Cerebrospinal Fluid Lavage Research Articles

Tranexamic acid-associated intrathecal toxicity during spinal anaesthesia: A narrative review of 22 recent reports.

Therapeutic use of tranexamic acid (TXA) to minimise blood loss is common during a wide range of surgical procedures. This review aims to explore the clinical features of the accidental intrathecal administration of TXA and to identify contributory factors that might prevent future incidents. The author searched published reports of accidental intrathecal administration of TXA using Medline and Google Scholar databases from July 2018 to September 2022, including error reports in any language but excluding errors via nonintrathecal routes. The human factors analysis classification system (HFACS) framework was used to examine and classify the human and systemic factors that contributed to the errors. Twenty-two errors of accidental intrathecal administration were reported during the search period. The analysis showed that the outcome was death in eight patients (36%) and permanent harm in four (19%). The fatality rate was higher among female individuals (6/13 versus 2/8 male individuals). Two-thirds of errors (15/22) occurred during orthopaedic surgery (10) and lower segment caesarean sections (5). Nineteen of 21 patients developed refractory or super refractory status epilepticus, requiring mechanical ventilation and intensive care for 3 days to 3 weeks for those who survived the initial few hours. Severe sympathetic stimulation resulting in refractory ventricular arrhythmias was the final event in some patients, with death within a few hours. Lack of familiarity with clinical characteristics caused delayed diagnosis or confusion with other clinical conditions. A proposed plan to manage intrathecal TXA toxicity is presented, including immediate cerebrospinal fluid lavage; however, there is no specific approach. The HFACS suggested mistaking look-alike TXA ampoules for local anaesthetic was the predominant cause. The author concludes that inadvertent intrathecal TXA is associated with mortality or permanent harm in more than 50% of patients. The HFACS demonstrates that all errors are preventable.

Accidental intrathecal injection of tranexamic acid: a case report

BackgroundTranexamic acid is a well-known antifibrinolytic medication frequently prescribed to individuals with bleeding disorders. Following accidental intrathecal injection of tranexamic acid, major morbidities and fatalities have been documented. The aim of this case report is to present a novel method for management of intrathecal injection of tranexamic acid.Case presentationIn this case report, a 400 mg intrathecal injection of tranexamic acid resulted in significant back and gluteal pain, myoclonus of the lower limbs, agitation, and widespread convulsions in a 31-year-old Egyptian male with history of left arm and right leg fracture. Immediate intravenous sedation with midazolam (5 mg) and fentanyl (50 μg) was delivered with no response in seizure termination. A 1000 mg phenytoin intravenous infusion and subsequently, induction of general anesthesia was performed by thiopental sodium (250 mg) and atracurium (50 mg) infusion, and the trachea of the patient was intubated. Maintenance of anesthesia was achieved by isoflurane 1.2 minimum alveolar concentration and atracurium 10 mg every 20 minutes, and subsequent doses of thiopental sodium (100 mg) to control seizures. The patient developed focal seizures in the hand and leg, so cerebrospinal fluid lavage was done by inserting two spinal 22-gauge Quincke tip needles, one on level L2–L3 (drainage) and the other on L4–L5. Intrathecal normal saline infusion (150 ml) was done over an hour by passive flow. After cerebrospinal fluid lavage and the patient’s stabilization was obtained, he was transferred to the intensive care unit.ConclusionsEarly and continuous intrathecal lavage with normal saline, with the airway, breathing, and circulation protocol is highly recommended to decrease morbidity and mortality. The selection of the inhalational drug as a sedative and for brain protection in the intensive care unit provided possible benefits in management of this event with medication errors.

Unintentional subarachnoid administration of tranexamic acid during spinal anesthesia

An accidental intrathecal tranexamic acid injection is a rare but extremely unpleasant case, which can lead to severe complications, including death. This review aimed to describe the clinical, pathophysiological changes and outcomes occurring in patients with unintentional tranexamic acid subarachnoid injection during spinal anesthesia. The review includes studies published in PubMed, The Cochrane Library, Google Scholar, and the Russian Science Citation Index databases. There were 31 reports (27 literature reports and 4 own observations) of unintended tranexamic acid administration during spinal anesthesia, including 12 cases in traumatology and orthopedics, 11 cases in cesarean section, and 8 cases in urology and general surgery. Typical signs and symptoms reported by the authors include severe pain in the lower back, buttocks, and lower extremities, seizure syndrome, marked tachycardia and arterial hypertension, and ventricular arrhythmias. Ten (32.1%) patients recovered without any consequences and six (19.4%) patients required long-term rehabilitation after hospital discharge due to severe neurological deficits or cognitive impairment. Of 11 females, 9 died during cesarean section and 4 of 12 patients died in traumatology and orthopedics. Overall, 15 (48.4%) patients had a fatal outcome. An unintentional subarachnoid tranexamic acid injection is a catastrophic event with extremely high patient risk and is accompanied by high mortality, especially in obstetric practice. Intensive care should include intravenous propofol or sevoflurane inhalation in the case of unintentional intrathecal tranexamic acid injection, and cerebrospinal fluid lavage is promising. Developing a formalized protocol for intrathecal administration of local anesthetic solutions is advisable to avoid errors associated with accidental drug administration not intended for spinal anesthesia.

Tranexamic acid: Beware of anaesthetic misadventures

Tranexamic acid (TXA) is an antifibrinolytic agent that is commonly used in cardiac, gynecologic, and obstetric surgeries. Inadvertent intrathecal injection of the TXA may lead to serious side effects, including back pain, myoclonus, seizure, and ventricular fibrillation that can be attributed to similar appearance of ampoules, location of ampoules, and incorrect labeling of prefilled syringes and can be avoided by vigilance, correct labeling of syringes and ampoules, double checking medications prior to administration, and preventing manufacturing of vials of different drugs with similar appearance. Treatment of intrathecal injection of the TXA includes administration of the anticonvulsants, general anaesthetics, MgSO4, along with intensive haemodynamic monitoring, scalp electroencephalography monitoring guided burst suppression with thiopentone infusion and cerebrospinal fluid lavage.

Inadvertent intrathecal injections and best practice management.

The intrathecal space has become an important anatomic site for medical intervention not only in anesthesia practice, but also in many other medical specialties. Undesired/inadvertent intrathecal injections (UII) are generally rare. There is tremendous variation in reported inadvertent administrations via an intrathecal route in the literature, mainly as individual cases and very small case-series reports. This review aims to identify potential sources of UII, its clinical presentations, and appropriate management. The inadvertent injectants are classified as anesthetic agents and pain medicines, chemotherapeutics, radiological contrast agents, antibiotics and corticosteroids, and miscellaneous chemical agents such as tranexamic acid. The clinical effects of UII are dependent upon inadvertent injectant(s) and dose being administered intrathecally, and can range from no adverse effect to profound neurological consequences and/or death. Prompt cerebrospinal fluid (CSF) lavage and cardiopulmonary support seem to be the mainstay of treatment. If serious consequences are anticipated, CSF lavage could be lifesaving. This review additionally provides some options for comprehensive management and preventing strategies.

Inadvertent Intrathecal Vincristine Administration with Widespread Axonal Injury Demonstrated by Amyloid Precursor Protein Immunohistochemistry

Vincristine is a Vinca alkaloid chemotherapeutic agent used to treat hematologic and some solid organ neoplasms. As a microtubule inhibitor, an unfortunate side effect of this drug is disruption of axonal transport. Thus, the drug is intended for intravenous use only. We report a 59-year-old man with diffuse large B-cell lymphoma who inadvertently received intrathecal vincristine. The patient experienced progressive neurologic decline despite attempts at cerebrospinal fluid lavage with fresh frozen plasma and died five days after the incident. Grossly, there was evidence of prior shunt placement, the brain was mildly swollen, and the white matter appeared congested. Histological study revealed pallor of the centrum semiovale, focal perivascular hemorrhages, and widespread axonal spheroids that were demonstrated by immunohistochemical study for amyloid precursor protein (APP). There was subependymal spongiosis and focal hydropic-like change of the ependyma. Proximal axon segments of anterior horn neurons showed many APP-reactive spheroids as they exited the spinal cord. Anterior spinal nerve roots also contained APP-positive swellings. No significant pathologic changes were identified in the gray matter. In particular, there was no Purkinje cell loss. No evidence of residual lymphoma was identified. This case illustrates diffuse axonal injury that was caused by toxic disruption of axonal transport and was clearly demonstrated by immunohistochemistry for APP. This case emphasizes the need for continued awareness of this preventable medical error.

Efficacy of cerebrospinal fluid lavage replacement in severe tuberculous hydrocephalus

Efficacy of cerebrospinal fluid lavage replacement in severe tuberculous hydrocephalus

Accidental spinal potassium chloride injection successfully treated with spinal lavage

We describe the management of a 62-year-old man who developed severe pain, cramps, paraplegia and pulmonary oedema after the accidental administration of potassium chloride into the subarachnoid space. In addition to supportive treatment, we performed cerebrospinal fluid lavage with saline 0.9%. The patient recovered well without any permanent injury.

Effect of artificial cerebrospinal fluid lavage time on the edema of traumatic brain injury

To detect the impact of artificial cerebrospinal fluid lavage time on the edema of traumatic brain injury. A total of 240 SD rats were randomly divided into a sham group, a traumatic brain injury model group, 3 artificial cerebrospinal fluid lavage groups (3 h, 6 h and 9 h). Each group was divided into 4 sub-groups by time of sacrifice namely 12 h, 1 d, 3 d and 7 d postoperatively. We detected the content of brain water, sodium, and potassium, and the VEGF expression to confirm whether the duration of lavage could reduce the traumatic brain edema. Compared with the sham group and the traumatic brain injury model group, brain water content and sodium content were decreased, while the potassium content and the VEGF levels were increased in the artificial cerebrospinal fluid lavage groups. Significant difference was found at 12 h, 1 d, and 3 d after the injury (P<0.05). With the increase of artificial cerebrospinal fluid lavage time, the difference was more obvious. Artificial cerebrospinal fluid lavage can reduce the brain edema after traumatic brain injury. The longer the lavage, the more obvious the effect.

Delayed CSF lavage for arteriographic and morphological vasospasm after experimental SAH.

Irrigation of the subarachnoid space after aneurysmal subarachnoid hemorrhage (SAH) has been reported to alleviate subsequent arterial vasospasm. The authors have investigated the effect of lavage of the cerebrospinal fluid (CSF) space in the two-hemorrhage canine model of vasospasm. Twelve dogs had basilar cistern lavage with 120 cc of artificial CSF 24 hours after each of two SAH's, and 12 control dogs had two sequential SAH's without intervening lavage of clot. The amount of clot on the ventral brain stem was evaluated at sacrifice and was graded from 0 (no clot) to 4 (maximum clot) to assess the adequacy of clot removal. Dogs that had undergone lavage had a median grade of 1 (range Grade 0 to 2); control dogs had a median grade of 2 (range Grade 1 to 3.5, p less than 0.001. Wilcoxon rank sum test), indicating significant reduction of gross clot by lavage. The neurological findings were graded from 0 to 5, based on meningismus, ataxia, paresis, and cranial nerve deficits. No significant differences in neurological grade were found on any day between the two groups. Satisfactory angiograms were obtained before and 7 days after hemorrhage and were controlled for blood pressure and blood gases; these showed significant spasm in both groups. There was a mean reduction (+/- standard deviation) of 21.6% +/- 16.2% in basilar artery diameter in control dogs, compared to a 28.8% +/- 15.1% reduction in dogs with lavage (difference not significant, t-test). There was a strong, but insignificant, trend toward reduction of endothelial desquamation in the basilar and middle cerebral arteries in dogs with lavage compared to control animals (p = 0.06). Corrugation and tearing of the elastica, thickened intima, intimal fibroplasia, vacuolization of the endothelial or smooth-muscle cells, and presence of blood cells in the adventitia occurred similarly in both groups. It appears that cisternal lavage 24 hours after hemorrhage in this model has no effect on the angiographic, neurological, or most morphological sequelae of SAH, in spite of evidence for removal of clot as seen at sacrifice. Any postulated interaction of clot and vessel resulting in chronic vasospasm must occur before this time. Evaluation of the effect of much earlier lavage (for instance, 1 hour after hemorrhage) may elucidate the point at which vasospasm is instigated after SAH, and help in determining what factors cause vasospasm.