Nicolas Gagnon

Complication of intraosseous administration of systemic fibrinolysis for a massive pulmonary embolism with cardiac arrest.

We managed a 53-year-old man for suspected acute respiatory failure. Accessing a peripheral vein was very difficult. efore insertion of venous access, the patient developed ventriclar fibrillation (VF) cardiac arrest. We started cardiopulmonary esuscitation (CPR) with chest compressions. An intraosseous (IO) atheter (EZ-IO®, Vidacare®) was inserted into the proximal tibia. fter 30 min of resuscitation, including injection of adrenaline, e remained in asystole. Echocardiography showed marked right entricular dilatation and a collapsed left ventricle. We susected massive pulmonary embolism (MPE) and gave thrombolysis Acteplase 0.6 mg kg−1). Five minutes later, sinus rhythm was estored. Femoral venous access was inserted and the IO catheter as removed. The patient was treated successfully in the intensive are unit (ICU) for post cardiac arrest syndrome with multi-organ ailure. He had few residual neurological sequelae. A large extensive ecrosis of the anteromedial side of the right leg appeared in the IO nsertion area (Fig. 1) 48 h later. Medical treatment failed, thus surical excision was performed followed by vacuum-assisted closure. fter 5 weeks in the ICU, vacuum therapy was pursued for 3 weeks n the dermatology department with repetitive surgical dressing. lceration persisted on the whole anteromedial side of the right eg with direct exposure of bone. The computed tomography (CT)

Ebola Virus–Related Encephalitis

Ebola patients frequently exhibit behavioral modifications with ideation slowing and aggressiveness, sometimes contrasting with mild severity of Ebola disease. We performed lumbar punctures in 3 patients with this presentation and found Ebola virus in all cerebrospinal fluid samples. This discovery helps to discuss the concept of a specific Ebola virus encephalitis.

Seizures associated with local anaesthetic intoxication

cannot support specific recommendations. The cardiovascular profile of pancuronium suggests that it can produce cardiovascular stimulation possibly by a direct action and an increased release/decreased reuptake of catecholamines at the adrenergic nerve terminals. b-Adrenoreceptors and M2 muscarinic receptors possibly play a significant role in pancuronium-induced cardiac responses. 6 Pancuronium has been found to have a higher potency for interaction with cardiac muscarinic receptors compared with newer neuromuscular blockers. On the other hand, as shown in Supplementary Table S1 of our review, there is sufficient evidence supporting the lack of significant cardiac effects of newer neuromuscular blockers, such as atracurium, cisatracurium, and rocuronium. Based on the above, we consider that pancuronium is probably not the first-choice neuromuscular blocker for patients with arrhythmogenic syndromes (as ARVD), even though serious adverse effects have not been observed in the authors’ clinical practice, or confirmed in relevant clinical reports. In conclusion, pancuronium seems to have a less favourable cardiovascular profile compared with newer neuromuscular blockers according to electrophysiological studies. Regarding neuromuscular blockers and ARVD, relevant literature is inadequate to support specific recommendations. On the other hand, as it is prudent for the physicians always to be on the safe side, we consider that neuromuscular blockers with minimal cardiovascular effects should be preferred over pancuronium in patients who are at risk of arrhythmias, as are patients with ARVD.

Occupational Exposures to Ebola Virus in Ebola Treatment Center, Conakry, Guinea

We report 77 cases of occupational exposures for 57 healthcare workers at the Ebola Treatment Center in Conakry, Guinea, during the Ebola virus disease outbreak in 2014−2015. Despite the high incidence of 3.5 occupational exposures/healthcare worker/year, only 18% of workers were at high risk for transmission, and no infections occurred.

Comments on Rees et al.: safety and feasibility of a strategy of early central venous catheter insertion in a deployed UK military Ebola virus disease treatment unit

Dear Editor, We read with great interest the article by Rees et al. published in your journal [1]. First of all, we would like to congratulate Dr. Rees and his team for their valuable work which gives Ebola healthcare workers access to very useful data. As part of France’s contribution, a ten-bed military Ebola virus disease treatment unit has been deployed since January 2015 in Conakry, Guinea, where the epidemic remains active. The unit comprises a multidisciplinary team of senior physicians combined with nurses, laboratory technicians, pharmacists, administrative and command elements. Our medical team also discussed the potential advantages of early central venous access with two goals: (1) to allow reliable venous access to facilitate fluid replacement that is a key point in the care of Ebola patients, and (2) to prevent the personnel from risk of contamination by reducing the number of venous punctures. Data published in the article by Rees et al. showed that this strategy may be successful, which is concordant with our local experience. However, we observed that patients frequently experienced agitation and confusion as a result of encephalopathy. To date, this encephalopathy physiopathology remains to be elucidated, but we can hypothesize that it may be enhanced by direct viral encephalopathy, systemic inflammatory response syndrome and the isolation imposed by the ‘‘red zone’’. Above all, agitation may complicate the central venous catheter insertion, and increase the risk of accident. We would like to know if the authors observed such agitation in their patients, and how they dealt with this concern when central venous access was decided upon. Is it a contraindication to central venous access? Do they perform deep sedation that may be challenging and unsafe in the red zone? Conflicts of interest The authors have no conflict of interest related to the topic of this letter.

Organ failures on admission in patients with Ebola virus disease

Dear Editor, The actual outbreak of Ebola virus disease (EVD) started in December 2013 in West Africa, and spread from Guinea to Sierra Leone and Liberia. Organ dysfunctions during EVD have only been described through case reports managed in high income countries, and data are still lacking [1]. The Sepsis-related Organ Failure Assessment (SOFA) score has been developed to quantitatively describe the degree of organ dysfunction in intensive care unit septic patients [2]. We aimed to characterize the severity of Ebola patients admitted to our center by calculating the SOFA score on admission. After approval by the local ethics committee, SOFA score was calculated in Ebola-infected patients using the most abnormal values from the first 24 h after admission. Data were collected between January and April 2015. A total of 38 patients were admitted, of whom 22 were infected with Ebola. Results are expressed as mean ± standard deviation. The mean age of confirmed cases was 33 years (±9). Mean viral load expressed as cycle threshold (CT) at admission was 21.6 (±3.9). On the 22 patients, six died (mortality rate of 27.3 %). Mean SOFA score at admission was 2.6 (±1.7). SOFA score at admission was significantly higher in non-survivors than in survivors (4.8 ± 1.7 versus 1.7 ± 1, P = 0.001). Mean viral load was also higher in non-survivors (CT at 17.7 ± 3.8 versus 23 ± 3.1, P = 0.006). Renal dysfunction was the most frequent dysfunction on admission in non-survivors (Fig. 1). Relationships between admission patients’ conditions and outcome have never been explored during EVD, except for age and viral load [3]. A study analyzing the WHO case investigation form data of 3343 infected patients reported a high mortality rate above 70 %, but patients’ organ dysfunctions could not have been scored [4]. In this study, hemorrhage, coma, and ‘‘difficulty breathing’’ were not commonly reported in patients who died, suggesting that massive fluid loss due to gastrointestinal disorders may be the main factor of worse outcome. Another study reported a lower mortality rate of 43 % [3]. Risk of death was associated with an older age, but this study failed in identifying other factors, mainly because biological data on admission were also limited as no routine clinical laboratory testing was available. Presented data showed that patients were hemodynamically stable on admission and had no respiratory dysfunction (3 % of patients with oxygen therapy). Our results highlighted two main points. The first is that cardiovascular, respiratory, and neurological dysfunctions were not common on admission in Ebola patients, even in non-survivors. The second is the frequency of renal dysfunction. Acute kidney injury during EVD may be promoted by several factors: hypovolemia due to gastrointestinal fluid loss, inflammatory response, viral injury as suggested by histopathological examination of tissues from infected animals showing indications of interstitial nephritis [5]. Larger studies are needed to describe objectively organ dysfunction in Ebola patients and evolution during stay. It may also help to optimize the preparation of treatment facilities according to local available resources for the next outbreaks.

Dyspnea and risk of death in Ebola infected patients. Is lung really involved

TO THE EDITOR—We read with great interest the article of Barry et al, published in a previous issue of this journal. In this observational cohort study of Ebola patients, authors identified difficulty breathing as an independent predictor of death (adjusted odds ratio [OR], 5.75; P = .1) [1]. In the discussion, the authors postulate that difficulty breathing could be linked to parenteral rehydratation that could lead to edema in patients with respiratory disease. The authors did not provide data to support it. In our point of view, this hypothesis is not supported by local experience. Pulmonary edema may be favored both by vascular leakage syndrome and fluid replacement if it is massive. A case report of a healthcare worker who contracted Ebola infection in Sierra Leone and was airlifted to a German intensive care unit showed that pulmonary edema may occur late in the disease after massive rehydration [2]. In an Ebola treatment center, providing intensive care is very challenging due to the number of patients, heavy climatic condition, and lack of medical staff, which seriously limits the time spent at the patient’s bedside. Working in personal protective equipment is also a barrier in providing accurate care and may complicate vascular access in dehydrated patients. As a result, all of these factors limit seriously the crystalloid volume that could be perfused to Ebola patients. In a previously published study regarding the Donka center, it was described that the median crystalloid volume perfused to Ebola patients was 1 liter the first 24 hours, with interquartile range at 1–1. It means that 75% of patients received only 1 liter of crystalloid during the first 24 hours, which is not consistent with the occurrence of pulmonary edema [3].Moreover, we performed in our center systematic transthoracic echocardiography in 9 consecutives patients; we did not find elevated ventricular filling pressure in any patients, even in dyspneic patients. Difficulty breathing has been reported for years in Ebola patients. Previous studies described a “sine materia” dyspnea, suggesting that dyspnea could be the symptom of another organ dysfunction [4]. Others causes of dyspnea such as muscle weakness, encephalitis, and metabolic acidosis remain to be explored. Unfortunately, biological data are poor on the actual Ebola outbreak to describe objectively the organ dysfunctions. However, metabolic acidosis may be one of the key points in the Ebola infection course and has been reported in some patients [3]. It might be promoted by several factors such as bicarbonates loss during diarrhea, acute kidney injury, and lactic acidosis during the late shock phase. Finally, difficulty breathing in Ebola patients should probably be linked to metabolic disorders rather than pulmonary aggression. Paraclinical data are required to clearly identify the organ dysfunctions during Ebola virus disease.

Another use of the ultrasound-guided transversus abdominis plane block in the ED

We read with interest the article published by Herring et al [1], describing the interest of the transversus abdominis plane (TAP) block for analgesia in emergency situations. We describe another interest of the technique. We used the TAP block for a woman with acute hyperalgesic pancreatitis for analgesia in a clinical situation with opiate resistance. We took care in the emergency department (ED) a 51-yearold patient for an acute pancreatitis. She was hospitalized 1 month before for previous pancreatitis. Her medical history indicated a Harrington implant surgery for a scoliosis in 1977. Initially, she had no clinical complications of the pancreatitis but a CT Balthazar E grade score. She had severe pain. The patient evaluated her pain at 8/10 at the numerical rating scale (NRS). A multimodal analgesia was started with the association of paracetamol, nefopam, and morphine titration. After 12 mg of morphine, the patient began to present adverse effects of the treatment: drowsiness, bradypnea, and desaturation without effective analgesia (NRS, 7/10). We were not able to perform any neuraxial anesthesia because of her former spine surgery. A bilateral ultrasound-guided subcostal TAP block was realized. We injected 20 mL of ropivacaine 0.5% on each side. It allowed rapid pain control (NRS, 3/10). Noninvasive ventilation remained possible. A intravenous patient controlled analgesia (IV-PCA) with morphine was also installed. The patient was transferred to the intensive care unit. Numerical rating scale remained low (b30) during 48 hours. Morphine consumption was 1 mg on day 1 and 3 mg on day 2. The third day, pain came back. The patient needed 8 mg of morphine (PCA), and NRS was 6/10. We decided to realize another TAP block. The patient was discharged on day 5 without serious pain in the medical ward. Pain during acute pancreatitis has to be treated properly. Italian and Japanese recent guidelines in acute pancreatitis published the dramatic impact of analgesia to control severe persistent abdominal pain in this clinical situation (A-grade recommendation) [2,3]. Morphine in pain treatment for an acute pancreatitis could have negative effect because of its presumed hypertony of the sphincter of Oddi hypertony [4]. However, a meta-analysis published in 2001 concluded that no studies or evidence exists to indicate that morphine is contraindicated to be used in acute pancreatitis [5]. Anyway, in our case, morphine was ineffective. According to a previous study, an excellent level of analgesia can be expected when epidural anesthesia is used in case of acute hyperalgesic pancreatitis [6]. In our case report, there was a contraindication to neuraxial anesthesia. That is why we proposed the TAP block. Transversus abdominis plane block was first described in 2001 in a letter by Dr Rafi [7]; the lumbar triangle of Petit is used as a landmark for injecting local anesthetic into the neurovascular plane of the abdominal wall. Over the past years, with the “revolution” of ultrasound in regional anesthesia, there has been a growing interest for the TAP block. The technique realized under ultrasound guidance involves injection of local anesthetic into a plane between internal oblique and transversus abdominis muscles. This plane contains the thoracolumbar nerves from T7 to L1, which supply anterolateral abdominal wall innervation [8]. The analgesic efficacy of the TAP block has been demonstrated in prospective randomized trials compared with placebo, in different surgical procedures such as abdominal surgery, hysterectomy, retropubic prostatectomy, cesarean section, laparoscopic cholecystectomy, and appendicectomy [8]. Catheter insertion is possible to provide boluses as an effective alternative to epidural infusion to provide postoperative analgesia after upper abdominal surgery [9]. The interest of the TAP block for supraumbilical incision allowed us to think about the efficacy of the TAP block for pain linked to acute pancreatitis. In the case of the pancreatitis, we do not have only abdominal wall pain. The TAP block is efficient not only for abdominal wall pain but also for intra-abdominal pain [10]. That is why TAP block can be effective in acute pancreatitis pain [10]. Few complications of the TAP block are described [11]. We did not find recent study or case report presenting the interest of the TAP block for analgesia in acute pancreatitis. Subcostal ultrasound-guided TAP block is a safe and easy technique. Emergency physicians training in sonography can quickly identify relevant structures and perform the block efficiently [1]. It can be used for analgesia in case of hyperalgesic acute pancreatitis. As Herring et al [1], we presented another use of www.elsevier.com/locate/ajem

Hyperalgesic acetabular fracture treated by transversus abdominis plane block in the ED.

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