Viviane Chalhoub

Prophylactic ondansetron is effective in the treatment of nausea and vomiting but not on pruritus after cesarean delivery with intrathecal sufentanil-morphine

STUDY OBJECTIVES To assess the safety and efficacy of ondansetron for prevention of pruritus, nausea and vomiting after cesarean delivery with intrathecal sufentanil-morphine. DESIGN Randomized, double-blind, placebo-controlled study. SETTING Referral center, institutional practice. PATIENTS 100 nonbreastfeeding women undergoing elective cesarean delivery with sufentanil-morphine-bupivacaine anesthesia. INTERVENTIONS After the umbilical cord was clamped, patients in Group 1 received ondansetron 8 mg intravenously (IV) and patients in Group 2 received placebo. MEASUREMENTS Frequency and severity of postoperative (24-hour) pruritus, nausea and vomiting, surgical pain, and side effects related to ondansetron were recorded. MAIN RESULTS In the ondansetron group, 38 patients had pruritus (16 mild and 22 severe) and 9 patients had nausea and vomiting (5 mild and 4 severe). In the placebo group, 41 patients had pruritus (21 mild and 20 severe) and 29 patients had nausea and vomiting (9 mild and 15 severe). The frequency and severity of the nausea and vomiting episodes were significantly reduced in the ondansetron group. Pain scores were comparable between groups. No side effects related to ondansetron were reported. CONCLUSIONS Prophylactic IV ondansetron 8 mg is safe and effective in reducing the frequency and the severity of nausea and vomiting, but not pruritus, following cesarean delivery with intrathecal sufentanil-morphine.

Intracranial Aneurysm and Recessive Polycystic Kidney Disease: The Third Reported Case

OBJECTIVE To highlight the possible association of intracranial aneurysm with autosomal recessive polycystic kidney disease. DESIGN, SETTING, AND PATIENT To our knowledge, this association has been reported only twice in the medical literature. We herein report the case of a 21-year-old man with autosomal recessive polycystic kidney disease, presenting with subarachnoid hemorrhage secondary to a ruptured intracranial aneurysm, at our institution. RESULTS In the presence of only 3 cases in the medical literature, one might conclude they are a simple coincidence. However, should this association exist, such as with the dominant form, then the neurologic prognosis and even the life of young patients may be at stake. CONCLUSIONS Given the devastating consequences of intracranial bleeding in young patients, early neurologic screening may be warranted.

Coma profond aréactif réversible après intoxication par des abats d’un poisson méditerranéen

INTRODUCTION Neurotoxic fish poisoning appears to be a recent phenomenon in the Mediterranean Sea. We report a case of deep non-reactive reversible coma after ingestion of Mediterranean fish innards. CASE REPORT An 80 year-old man, heavy smoker who had a previous cerebral infarct in the posterior territory, was admitted for rapid deterioration of his neurological condition. He started having perioral tingling, then dysarthria, then became quadriparetic, then developed respiratory and hemodynamic failure and within 3-4h, entered a state of deep non-reactive coma with absence of all brainstem reflexes. He started to improve after 20 h and recovered his neurological baseline within 36 h. Later on, he stated that all his symptoms started after he ingested the gonads of a toxic fish, Lagocephalus scleratus. DISCUSSION Tetrodotoxin blocks voltage-gated sodium channels and inhibits the production and propagation of action potentials. This toxin is highly concentrated in the liver, gonads, intestines and skin of this fish that is well-known in Japan (where it is considered as a delicacy) and South-East Asia and seems to have migrated recently to the Mediterranean Sea. There is no known antidote to tetrodotoxin but intensive supportive treatment can be life-saving.

Ondansetron for prevention of intrathecal opioids-induced pruritus, nausea and vomiting after cesarean delivery.

We have read with interest the article by Charuluxananan et al. (1) that compares the effectiveness of nalbuphine and ondansetron in the prevention of intrathecal morphine-induced pruritus after cesarean delivery. The authors found that prophylactic nalbuphine and ondansetron were both effective in reducing pruritus but not nausea and vomiting induced by 0.2 mg of intrathecal morphine. In a similar study (2), we assessed the efficacy of ondansetron for the prevention of pruritus, nausea, and vomiting induced by intrathecal sufentanil-morphine in 100 patients undergoing cesarean delivery. Doses of drugs used were 8 mg of ondansetron, 0.1 mg of morphine, and 2.5 g of sufentanil. The incidence of nausea and vomiting, in this study, was significantly reduced in the treatment group when compared with the placebo group (18% vs 48%; P 0.001). However, the incidence of pruritus was not decreased in the treatment group when compared with the placebo group (76% versus 82%; P 0.46). These results are not in agreement with the data reported by Charuluxananan et al. Failure of ondansetron to prevent pruritus in our study may be explained by the fact that sufentanil—which is a highly lipophilic opioid with a quick onset of action—was added to intrathecal morphine. The serotonin receptors in the spinal cord were probably activated by sufentanil before they were blocked by ondansetron. Furthermore, and because the incidence of nausea and vomiting following intrathecal opioids is dosedependent (3), the effectiveness of ondansetron in our study could be related to the low dose (0.1 mg) of the intrathecally administrated morphine as compared with the higher dose (0.2 mg) used by Charuluxananan et al. In conclusion, prophylactic ondansetron decreases the incidence of intrathecal opioid-induced pruritus, nausea, and vomiting after cesarean delivery. However, ondansetron may not be effective when highly lipophilic opioids or increased doses of morphine are administrated.

Pulmonary Migration of a Fragment of Plastic Coating Sheared from a Stylet

BACKGROUND In trauma patients, particularly with head immobilization, tracheal intubation without the use of a stylet may be impossible. OBJECTIVES To report a very rare but potentially fatal complication that may happen in any Emergency Department: fracture of the plastic sheath of an intubation stylet, reported only twice before in the literature. CASE REPORT Two large plastic fragments detached from a stylet while intubating a trauma patient. One piece was removed from the endotracheal tube a few hours later in the operating room. The second fragment migrated asymptomatically into the pulmonary airway. It was successfully retrieved from the right bronchus 24 h later. CONCLUSION This potentially life-threatening event may go unnoticed after intubation if the endotracheal tube is not obstructed by the fragment. Gentle withdrawal of the stylet from the tube is essential to avoid stylet fracture. Careful examination of the stylet after intubation may suggest a stylet fracture.

Subdural hematoma with cranial nerve palsies after obstetric epidural analgesia

We report a case of intracranial subdural hematoma (SDH) with trigeminal and facial nerve paresis in a pregnant woman receiving epidural analgesia without evidence of dural puncture. A 35-year-old patient, with no medical history, was admitted in active labour at 38 weeks of gestation. An epidural catheter was inserted and advanced 3 cm at L3–4 without difficulty or evidence of dural puncture. A test dose of 2% lidocaine 40 mg excluded intrathecal catheter placement and a continuous infusion of bupivacaine and sufentanil was started. Uncomplicated vaginal delivery took place 5 h later, and the patient was discharged home on the second postpartum day. Three days later, she developed a postural occipitofrontal headache. Conservative therapy for mild post-dural puncture headache (PDPH) was started. On postpartum day 9, she presented to the emergency department with headache. An epidural blood patch (EBP) was performed at L4–5 and resulted in 50% improvement of her headache. However, the following morning she was hospitalized urgently for severe headache unrelated to posture, with paraesthesia and numbness of the left side of the face. Magnetic resonance imaging revealed bilateral 10 day-old temporal SDHs. The following day the patient was conscious, afebrile, and with minimal neck stiffness. Left-sided facial weakness had progressed with drooping of the lip, inability to close the eyelid, and weakness of the frontalis, orbicularis oculi and orbicularis oris muscles, with hypoalgesia and hypoesthesia. Kernig and Brudzinsky signs were absent. Bilateral pupillary reactions to light and ocular motility were normal. Neurological examination was otherwise normal, as were electrocardiogram, chest X-ray and laboratory tests. With SDH thickness of <15 mm, an estimated volume of <30 mL, a midline shift of <5 mm, and in the absence of clinical symptoms, the patient was managed conservatively. The trigeminal and facial nerve paresis recovered completely over six months. The association of SDH and trigeminal and facial nerve paresis as a complication of epidural analgesia has not been reported previously. Accidental dural puncture occurs in approximately 1% of the cases and was usually noted at the epidural insertion time. However, in one third of cases, no sign of dural puncture is seen at the catheter insertion time and retrospective diagnosis is made after PDPH appears. Cases of delayed diagnosis have been reported. In the absence of obvious dural puncture, other etiologies such as traumatic brain injury, coagulopathy or intense Valsalva maneuvers should be considered if the patient presents with symptoms suggestive of PDPH. A traumatic etiology was unlikely in our case given the bilateral hematomas, and coagulopathy was eliminated by laboratory tests. Intense and repeated Valsalva maneuvers during labour, leading to elevated intracranial and intraspinal pressures, could explain the subdural bleeding. If accidental dural puncture occurs, cerebrospinal fluid (CSF) may leak into the lumbar perispinal fatty tissue leading to CSF hypotension, arachnoid membrane lacerations or venous rupture, and finally SDH. The role of an EBP in the etiology of SDH in our case is controversial. It was performed to treat PDPH by tamponading the CSF leak. Guido et al. reported improvement in severe focal neurologic deficits with EBP. However, SDHs were found to develop after inadvertent dural puncture even when an EBP was performed. An EBP may exacerbate neurologic symptoms following dural puncture, and may lead to neurologic complications ranging from cranial nerve palsy to coma. The increased epidural and subarachnoid pressure secondary to the injection of blood may damage neural fibres, compromising neural blood flow, and oedema or nerve stretching during pregnancy may further contribute to injury if EBP is performed. The seventh cranial nerve is more liable to stretching, and the third, fourth, sixth and eighth cranial nerves are more affected when CSF loss has occurred. We feel that our patient had an unrecognised dural puncture with CSF leakage that continued in the postpartum period, leading to CSF hypotension and SDH. We consider that the hematoma, not the EBP, was the principal cause of cranial nerve palsies. Earlier EBP might have prevented both the haematoma and the cranial nerves palsies. In cases where clinical history, signs, and symptoms are not clearly consistent with dural puncture, neuroimaging should be strongly considered before performing an EBP.

Rupture of an infected radial artery false aneurysm

A 67-yr-old male obese smoker was admitted to the intensive care unit with respiratory failure due to exacerbation of chronic obstructive pulmonary disease. A 20G, 5-cm catheter (Seldicath; Plastimed , Paris, France) was placed in the right radial artery under aseptic conditions with a single puncture. The catheter was removed on day 5 and its tip sent for routine culture. On day 7, a red, painful, pulsatile mass (Figure A) with purulent discharge appeared at the puncture site. The discharge was sent for culture. Arterial ultrasonography of the lesion revealed a radial artery pseudoaneurysm (Figures B and C). The cultures from both the catheter tip and discharge were positive for methicillin-resistant Staphylococcus aureus. Antibiotic treatment was initiated with teicoplanine on day 9. On day 11, active bleeding at the puncture site developed. A suspected rupture of the

Dexmedetomidine sedation for a claustrophobic patient with obstructive sleep apnea undergoing magnetic resonance imaging.

Tizanidine is a commonly prescribedmedication formuscle spasms [1]. The pharmacokinetics of Tizanidine are altered by the use of CYP1A2 inhibitors as Ciprofloxacin in healthy subjects; elevation of Tizanidine levels leads to a decrease in psychomotor activity and hemodynamic changes which are manifested as a decrease in blood pressure and heart rate [2,3]. A 51-year-old woman with chronic low back pain was on treatment with Oxycodone 5/325 mg 3 times daily as needed, Oxycontin 10 mg twice daily, and Tizanidine 4 mg three times daily as needed. The patient was prescribed Ciprofloxacin 500 mg twice daily andMetronidazole 500mg three times daily for diverticulitis by her primary care physician. Four days after starting treatment the patient developed severe abdominal pain, nausea, and vomiting. The patient was admitted to the hospital, had abdominal computed tomography and ultrasound which showed an enlarged gall bladder. The gastroenterology team and gynecology team were consulted, and they both excluded the gastrointestinal tract and genitourinary tract, respectively, to have any disease condition that caused this pain. The patient was afebrile on presentation and her white blood cell count was 5.9. The patient also presented with acute kidney dysfunction, thrombocytopenia, orthostatic hypotension, dizziness, and headache. She was also diagnosed with Clostridium difficile infection. The abdominal pain in this patient can be attributed to the infection with C difficile or the interaction between Ciprofloxacin and Metronidazole. Tizanidine is a common medication to be prescribed by a pain physician for treating muscle spasms. It is very important to check the patient medication list as they might be on Ciprofloxacin for urinary tract infection. Although the interaction between both medications is very rare, it can be life threatening.

Contributing Factors to Inferior Vena Cava Filter Migration

We read with great interest the study published by Laborda et al. about the relationship between inferior vena cava size and pressure, and filter migration or penetration [1]. We agree completely with their findings concerning the effects of ventilation and valsalva maneuvers on the hemodynamics and anatomy of the inferior vena cava (IVC). These changes may be a risk factor for the migration of a previously inserted IVC filter. We would like to draw attention to an overlooked additional element that may also contribute to IVC filter migration: Prone positioning in association with positive pressure ventilation. We recently experienced an IVC filter migration during spinal surgery in a prone position. The IVC is a dynamic compliant vessel, subject to many physiologic variables that may affect its anatomy and hemodynamics [2]. Bariatric surgery illustrates best the dynamic nature of the vena cava, the vessel being under constant stress from fluid resuscitation and pneumoperitoneum, and acute migration of IVC filters have been reported during surgery [3]. Migrations have also been reported during cardiopulmonary resuscitation, where the IVC takes its maximal diameter as a result of aggressive fluid replacement, pump failure, and positive pressure ventilation [2]. Prone positioning of the patient in the operating room may also acutely modify the pressure in the IVC and contribute to the change in its diameter [4–6]. Prone positioning patients is widely practiced during lumbar spinal surgery, but these positions vary according to the available operating facilities and frames used. A positioning frame allowing the patient’s abdominal viscera to hang freely significantly reduces their inferior vena caval pressure, whereas proning on a conventional pad increases IVC pressure 1.5 times [6]. The patient we hereby describe was positioned on a conventional convex pad. In addition to proning, caval morphology and hemodynamics have probably been also affected by positive pressure ventilation, as demonstrated by Laborda et al. Device migration to the heart chambers is a serious complication, with a potentially fatal outcome. In 3 reviews of filter migrations between 1996 and 2008, we collected 59 cases of devices migrating up to the heart [3, 7, 8]. Four patients (7 %) died from the cardiac complications and half of the patients presented with potentially life-threatening complications including cardiogenic shock, arrhythmias, and acute myocardial infarction. Once again, we congratulate Laborda et al. on their work. We think that anesthesiologists should be aware of the risks related to the sudden increase of IVC pressure in the presence of an indwelling device. The use of proper frames that allow for less abdominal compression, and the avoidance of high positive ventilation pressures should be considered in these patients.

Inferior vena cava filter migration during the prone position for spinal surgery: a case report

PurposeInferior vena cava (IVC) filters have been used as an alternative therapy for patients with a contraindication to anticoagulation. We present a case of an IVC filter migration to the right ventricle occurring while a trauma patient was undergoing spinal surgery in the prone position. The patient provided written consent to describe this case.Clinical featuresA 54-yr-old multiple trauma male patient with an unstable fracture of the T6 vertebra and a stable fracture of the T10 vertebra developed a pulmonary embolism secondary to a left common femoral deep vein thrombosis. An IVC filter was placed so that an intravenous unfractionated heparin infusion could be stopped two days before scheduled spinal surgery. Intraoperatively, the patient was placed in the prone position on conventional convex support pads. At the end of the procedure, he developed ventricular trigeminy which lasted three minutes.During the next 48 hr, the patient developed a fever of 39°C. An echocardiogram was performed to rule out endocarditis, and results showed that the IVC filter had migrated into the right ventricle. After a failed attempt at percutaneous removal of the filter in the catheterization laboratory, the patient was transferred to the operating room and the IVC filter was extracted through a midline sternotomy under cardiopulmonary bypass.ConclusionsThe prone position during surgery can induce anatomic and hemodynamic changes in the IVC. This may contribute to the migration of IVC filters—especially flexible retrievable filters. Careful handling and positioning of patients with IVC filters is recommended to avoid a sudden increase in IVC pressure that may predispose to IVC filter migration.RésuméObjectifOn utilise les filtres de la veine cave inférieure (VCI) comme traitement alternatif chez les patients lorsque l’anticoagulation est contre-indiquée. Nous présentons un cas de migration du filtre de la VCI dans le ventricule droit survenue alors qu’un patient traumatisé subissait une chirurgie de la colonne en position ventrale. Le patient a consenti par écrit à la publication de ce cas.Éléments cliniquesUn patient polytraumatisé de 54 ans avec une fracture instable de la vertèbre T6 et une fracture stable de la vertèbre T10 a subi une embolie pulmonaire suite à une thrombose veineuse profonde de la veine fémorale commune gauche. Un filtre de VCI a été placé de façon à ce qu’une perfusion intraveineuse d’héparine non fractionnée puisse être interrompue deux jours avant la chirurgie planifiée de la colonne. Pendant l’opération, le patient a été placé en position ventrale sur des coussins de soutien convexes conventionnels. À la fin de l’intervention, il a manifesté un trigéminisme ventriculaire d’une durée de trois minutes.Au cours des 48 h suivantes, le patient a manifesté une fièvre de 39 °C. Une échocardiographie, réalisée afin d’exclure une endocardite, démontra que le filtre de la VCI avait migré dans le ventricule droit. Après une tentative infructueuse pour retirer le filtre de façon percutanée dans le laboratoire de cathétérisation, le patient a été transféré en salle d’opération et le filtre de la VCI retiré via une sternotomie médiane sous circulation extracorporelle.ConclusionPendant une chirurgie, la position ventrale peut entraîner des changements anatomiques et hémodynamiques dans la VCI. Cela pourrait favoriser la migration des filtres de la VCI – particulièrement les filtres récupérables souples. Une manipulation et un positionnement minutieux des patients ayant des filtres de la VCI sont recommandés afin d’éviter une augmentation soudaine de la pression dans la VCI qui pourrait favoriser une migration du filtre.