Carboxyhemoglobin half-life toxicokinetic profiles during and after normobaric oxygen therapy: On a swine model.

Investigations on acute carbon monoxide (CO) poisoning struggle to highlight a relevant discriminant criterion related to CO poisoning severity for predicting complications, such as delayed neurological syndromes. In this context, it remains difficult to demonstrate the superiority of one method of oxygen (O2) administration over others or to identify the optimal duration of normobaric 100% oxygen (NBO) treatment. Myoglobin, as hemoglobin, are a potential binding site for CO, which could be a source of extravascular CO storage that impacts the severity of CO poisoning. It is not possible in routine clinical practice to estimate this potential extravascular CO storage. Indirect means of doing so that are available in the first few hours of poisoning could include, for example, the carboxyhemoglobin half-life (COHbt1/2), which seems to be influenced itself by the level and duration of CO exposure affecting this store of CO within the body. However, before the elimination of CO can be assessed, the COHbt1/2 toxicokinetic model must be confirmed: research still debates whether this model mono- or bi-compartmental. The second indirect mean could be the assessment of a potential COHb rebound after COHb has returned to 5% and NBO treatment has stopped. Moreover, a COHb rebound could be considered to justify the duration of NBO treatment. On an experimental swine model exposed to moderate CO poisoning (940 ppm for ±118 min until COHb reached 30%), we first confirm that the COHb half-life follows a bi-compartmental model. Secondly, we observe for the first time a slight COHb rebound when COHb returns to 5% and oxygen therapy is stopped. On the basis of these two toxicokinetic characteristics in favor of extravascular CO storage, we recommend that COHbt1/2 is considered using the bi-compartmental model in future clinical studies that compare treatment effectiveness as a potential severity criterion to homogenize cohorts of the same severity. Moreover, from a general toxicokinetic point of view, we confirm that a treatment lasting less than 6 hours appears to be insufficient for treating moderate CO poisoning.

Long-term intensive care unit outbreak of carbapenemase-producing organisms associated with contaminated sink drains.

BACKGROUND: Between 2018 and 2022, a Belgian tertiary care hospital faced a growing issue with acquiring carbapenemase-producing organisms (CPO), mainly VIM-producing P. aeruginosa (PA-VIM) and NDM-producing Enterobacterales (CPE-NDM) among hospitalized patients in the adult intensive care unit (ICU). AIM: To investigate this ICU long-term CPO outbreak involving multiple species and a persistent environmental reservoir. METHODS: Active case finding, environmental sampling, whole-genome sequencing (WGS) analysis of patient and environmental strains, and implemented control strategies were described in this study. FINDINGS: From 2018 to 2022, 37 patients became colonized or infected with PA-VIM and/or CPE-NDM during their ICU stay. WGS confirmed the epidemiological link between clinical and environmental strains collected from the sink drains with clonal strain dissemination and horizontal gene transfer mediated by plasmid conjugation and/or transposon jumps. Environmental disinfection by quaternary ammonium-based disinfectant and replacement of contaminated equipment failed to eradicate environmental sources. Interestingly, efflux pump genes conferring resistance to quaternary ammonium compounds were widespread in the isolates. As removing sinks was not feasible, a combination of a foaming product degrading the biofilm and foaming disinfectant based on peracetic acid and hydrogen peroxide has been evaluated and has so far prevented recolonization of the proximal sink drain by CPO. CONCLUSION: The persistence in the hospital environment of antibiotic- and disinfectant-resistant bacteria with the ability to transfer mobile genetic elements poses a serious threat to ICU patients with a risk of shifting towards an endemicity scenario. Innovative strategies are needed to address persistent environmental reservoirs and prevent CPO transmission.

Extreme Rhabdomyolysis, Acute Renal Failure, and Protracted Ileus in a Case of Legionella Pneumonia.

A 53-year-old man developed a Legionella pneumophila pneumonia complicated by rhabdomyolysis, acute kidney injury, and protracted ileus. Risk factors were smoking and chronic alcoholism, but the patient had no history of previous abdominal surgery. Hemodialysis was required for a period of 5 weeks with a full renal recovery. Pneumonia required respiratory support but for a limited period of 6 days. The protracted course of the ileus led to explorative laparotomy despite negative computed tomography findings. No cause of mechanical obstruction was found at surgery and common etiologies of intestinal obstruction were excluded. Parenteral nutrition was needed for a total of 4 weeks, before recovery of intestinal motility. This case illustrates the apparent discrepancy between the pulmonary symptoms and the extrapulmonary manifestations that could be seen as a consequence of an exaggerated immune response.

Acute Bacterial Meningitis and Systemic Abscesses due to Streptococcus dysgalactiae subsp. equisimilis Infection.

Disseminated abscesses due to group G ß-hemolytic Streptococcus dysgalactiae were observed in a 57-year-old cirrhotic patient with the skin being the putative way of entry for the pathogen. S. dysgalactiae is a rare agent in human infections responsible for acute pyogenic meningitis. The mortality rate associated with S. dysgalactiae bacteraemia and meningitis may be as high as 50%, particularly in the presence of endocarditis or brain abscesses. In our patient, main sites of infections were meningitis and ventriculitis, spondylodiscitis, septic arthritis, and soft-tissue infections. In contrast, no endocarditis was evidenced. Cirrhosis-related immune suppression was considered as a pathophysiological cofactor for the condition. Fortunately, clinical status improved after long-term (3 months) antimicrobial therapy.

Neuroinvasive Infection from O117:K52:H-Escherichia coli following Acute Pyelonephritis.

Spontaneous or nosocomial Escherichia coli meningitis remains rare in healthy adults but is still carrying a high mortality rate despite adapted antimicrobial treatment for susceptible strains. A 39-year-old woman was admitted to the hospital with severe subarachnoid haemorrhage complicated by acute hydrocephalus. On hospital day 10, she developed Streptococcus anginosus septicaemia and urinary tract infection due to a multisensitive strain of E. coli. This infection was successfully controlled by antimicrobial therapy. As a late complication in the neurosurgical ward (day 39), she developed fever, alteration of consciousness, and shock, leading to the diagnosis of bacterial meningitis. The culture of blood, cerebrospinal fluid, and urine grew positive for a multisensitive E. coli. The strain was identified as O117:K52:H, a serotype that was until now never associated with acute meningitis or brain abscesses. The source appeared to be the urinary tract with the demonstration of acute pyelonephritis. The patient died on day 94 from delayed complications of multiple brain abscesses.

Susac-like syndrome in a chronic cocaine abuser: could levamisole play a role?

INTRODUCTION: Toxic leukoencephalopathy is a possible but rare complication of chronic cocaine abuse. The role of adulterants, mainly levamisole, is still debated. CASE REPORT: We describe an atypical case of fatal leukoencephalopathy mimicking Susac syndrome in a 22-year-old man who was chronically abusing cannabis and cocaine. Exposure to levamisole as adulterant to cocaine was proven by hair analysis. Despite cessation of exposure to cocaine and aggressive immunosuppressive therapy, the patient remained in a minimally conscious state until death. DISCUSSION: Susac syndrome is a rare entity, and its etiology is not yet fully elucidated. The toxic etiologies have been poorly investigated to date. Further observations are required to determine if cocaine and/or adulterants might play a significant role.

Oesophageal and gastric obstruction in a cocaine body packer.

While the management of asymptomatic body packers is mainly conservative, few individuals will require surgery for acute toxicity related to packets rupture, intestinal obstruction or very slow progression of the packages. Obstruction of the lower oesophagus or stomach is not frequently reported. We report the case of a 49-year-old woman who had ingested 92 cocaine-containing packages. She was admitted to the hospital after opioid syndrome related to the intake of morphine and codeine to decrease intestinal transit. The presence of more than 80 packages was suspected in the stomach on the initial abdomen computed tomography. Due to the absence of progression of the packages after four days of well-conducted laxative therapy and to major gastric distension at abdomen tomography, surgery was decided and gastrotomy allowed the evacuation of 80 packages that were still present in the stomach or in the lower oesophagus. In addition, 12 other packages had been retrieved either after laxative therapy (9) or by evacuation via the anal canal (3) after palpation of the intestine during the surgical procedure. No complication was observed.

Pink urine.

A 55-year-old man was admitted after a suspected hypnotic overdose of valerian extracts. In addition to altered consciousness, the first clinical symptoms included not only diffuse rash on the face, trunk, and limbs, but also an inspiratory dyspnea with a marked hypoxemia. A major laryngeal edema was noted during orotracheal intubation. After correction of hypoxemia, the patient became agitated and propofol was administered by continuous infusion. In addition, the patient passed pink urine staining the urine collection bag. The presence of an unidentified toxic substance was suspected.

Spontaneous pneumomediastinum and epidural pneumatosis after oral ecstasy consumption.

A 19-year-old man was admitted with acute dyspnoea. Physical examination revealed subcutaneous emphysema in the cervical and thoracic area. This was further confirmed by the total body computed tomography that also demonstrated mediastinal emphysema. Epidural pneumatosis of the thoracis spine was also evident. There was no history of trauma, but well of a recent oral ecstasy consumption during a techno rave party, associated with intense dancing and jumping. Clinical course was favourable with conservative therapy.

Pregabalin-associated myoclonic encephalopathy without evidence of drug accumulation in a patient with acute renal failure.

Pregabalin, used for treating partial epilepsy and neuropathic pain, is usually well tolerated. Patients with impaired renal function are at risk to develop more serious adverse events. A 64-year-old woman was admitted in the Emergency Department for altered consciousness and abnormal movements. She recently started to take pregabalin (150 mg/day) for neuropathic pain. The drug was withdrawn 36 h before hospitalization following worsening of neurological symptoms. At physical examination, myoclonus was noted as main finding in the limbs and head, with encephalopathy. Laboratory investigations revealed acute renal failure with serum creatinine at 451.3 µmol/l. Urine output was preserved. After supportive care alone, myoclonus resolved after 24 h and consciousness was normal after 48 h. Renal function was also recovered. At the time of admission, the concentration of plasma pregabalin was 3.42 µg/ml, within therapeutic range. The calculated terminal elimination half-life was 11.5 h. Pregabalin-induced myoclonus may not be strictly related to drug accumulation in acute renal failure, with the possibility of a threshold phenomenon.

The spectrum of acute heart failure after venlafaxine overdose.

OBJECTIVE: Venlafaxine is a bicyclic antidepressant that may be associated with severe cardiotoxicity following large overdose. The purpose of this short case series is to present different patterns of venlafaxine-related cardiotoxicity and to discuss the potential mechanisms. CASE SERIES: Between January 2010 and July 2011, four patients were admitted to an ICU with acute left ventricular failure following large venlafaxine overdoses. The age of the four female patients ranged from 35 to 65 years. None of them had no history of cardiovascular disease. The amount of venlafaxine ingested by history ranged from 3150 to 13500 mg (extended-release preparation in two cases). The peak serum venlafaxine concentration was between 2153.3 and 9950 ng/ml. Three patients died and one recovered rapidly. The initial ECG revealed only mild abnormalities in two cases. In two patients, at least one ECG recording demonstrated a widening of QRS interval. In three patients, echocardiography disclosed a left ejection fraction of 15%-18%. Two patients presented a severe serotonin syndrome, with major rhabdomyolysis. Seizures were noted in two cases, including one patient with status epilepticus. Three patients were mechanically ventilated. The causes of death were refractory hypoxemia, malignant arrhythmias, and cardiogenic shock, respectively. DISCUSSION: Severe and diffuse left ventricular dysfunction may be observed after large venlafaxine overdoses and this is not always associated with severe cardiac conduction function abnormalities. The mechanisms underlying venlafaxine-related cardiac failure with preserved normal cardiac conduction are discussed. A possible explanation may be a catecholamine-induced myocardial damage in relationship with the inhibition of norepinephrine (and dopamine) reuptake.

Locked-in syndrome as an unusual complication of acute otitis media.

BACKGROUND: A 32-year-old woman developed altered consciousness two days after initial symptoms of acute otitis media, with purulent discharge from the right ear. She was quadriplegic, with spontaneous eye opening, mild neck stiffness, and lacking vestibular-ocular reflexes. METHODOLOGY: Upon admission, the patient was subjected to brain computed tomography (CT), magnetic resonance imaging (MRI), and lumbar puncture. RESULTS: CT was consistent with pansinusitis, right middle ear otitis, mastoiditis, and sphenoiditis. No brainstem lesion was evident; brain MRI demonstrated ischemic and secondary hemorrhagic lesions in the pons and cerebral peduncles. The dura mater in the petroclival space was intensely inflamed, and likely responsible for reduced basilar arterial blood flow. Lumbar puncture yielded clear cerebrospinal fluid; gram stain examination was negative and culture remained sterile. Streptococcus pneumoniae and Haemophilus influenzae were cultured from the purulent ear discharge. CONCLUSION: The final diagnosis was locked-in syndrome consecutive to inflammatory changes compressing the basilar artery.

Refractory hypercapnia: a simplified technique for extracorporeal CO2 removal (ECCO2R) in the presence of therapeutic limitations.

Refractory hypercapnia with severe acidosis appeared in a 67-year-old man who presented with lung fibrosis and a left pneumothorax as delayed complications of bleomycin chemotherapy for advanced grade lymphoma. Due to failure of noninvasive ventilation using a high-flow nasal cannula oxygen system, the patient was mechanically ventilated with two ventilators at different settings, after intubation with a double-lumen tube. As he had a poor haematological prognosis, extracorporeal membranous oxygenation was not considered. To remove some amount of carbon dioxide, we used a simplified method based on a veno-venous hemofiltration circuit coupled to a paediatric oxygenator and an air/oxygen blender. The efficacy on carbon dioxide removal was modest, with a percentage of CO2 total extraction ranging from 10.5 to 20.4%, but the system was immediately available, well tolerated and not very expensive.

Reversible splenial lesion syndrome in cerebral malaria.

A 71-year-old Caucasian man living in Congo was investigated by serial magnetic resonance imaging (MRI) after having presented cerebral malaria due to Plasmodium falciparum. The clinical picture was characterized initially by coma and seizures. The patient developed multiple organ failure. There was, at 4 months follow-up only, a minimal neurological improvement consistent with minimally conscious state. The first cerebral MRI on day 17 showed a lesion of the splenium of corpus callosum with high signal intensity on DWI and FLAIR sequence and reduced ADC, and small cortical infarcts in the internal occipital regions. Follow-up MRI obtained 36 days later showed a complete resolution of splenial lesion, though without clinical improvement. Cerebral malaria should be added to the list of possible causes of reversible lesion of the splenium of corpus callosum.