balloon entrapment comes second after coronary guidewires. We present the case of 68-years-old man, smoker, hypertensive and type2 diabetic that presents angina with evidence of ischemia on myocardial tomoscintigraphy and in whom the radial coronary angiography reveals a tight calcified mid LAD stenosis. During his PCI and after dilatation with an NC balloon 2.5 × 12 the latter refuses to deflate and remains trapped in the lesion with the appearance of pain and ST-elevation despite several attempts to dilute the product in the inflator and to burst it by overexpansion. Traction on the balloon resulted in the deep intubation of the guiding-catheter, which comes in contact with the trapped balloon, and the rupture of the latter’s hypotube, which remains inflated at the site of the lesion and mounted on the 0.014 guidewire. We put a second 0.014 guidewire distally in the LAD and twisted with the distal part of the first guidewire, then we introduced a second balloon 2.0 × 20 over the second guidewire until the distal part of the guiding-catheter and inflated to trap the stucked balloon. We gradually removed this emergency assembly that allowed us to retrieve the trapped balloon. The control injection revealed a thrombotic occlusion of the LAD treated by thrombectomy and anti-GPIIbIIIa followed by a DES 2.75 × 28 placement. The patient was discharged 48 hours later with a good LVEF. The possible balloon entrapment mechanisms are an acute recoil of a highly calcified lesion with compression of the incompletely deflated balloon, which seems to be the case in our patient, strangulation of the proximal balloon end by the guiding-catheter if the balloon is removed before complete deflation and break or bend of the hypotube. The solutions in case of undeflatable balloon entrapment are to dilute the product in the inflator, to burst it by overexpansion, to pierce it through a stiff guidewire (or through its other end on a Microcatheter or OTW balloon), to cut its outer part and let it empty passively, to introduce a second guide-wire and perform a Buddy-Balloon or to transfer the patient to Surgery. Material entrapment remains a rare but life-threatening complication, its eviction requires the choice of material size and gentle manipulations (small balloons in the event of a calcified lesion) and its management uses different techniques, the choice of which depends on the clinical and anatomical situation. 

Portal vein thrombosis (PVT) is a rare condition that may congest bowel venous drainage and cause mesenteric ischemia. In acute settings, gastrointestinal bleeding (GIB) is rare, and acute abdominal pain is the most common clinical presentation. A 24-year-old man who presented with acute abdominal pain and a single episode of hematemesis is reported. Workups revealed evidence of thrombosis in the portal vein, but upper endoscopy was incapable to detect the source of the bleeding. We discuss the possible scenarios for the GIB in this case and review similar reports in the literature.

SARS-CoV-2 is a new pandemic infection that affects at the beginning the upper respiratory system, and, successively, all the organisms, due to cytokine storm, with serious consequences that can reach death. The aim of this work was the observation of the nasal mucosa of enrolled 60 patients, resulting negative for two weeks to the molecular swab for SARS-CoV-2, versus the control group. Rhino-fibroscopy and nasal cytology of nasal mucosa were performed for both the investigated groups. The observation of the samples showed the occurrence of plasmablastic lymphocytes and Downey II lymphocytes type. The former type of lymphocytes was prevalent against the second one, probably because of an immunological “scar”. The rhino-fibroscopy showed a “pseudo ischemia of nasal submucosa” at pre and pericranial levels, not occurred in the control group.The occurrence of atypical lymphocytes in the nasal smear was analog to that observed in the blood peripheral smear, probably caused by mechanisms of local immune reaction and dysregulation like those observed in other virus infections. Our findings suggest that the nasal mucosa study through the nasal cytology, can represent an important predictive tool of the SARS-CoV-2 infection.

Aims: There is no study in the literature about ischemia-modified albumin (IMA) and hepatocyte growth factor (HGF) levels in amniotic fluid for Down syndrome cases. The aim of this study was to investigate the changes of IMA and HGF in Down syndrome cases at 16-20 weeks of gestation compared to normal fetuses.Methods: For this prospective case-control study, following reaching the number of 20 women (study group) who had the prenatal diagnosis of Down syndrome, maternal and gestational age-matched pregnant women with normal constitutional karyotype were selected for the control group (n = 74) from the stored amniotic fluid samples. Results: Mean women and gestational ages were comparable between the two groups. Amniotic fluid IMA (1.32 ± 0.13 vs. 1.11 ± 0.11 ABSU, respectively, p < 0.001) and HGF (2743.53 ± 1389.28 vs. 2160.12 ± 654.63 pg/mL, respectively, p = 0.008). Levels were significantly higher in pregnant women having Down syndrome fetuses compared with women having normal fetuses. The amniotic fluid IMA levels for the diagnosis of Down syndrome, and the sensitivity and specificity were calculated as 95.0% and 71.6% for the limit value 1.171 cm3, respectively. Conclusion: In cases with suspected Down syndrome, the diagnosis of Down Syndrome may be made in approximately 1 hour with high sensitivity and specificity by measuring the IMA level in the amniotic fluid sample taken for fetal karyotyping.

Objective: Assessment of heart rate variability (HRV) is a non-invasive and reliable method to evaluate autonomic disorders after cerebral ischemia. The present study was conducted to investigate the therapeutic potential of IC87201 in reducing post-stroke cardiac dysfunction. Materials and methods: Cerebral ischemia was induced by the middle cerebral artery occlusion (MCAO) method in 15 anesthetized adult male rats in three MCAO, MCAO+ DXM, and MCAO+ IC87201 groups, for one hour. Electrocardiogram was recorded before, and 48 hours after ischemia and drug administration, and HRV parameters were calculated from R-R intervals. In the treatment groups, IC87201 and Dextromethorphan hydrobromide monohydrate (DXM) were injected after an ischemic period. Results: After brain ischemia, the R-R interval decreased and consequently heart rate increased. The R-R intervals were used to extract the HRV frequency and time domains, including normalized low frequency (LF), high frequency (HF), LF/HF ratio, and standard deviation of R-R interval (SDRR). Normalized LF and LF/HF ratio enhanced 48 hours after ischemia, while normalized HF and SDRR significantly reduced compared to the pre-ischemic state. All HRV parameters had returned to their pre-ischemic level 48 hours after IC87201 and DXM administration, except SDRR, which recovered only in the IC87201 administered group. Conclusion: Based on our findings, it can be concluded that cerebral ischemia significantly worsens HRV parameters as a result of sympathetic overactivity. These changes were reversed by administering DXM and IC87201, but IC87201 has generally been more effective in lowering lesions. As a result, IC87201 can be introduced as an effective substance for the treatment of post-ischemic cardiac side effects.

Ischemia-Reperfusion Injury (IRI) is the outcome of two intertwined pathological processes resulting from the shortage of blood flow to tissues and the subsequent restoration of circulation to a previously ischemic area. IRI (sometimes just one side of the dyad) remains one of the most challenging problems in several branches of emergency medicine. Mitochondrial and endoplasmic reticulum dysfunction is a crucial pathological factor involved in the development of IRI. The sigma-1 receptor (Sig1-R) is an intracellular chaperone molecule located between the mitochondria and endoplasmic reticulum with an apparent physiological role in regulating signaling between these cell organelles and serves as a safety mechanism against cellular stress. Therefore, amelioration of IRI is reasonably expected by the activation of the Sig1-R chaperone. Indeed, under cellular stress, Sig1-R agonists improve mitochondrial respiration and optimize endoplasmic reticulum function by sustaining high-energy phosphate synthesis. The discovery that N, N-dimethyltryptamine (DMT) is an endogenous agonist of the Sig1-R may shed light on yet undiscovered physiological mechanisms and therapeutic potentials of this controversial hallucinogenic compound. In this article, the authors briefly overview the function of Sig1-R in cellular bioenergetics with a focus on the processes involved in IRI and summarize the results of their in vitro and in vivo DMT studies aiming at mitigating IRI. The authors conclude that the effect of DMT may involve a universal role in cellular protective mechanisms suggesting therapeutic potentials against different components and types of IRIs emerging in local and generalized brain ischemia after stroke or cardiac arrest.