Does prolonged prone position affect intracranial pressure? prospective observational study employing Optic nerve sheath diameter measurements.

BACKGROUND: Our aim in this observational prospective study is to determine whether the prone position has an effect on intracranial pressure, by performing ultrasound-guided ONSD (Optic Nerve Sheath Diameter) measurements in patients with acute respiratory distress syndrome (ARDS) ventilated in the prone position. METHODS: Patients hospitalized in the intensive care unit with a diagnosis of ARDS who were placed in the prone position for 24 h during their treatment were included in the study. Standardized sedation and neuromuscular blockade were applied to all patients in the prone position. Mechanical ventilation settings were standardized. Demographic data and patients' pCO2, pO2, PaO2/FiO2, SpO2, right and left ONSD data, and complications were recorded at certain times over 24 h. RESULTS: The evaluation of 24-hour prone-position data of patients with ARDS showed no significant increase in ONSD. There was no significant difference in pCO2 values either. PaO2/FiO2 and pO2 values demonstrated significant cumulative increases at all times. Post-prone SPO2 values at the 8th hour and later were significantly higher when compared to baseline (p < 0.001). CONCLUSION: As a result of this study, it appears that the prone position does not increase intracranial pressure during the first 24 h and can be safely utilized, given the administration of appropriate sedation, neuromuscular blockade, and mechanical ventilation strategy. ONSD measurements may increase the safety of monitoring in patients ventilated in the prone position.

Kratom-induced Liver Failure and Death: A Case Report

Introduction: Kratom (mitragynine speciosa) is a tree native to Southeast Asia that has both opioid, stimulant, and other unknown properties. It is currently legal in the United States and used for therapeutic and recreational purposes. There is a dearth of literature on kratom’s effects on the body. At least half of reported kratom exposures resulted in a serious medical outcome, including death (1). In contrast, there are no controlled clinical trials on safety and efficacy of kratom as a treatment (2). Case: A 32-year-old Caucasian, currently unemployed, unmarried, mother of two children presented intubated to the MICU from an outside hospital with acute fulminant hepatic failure in the setting of significant kratom use. The patient also presented febrile with intracranial hemorrhage, cerebral edema, GI bleeding, acute renal failure, and diffuse intravascular coagulation. Psychiatry was consulted for potential liver transplant candidacy. Her previous history included six years of opioid use and transition to kratom 1-2 years prior to admission, with recent ingestion up to twenty-five times the patient’s usual amount (up to 125mg). Pertinent positive labs included elevated troponin (0.4), transaminitis ( >11,000), elevated PT/PTT (99/52), D-dimer ( >20), hematuria, pyuria, serum ferritin, prolonged QTc (514), and hypoglycemia. Pertinent negatives included unrevealing serum ethanol, phosphatidylethanol, viral hepatitis, HIV, COVID-19, EBV, CMV, other viral panels, acetaminophen level, toxicology screen, and EEG. Imaging revealed interstitial pulmonary edema and diffuse cerebral edema. Given lack of published information on kratom, the team emergently listed the patient for liver transplant despite significant concern for kratom use disorder. Over the course of three days, the patient’s mental status and labs continued to worsen, ultimately resulting in death. Interventions pursued included dialysis, mechanical ventilation, intracranial pressure monitoring with pressure optimization, anticonvulsant therapy, antibiotic therapy, N-acetylcysteine, and other routine MICU care. Due to relatively unremarkable health before ingestion, lack of other significant events, and severe rapid decline, multidisciplinary team consensus cause of death was due to kratom ingestion causing “acute liver failure with hepatic coma”. Discussion: This case report will go into further detail on kratom by analyzing kratom’s mechanism of action, therapeutic use, known side effects including addictive potential, effects on the liver including acute fulminant injury, and current laws and regulations surrounding kratom in the United States with relevance to public health. This is relevant to psychiatrists in the general consult, transplant, and addictions services. References: 1. Post S, Spiller HA, Chounthirath T, Smith GA. Kratom exposures reported to United States poison control centers: 2011–2017. Clinical Toxicology. 2019 57:10,847-854. DOI:10.1080/15563650.2019.1569236 2. Prozialeck W. Update on the Pharmacology and Legal Status of Kratom. J of the AOA. 2016, 116, 802-809. DOI: https://doi.org/10.7556/jaoa.2016.156

Pediatric Multi-System Inflammatory Syndrome With Fatal Cerebral Edema in a Patient With COVID-19

INTRODUCTION: There are increasing reports of a pediatric multisystem inflammatory syndrome associated with coronavirus disease 2019 (COVID-19) that presents with varying clinical features, but includes features of Kawasaki disease or toxic shock syndrome. Symptoms include fever, rash, abdominal pain, vomiting, and diarrhea. Many patients present without any respiratory symptoms and testing for SARS-CoV-2 is often negative. METHODS: A retrospective chart review was performed. RESULTS: A 7-year-old previously healthy male presented with 3 days of fevers up to 102.4F, headaches, abdominal pain, and intractable vomiting. Both parents had tested positive for SARS-CoV-2 four weeks prior. Nasopharyngeal swab tested positive for SARS-CoV-2 RNA. Echocardiogram was normal. CT venogram of his head was negative for any pathology. He developed severe neck pain and persistent headache during his hospitalization. Soon after receiving hydroxychloroquine, he developed a facial rash and altered mental status with episodes of aphasia, agitation, and pinpoint pupils. He then became unresponsive with left gaze deviation. A non-contrast head CT and CT angiography were negative. He was given levetiracetam and cefazolin and transferred to the pediatric intensive care unit. An electroencephalogram (EEG) showed no epileptiform activity. Over the following 7 hours, the EEG demonstrated left frontotemporal slowing, which progressed into a loss of fast activity over the right hemisphere with increased delta activity in the left hemisphere, then abruptly changed to generalized voltage attenuation.He rapidly lost brainstem reflexes, developing fixed and dilated pupils. Repeat CT scan revealed diffuse cerebral edema with loss of gray-white differentiation. Lab results then were consistent with severe inflammation. An intracranial pressure monitor revealed pressures greater than 76 mmHg. His exam soon became consistent with brain death. Pathologic evaluation showed diffuse cerebral edema with perivascular mononuclear infiltrates. CONCLUSION: The cause of this pediatric multi-system inflammatory syndrome is unclear and the mechanism by which SARS-CoV-2 affects the nervous system is unknown. Pediatric patients with COVID-19 and neurologic symptoms should be closely monitored as they can rapidly decline due to fulminant cerebral edema.