Improving Communication in the Medical Intensive Care Unit Through Standardization of Handoff Format: A Quality Improvement Project.

Objective: To decrease interruptions in handoff, increase compliance with a structured verbal handoff format, and increase compliance with handoff template completion in electronic medical records without increasing the length of handoff time. Patients and Methods: The project timeline was from April 1, 2019, to February 1, 2020. Define phase data were obtained through a survey of stakeholders to identify the gap in needs. The baseline data included components from the illness severity, patient summary, action list, situational awareness and contingency plans, and synthesis by receiver (IPASS) handoff tool because this tool best aligned with information identified in the define phase. Observational data were collected in person and reviewed via audio recording for accuracy. Results were analyzed to determine adherence to the chosen intervention, the IPASS handoff tool, on which the stakeholders were educated and assessed prior to implementation. Five plan-do-study-act cycles were completed over 3 months to optimize the intervention. Final data were collected and analyzed using the same method as baseline data. Results: After implementation of the IPASS handoff tool, there were more care plan components mentioned in the provider handoffs across all unique IPASS components, there were fewer observed distracting events, and there was increased compliance with electronic medical record handoff completion. The time of handover increased by 3 minutes. Conclusion: A standardized handoff tool improved communication during provider handoffs by increasing the mention of pertinent details and reducing distracting events during handoff.

Diagnostic Dilemma in a Case of Lyme Borreliosis Presenting as Severe Anion Gap Metabolic Acidosis: A Case Report.

BACKGROUND Lyme disease is a common tickborne disease with a common presentation. Untreated Lyme disease can affect other organs. This can lead to anion gap metabolic acidosis through severe renal failure. Unlike anion gap metabolic acidosis, osmolar gap can be caused by ingestion of ethanol, toxic alcohols, solvents, and salicylates. Therefore, a presentation with osmolar gap and anion gap metabolic acidosis yields a variety of differential diagnoses. CASE REPORT A 72-year-old man presented after being found down. There were few historical cues, and workup was negative for seizures or any acute cerebrovascular incident. Laboratory results were revealing of severe anion gap acidosis with osmolar gap. During clinical decision making and diagnostic dilemma, toxidrome syndromes for potential ingestions and inhalations were sought in addition to thorough workup, which expanded to include infectious etiologies. This patient's presentation was unique: Lyme disease in the setting of severe anion gap metabolic acidosis with an osmolar gap. CONCLUSIONS The outcome of critically ill patients can be determined by the clinician's method to address the diagnostic dilemma and quality of supportive care. Critically ill patient outcomes can be subject to the clinician's method to address a diagnostic quandary. This unique case poses an important reminder for clinicians to maintain their standard methodologies of critical thinking amidst the noise of distracting medical information.

Clonidine use during dexmedetomidine weaning: A systematic review.

BACKGROUND: Dexmedetomidine is a centrally acting alpha-2A adrenergic agonist that is commonly used as a sedative and anxiolytic in the intensive care unit (ICU), with prolonged use increasing risk of withdrawal symptoms upon sudden discontinuation. As clonidine is an enterally available alpha-2A adrenergic agonist, it may be a suitable agent to taper off dexmedetomidine and reduce withdrawal syndromes. The appropriate dosing and conversion strategies for using enteral clonidine in this context are not known. The objective of this systematic review is to summarize the evidence of enteral clonidine application during dexmedetomidine weaning for prevention of withdrawal symptoms. AIM: To systematically review the practice, dosing schema, and outcomes of enteral clonidine use during dexmedetomidine weaning in critically ill adults. METHODS: This was a systematic review of enteral clonidine used during dexmedetomidine weaning in critically ill adults (≥ 18 years). Randomized controlled trials, prospective cohorts, and retrospective cohorts evaluating the use of clonidine to wean patients from dexmedetomidine in the critically ill were included. The primary outcomes of interest were dosing and titration schema of enteral clonidine and dexmedetomidine and risk factors for dexmedetomidine withdrawal. Other secondary outcomes included prevalence of adverse events associated with enteral clonidine use, re-initiation of dexmedetomidine, duration of mechanical ventilation, and ICU length of stay. RESULTS: A total of 3427 studies were screened for inclusion with three meeting inclusion criteria with a total of 88 patients. All three studies were observational, two being prospective and one retrospective. In all included studies, the choice to start enteral clonidine to wean off dexmedetomidine was made at the discretion of the physician. Weaning time ranged from 13 to 167 h on average. Enteral clonidine was started in the prospective studies in a similar protocolized method, with 0.3 mg every 6 h. After starting clonidine, patients remained on dexmedetomidine for a median of 1-28 h. Following the termination of dexmedetomidine, two trials tapered enteral clonidine by increasing the interval every 24 h from 6 h to 8h, 12h, and 24 h, followed by clonidine discontinuation. For indicators of enteral clonidine withdrawal, the previously tolerable dosage was reinstated for several days before resuming the taper on the same protocol. The adverse events associated with enteral clonidine use were higher than patients on dexmedetomidine taper alone with increased agitation. The re-initiation of dexmedetomidine was not documented in any study. Only 17 (37%) patients were mechanically ventilated with median duration of 3.5 d for 13 patients in one of the 2 studies. ICU lengths of stay were similar. CONCLUSION: Enteral clonidine is a strategy to wean critically ill patients from dexmedetomidine. There is an association of increased withdrawal symptoms and agitation with the use of a clonidine taper.

Diabetic ketoacidosis, cerebral venous sinus thrombosis and fulminant cerebral oedema in COVID-19 infection complicated by Klebsiella pneumoniae infection.

We present an unusual case of a woman in her 30s who was admitted for diabetic ketoacidosis (DKA) in the setting of newly diagnosed but late COVID-19 infection with associated Klebsiella pneumoniae infection. Her altered mental status, out of proportion with her metabolic decompensation, revealed a superimposed cerebral venous sinus thrombosis (CVST) with fulminant cerebral oedema and ultimately brain death. This unusual and fulminant case of cerebral oedema in the setting of COVID-19 infection with bacterial infection, DKA and CVST was the perfect storm with multiple interwoven factors. It offered diagnostic and treatment challenges with an unfortunate outcome. This unique case is a reminder that it is important to consider a broad neurological differential in patients with COVID-19 with unexplained neurological manifestations, which may require specific neurointensive care management.

Acute Epstein-Barr virus infection presenting as Guillain-Barre syndrome.

An 18-year-old man presented with 5-days of a lower extremity rash, sore throat, rapidly progressive bilateral facial numbness and paresthesias in his distal extremities. His neurological examination acutely deteriorated to include moderate bilateral facial weakness in a lower motor neuron pattern, mild flaccid dysarthria, mild bilateral interossei weakness, and diffuse hyporeflexia. In addition to neurological examination, EMG results of acute demyelinating polyradiculoneuropathy were suggestive of Guillain-Barre Syndrome (GBS). Infectious laboratory testing demonstrated acute infection of Epstein-Barr Virus (EBV) with relatively low EBV DNA quantitative values. The patient subsequently developed fever and cervical lymphadenopathy during his hospital course. Contrasting typical GBS, which presents weeks after an acute infection, the patient's presenting symptom of EBV infection was GBS. GBS as a presenting symptom of EBV has not previously been described. This case may represent a unique mechanism for the pathogenesis of GBS in acute infections as opposed to the traditional post-infectious antibody-mediated process.