Foodborne botulism, a forgotten yet life-threatening disease: a case report.

OBJECTIVE: Botulism is a very rare disease in Switzerland, with less than one case per year, an incidence of 0.01 cases for 100,000 inhabitants. Indeed, over the past ten years, 9 cases have been reported to Public Health registry. Foodborne botulism (FB) is caused by ingestion of preformed botulinum neurotoxin. Characteristic features should be rapidly recognized, and prompt treatment should be administered to avoid further progression towards respiratory failure and death. CASE REPORT: We report the case of a patient who developed gastrointestinal symptoms just after a sandwich consumption followed by rapidly progressive cranial nerve impairment, truncal muscle weakness in a descending pattern and respiratory failure requiring mechanical ventilation. The diagnosis of foodborne botulism was delayed due to differential diagnosis considerations. Specific antitoxin therapy was administered immediately after firm clinical conviction of botulism, without waiting for serologic results that later confirmed the diagnosis. As expected, muscle weakness recovery was slow, with persistent chronic deficits nine years later. CONCLUSIONS: This case highlights differential diagnosis issues of botulism. These include acute neuromuscular disorders such as myasthenia gravis, Guillain-Barré syndrome, or tick-borne encephalitis. The importance of careful medical history and repeated clinical evaluation to avoid misdiagnosis can be lifesaving. Our case highlights the typical warning signs.

Alleviative effects of glutamate against chemotherapeutic agent-induced intestinal mucositis.

5-Fluorouracil (5-FU) is one of the most widely used chemotherapeutic agents; however, it often causes intestinal mucositis with severe diarrhea. An efficient treatment strategy to reduce this side effect is lacking. Glutamate (Glu), a nonessential amino acid, is the most important energy source in the small intestine and has been shown to maintain intestinal morphology, barrier function, and antioxidative capacity. However, the effects of Glu on intestinal mucositis induced by chemotherapeutic agents have not been explored. This study aimed to demonstrate the alleviative effects of Glu on 5-FU-induced intestinal mucositis. Mucositis was induced in C57B/6N mice by intraperitoneal injection of 5-FU (50 mg/kg) for 6 days and assessed by histological and physiological analyses. Glu (500 or 1000 mg/kg) was orally administered as a pretreatment twice daily for 7 days before the initial treatment of 5-FU. Cellular proliferation and apoptosis were assessed using Ki-67 immunostaining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, respectively. Furthermore, fluorescein isothiocyanate-dextran infiltration was assessed to measure intestinal permeability. In vitro experiments using rat intestinal epithelial cells (IEC-6 cells) were performed to clarify the effect of Glu on 5-FU-induced barrier dysfunction. Glu alleviated 5-FU-induced intestinal mucositis by reducing villi shortening, enhancing cell proliferation, and suppressing apoptosis. It also alleviated the 5-FU-induced increased intestinal permeability. In vitro studies revealed significantly increased trans-epithelial electrical resistance (TEER) in Glu-pretreated IEC-6 cells compared to that in 5-FU-treated and control cells. In conclusion, the findings of this study provide evidence for the potential of Glu to protect against 5-FU-induced intestinal mucositis in patients with cancer.

Caution during endotracheal suctioning in case of skull base fractures!

OBJECTIVE: Cerebral exteriorization through the cribriform plate during routine endotracheal suctioning (ETS) in a coughing patient without sedation with multiple complex skull base fracture; this case has never been reported in the literature. CLINICAL PRESENTATION: We report the case of a polytrauma patient admitted in our ICU with severe traumatic brain injury (TBI) and multiple complex skull base fractures. After 48 hours of neurocritical care and stable neuromonitoring parameters, sedation was stopped for neurological assessment. During this period and while routine ETS was being performed, brain herniation with exteriorization through the nose occurred with a concomitant ICP elevation. CONCLUSIONS: ETS can induce the coughing reflex and provoke a rise in ICP. It is a simple routine procedure that should be performed with great precautions in order to avoid iatrogenic complications, particularly in patients with skull base fractures, such as brain herniation as described in our patient.

Video fluoroscopy for pulmonary artery catheter insertion in high-risk situation of knotting or misplacement.

Pulmonary artery catheter (PAC) insertion in patients with severe pulmonary hypertension, right heart dilation and failure, is very challenging. Misplacement and knotting are rare but could be serious complications leading to a delay of the monitoring and sometimes an emergent not expected intervention. Here we report a case of a patient admitted to Intensive Care Unit (ICU) with an acute hypoxemic respiratory failure. She had a history of chronic respiratory failure with pulmonary hypertension and right heart failure. We decided to monitor her cardiac output and pulmonary pressure with a PAC. Repeated attempts to reach the pulmonary artery (PA) were unsuccessful and the PAC was knotted and blocked at the distal tip of the introducer. Under fluoroscopy the knot was released by radiologist. Few days later, a monitoring of PA pressure was needed to guide a PA vasodilator treatment. Under fluoroscopic guidance with the supervision of radiologist, the catheter was successfully placed in the PA at the first attempt. Despite some limitations (patient displacement and radiation), this technique is more accurate than waveform guidance. We suggest in specific situations (low cardiac output, severe pulmonary hypertension, and severe tricuspid regurgitation) to consider first fluoroscopy.

Ischemic stroke and ST-elevation myocardial infarction revealing infective endocarditis.

In this clinical scenario, we report the case of a patient who presented multiple embolic complications due to mitral infective endocarditis (IE). A 68-year-old woman had extended right hepatectomy for hilar cholangiocarcinoma. Unfortunately, she had multiple postoperative complications and had to be transferred to the Intensive Care Unit. During this stay, we have diagnosed an Enterococcus faecium IE after the occurrence of multiple embolic complications (myocardial infarction, ischemic stroke, digital emboli, splenic emboli, and renal emboli). The case is presented hereunder with illustrative imagings. While embolism is a known complication of IE, the presence of multiple emboli in various organs is rare.

Reduction in the amplitude of shortening and Ca(2+) transient by phlorizin and quercetin-3-O-glucoside in ventricular myocytes from streptozotocin-induced diabetic rats.

Diabetes mellitus is the leading cause of cardiovascular morbidity and mortality. Phlorizin (PHLOR) and quercetin-3-O-glucoside (QUER-3-G) are two natural compounds reported to have antidiabetic properties by inhibiting sodium/glucose transporters. Their effects on ventricular myocyte shortening and intracellular Ca(2+) in streptozotocin (STZ)-induced diabetic rats were investigated. Video edge detection and fluorescence photometry were used to measure ventricular myocyte shortening and intracellular Ca(2+), respectively. Blood glucose in STZ rats was 4-fold higher (469.64+/-22.23 mg/dl, n=14) than in Controls (104.06+/-3.36 mg/dl, n=16). The amplitude of shortening was reduced by PHLOR in STZ (84.76+/-2.91 %, n=20) and Control (83.72+/-2.65 %, n=23) myocytes, and by QUER-3-G in STZ (79.12+/-2.28 %, n=20) and Control (76.69+/-1.92 %, n=30) myocytes. The amplitude of intracellular Ca(2+) was also reduced by PHLOR in STZ (82.37+/-3.16 %, n=16) and Control (73.94+/-5.22 %, n=21) myocytes, and by QUER-3-G in STZ (73.62+/-5.83 %, n=18) and Control (78.32+/-3.54 %, n=41) myocytes. Myofilament sensitivity to Ca(2+) was not significantly altered by PHLOR; however, it was reduced by QUER-3-G modestly in STZ myocytes and significantly in Controls. PHLOR and QUER-3-G did not significantly alter sarcoplasmic reticulum Ca(2+) in STZ or Control myocytes. Altered mechanisms of Ca(2+) transport partly underlie PHLOR and QUER-3-G negative inotropic effects in ventricular myocytes from STZ and Control rats.

Dapagliflozin reduces the amplitude of shortening and Ca(2+) transient in ventricular myocytes from streptozotocin-induced diabetic rats.

In the management of type 2 diabetes mellitus, Dapagliflozin (DAPA) is a newly introduced selective sodium-glucose co-transporter 2 inhibitor which promotes renal glucose excretion. Little is known about the effects of DAPA on the electromechanical function of the heart. This study investigated the effects of DAPA on ventricular myocyte shortening and intracellular Ca(2+) transport in streptozotocin (STZ)-induced diabetic rats. Shortening, Ca(2+) transients, myofilament sensitivity to Ca(2+) and sarcoplasmic reticulum Ca(2+), and intracellular Ca(2+) current were measured in isolated rats ventricular myocytes by video edge detection, fluorescence photometry, and whole-cell patch-clamp techniques. Diabetes was characterized in STZ-treated rats by a fourfold increase in blood glucose (440 ± 25 mg/dl, n = 21) compared to Controls (98 ± 2 mg/dl, n = 19). DAPA reduced the amplitude of shortening in Control (76.68 ± 2.28 %, n = 37) and STZ (76.58 ± 1.89 %, n = 42) ventricular myocytes, and reduced the amplitude of the Ca(2+) transients in Control and STZ ventricular myocytes with greater effects in STZ (71.45 ± 5.35 %, n = 16) myocytes compared to Controls (92.01 ± 2.72 %, n = 17). Myofilament sensitivity to Ca(2+) and sarcoplasmic reticulum Ca(2+) were not significantly altered by DAPA in either STZ or Control myocytes. L-type Ca(2+) current was reduced in STZ myocytes compared to Controls and was further reduced by DAPA. In conclusion, alterations in the mechanism(s) of Ca(2+) transport may partly underlie the negative inotropic effects of DAPA in ventricular myocytes from STZ-treated and Control rats.

[Multimodal neuromonitoring for the critical care management of acute coma]. / Neuromonitorage après coma aigu aux soins intensifs.

Management of neurocritical care patients is focused on the prevention and treatment of secondary brain injury, i.e. the number of pathophysiological intracerebral (edema, ischemia, energy dysfunction, seizures) and systemic (hyperthermia, disorders of glucose homeostasis) events that occur following the initial insult (stroke, hemorrhage, head trauma, brain anoxia) that may aggravate patient outcome. The current therapeutic paradigm is based on multimodal neuromonitoring, including invasive (intracranial pressure, brain oxygen, cerebral microdialysis) and non-invasive (transcranial doppler, near-infrared spectroscopy, EEG) tools that allows targeted individualized management of acute coma in the early phase. The aim of this review is to describe the utility of multimodal neuromonitoring for the critical care management of acute coma.

Mast cells as a source and target for nitric oxide.

Mast cells (MC), which are tissue-resident cells found widely distributed in the body, are derived from primitive hematopoietic cells. MC produce a variety of biologically active substances such as histamine, proteases, lipid derivatives and numerous cytokines and chemokines in response to immunologic or non-immunologic stimuli. Of interest, it has been reported that rodent MC can also be a source of nitric oxide (NO) derivatives, that they synthesize spontaneously, or only after activation, depending on their subtype. This synthesis appears to be under the control of the expression of the inducible isoform of the nitric oxide synthase (iNOS) and of the constitutive neuronal NOS (nNOS). MC might thus be able to influence the survival and functions of other types of NO-sensitive cells in close vicinity. Apart from being a source of NO, MC can also be the target for NO and its derivatives. Indeed, survival and reactivity of rodent MC is influenced by NO derivatives produced by MC themselves or by other cellular elements in close contact with the MC in tissues. By contrast, the existence of such mechanisms of cross-talk between MC and NO remains poorly documented in humans. If evidence are supplied in favor of such relationship, pharmacological modulation by agents acting at the level of the NO pathway might be of interest in order to regulate the functions of MC in immunologic, neoplastic, inflammatory and other conditions.