Honeybee bites are a common public health hazard, the incidence of which is gradually increasing. A bee sting incident involving more than fifty stings is categorized as massive envenomation. The clinical manifestations of honey bee stings can range from localized symptoms to severe allergic and systemic reactions.This case study presents a 60-year-old male who experienced multi-organ failure following a severe bee sting incident. According to our research, this is the first documented instance in Somalia of multi-organ failure resulting from a sting by a giant honey bee. The case highlights the potential severity of bee stings, which, while often considered minor, can lead to serious medical complications. Interestingly, despite the patient suffering numerous stings and receiving a substantial amount of venom, an immediate anaphylactic reaction did not occur. Instead, a delayed severe response leading to multi-organ failure emerged within 48 hours of the incident.

Facial appearance, whether consciously or subconsciously assessed, may affect clinical assessment and treatment strategies in the Intensive Care Unit (ICU). Nevertheless, the association between objective clinical measurement of facial appearance and multi-organ failure is currently unknown. The objective of this study was to examine whether facial appearance at admission is associated with longitudinal evaluation of multi-organ failure.
This was a sub-study of the Simple Intensive Care Studies-II, a prospective observational cohort study. All adult patients acutely admitted to the ICU between March 26, 2019, and July 10, 2019, were included. Facial appearance was assessed within three hours of ICU admission using predefined pictograms. The SOFA score was serially measured each day for the first seven days after ICU admission. The association between the extent of eye-opening and facial skin colour with longitudinal Sequential Organ Failure Assessment (SOFA) scores was investigated using generalized estimation equations.
SOFA scores were measured in 228 patients. Facial appearance scored by the extent of eye-opening was associated with a higher SOFA score at admission and follow-up (unadjusted 0.7 points per step (95%CI 0.5 to 0.9)). There was no association between facial skin colour and a worse SOFA score over time. However, patients with half-open or closed eyes along with flushed skin had a lower SOFA score than patients with a pale or normal facial skin colour (P-interaction < 0.1).
The scoring of patients\' facial cues, primarily the extent of eye-opening and facial colour, provided valuable insights into the disease state and progression of the disease of critically ill patients. The utilization of advanced monitoring techniques that incorporate facial appearance holds promise for enhancing future intensive care support.

Paraquat, a highly toxic herbicide, accounts for a substantial number of poisoning-related fatalities, primarily prevalent in agricultural regions. The ingestion gives rise to severe complications affecting various organs, including the lungs, gastrointestinal tract, kidneys and liver. This report details the case of an 18-year-old male who had been using cannabis for a year and inadvertently ingested paraquat. He presented at the emergency room exhibiting symptoms of vomiting characterized by hematemesis and regurgitated food particles, along with heartburn, dysphagia and reduced urine output. Given the absence of a specific antidote, the prognosis for paraquat poisoning remains generally unfavourable. Diagnosis relies on circumstantial evidence and clinical manifestations, necessitating a focus on supportive care. Presently, no specific antidote for paraquat poisoning is available. Efforts should concentrate on preventive measures, efficient decontamination strategies and vigilant stabilization protocols in instances of exposure.

Myocardial injury in the context of septic shock presents a multifaceted challenge in critical care medicine with implications for patient prognosis and therapeutic strategies. This comprehensive review explores the mechanisms, diagnostic approaches, and clinical implications of myocardial injury as a harbinger of multi-organ failure in septic shock. We delineate the pathophysiological processes underlying myocardial injury, including inflammation, oxidative stress, and microcirculatory dysfunction, and discuss the diagnostic utility of cardiac biomarkers and imaging modalities in identifying myocardial injury. Furthermore, we elucidate the prognostic significance of myocardial injury and its implications for patient management, highlighting the need for tailored therapeutic interventions to mitigate its adverse effects. Future research and clinical practice directions are also discussed, emphasizing the importance of personalized medicine approaches and multidisciplinary collaboration in optimizing outcomes for patients with septic shock-associated myocardial injury. This review aims to provide a comprehensive understanding of myocardial injury in septic shock and inform strategies for improving patient care in this challenging clinical scenario.

UNASSIGNED: Rickettsioses are infectious diseases which are caused by intracellular bacteria which belong to the family Rickettsiaceae. This zoonosis endemically prefers tropical and subtropical regions of which the Mediterranean is included. Murine typhus is a type of rickettsial disease that commonly presents with undulating fever, headache rash, chills, malaise, and myalgias. It can lead to complications such as multi-organ failure and has a lethality rate of <5% in such cases.
UNASSIGNED: A 70-year-old male was hospitalized at the Unit of Infectious Diseases, Mother Teresa Hospital, Tirana, Albania in a comatose condition. He had a seven-day history of fever up to 39-40°C, headache, fatigue, anorexia, vomiting, cough, and myalgia. He was a farmer and had contact with animals. Upon admission, he had scleral hemorrhages, hepatosplenomegaly, jaundice, maculopapular rash over the trunk, abdomen, and palms of his hands as well as severe acidosis, depressed bicarbonate levels, alteration in liver, kidney, and pancreas function tests. He was urgently transferred to the Intensive care unit of the Infectious Diseases Department. He was hemodynamically unstable and was put immediately on vasoactive agents and mechanical ventilation. ELISA Rickettsia typhi IgM resulted positive. Supportive treatment along with antibiotics Levofloxacin and Ceftriaxone was initiated. However, the patient died on the 4th day of hospitalization and the 11th of the disease onset.
UNASSIGNED: Murine typhus should be included in the investigation of possible causes when dealing with patients presenting with fever and maculopapular rash complicated by multi-organ failure and coming from a typhus-endemic area, especially in the summer season.

Organ transplantation is the primary therapy for organ failure caused by telomere biology disorder (TBD). We describe the first documented case of simultaneous liver and kidney transplantation (SLKTx) for TBD, although the diagnosis of TBD was reached only three months following SLKTx. The patient was born prematurely, displayed growth retardation, and developed chronic kidney and liver diseases. His pre-SLKTx autoimmune, metabolic, and viral assessments were negative, and persistent pancytopenia (bone marrow cellularity 70-80%) was attributed to renal disease-associated bone marrow changes. Following SLKTx, he was discharged with stable graft function on tacrolimus and prednisolone. Although mycophenolate mofetil was discontinued on the second postoperative day, his pancytopenia persisted. Despite extensive evaluations, including drug, immune, nutritional, and viral assessments, all results were negative. A bone marrow biopsy conducted three months post-transplant revealed significant hypocellularity (40-50%). Whole genome sequencing revealed a likely pathogenic variant of the TINF2 gene. The patient was subsequently treated with danazol. At the nine-month follow-up post-SLKTx, he exhibited stable graft function and improved cell counts while maintaining triple-drug immunosuppression. Given the lack of uniform diagnostic criteria for TBD, healthcare providers must be vigilant with patients presenting with multi-organ failure and persistent cytopenias. Effective pre-transplant screening for TBD can lead to timely diagnoses, better management, and improved post-transplant outcomes.

Delivering higher doses of protein to mechanically ventilated critically ill patients did not improve patient outcomes and may have caused harm. Longitudinal urea measurements could provide additional information about the treatment effect of higher protein doses. We hypothesised that higher urea values over time could explain the potential harmful treatment effects of higher doses of protein.
We conducted a reanalysis of a randomised controlled trial of higher protein doses in critical illness (EFFORT Protein). We applied Bayesian joint models to estimate the strength of association of urea with 30-day survival and understand the treatment effect of higher protein doses.
Of the 1301 patients included in EFFORT Protein, 1277 were included in this analysis. There were 344 deaths at 30 days post-randomisation. By day 6, median urea was 2.1 mmol/L higher in the high protein group (95% CI 1.1-3.2), increasing to 3.0 mmol/L (95% CI 1.3-4.7) by day 12. A twofold rise in urea was associated with an increased risk of death at 30 days (hazard ratio 1.34, 95% credible interval 1.21-1.48), following adjustment of baseline characteristics including age, illness severity, renal replacement therapy, and presence of AKI. This association persisted over the duration of 30-day follow-up and in models adjusting for evolution of organ failure over time.
The increased risk of death in patients randomised to a higher protein dose in the EFFORT Protein trial was estimated to be mediated by increased urea cycle activity, of which serum urea is a biological signature. Serum urea should be taken into consideration when initiating and continuing protein delivery in critically ill patients.
gov Identifier: NCT03160547 (2017-05-17).

Dengue fever is a prevalent viral disease caused by a single-stranded positive RNA virus belonging to the Flaviviridae family, genus flavivirus. It is characterized by fever, headache, myalgias, leukopenia, rash, and plasma leakage, which may progress to compensated or uncompensated shock and multi-organ failure. Liver involvement is a common feature of Dengue fever and is usually manifested by nausea, vomiting, abdominal discomfort, anorexia, hepatomegaly, and elevated serum transaminase levels. Severe disease is associated with laboratory parameters such as mean Platelet count < 20,000/mm, Aspartate Transaminase Levels >45 IU, and lymphocytes <1500. The Expanded Dengue Syndrome (EDS), a term coined by World Health Organization in 2012, refers to an atypical presentation of Dengue fever that manifests with generalized impacts on normal physiology. This case report presents a 29-year-old male with EDS who presented at a Tertiary Care Hospital in Karachi and died a week later due to liver failure.

A heat stroke (HS) is a medical emergency that can occur when the body is unable to cool itself down after overexertion in a hot condition. It is characterized by a high body temperature (usually greater than 40.5 degrees Celsius or 104.9 degrees Fahrenheit) and altered mental status. HS can cause a wide range of physiological changes in the body, including damage to the brain, heart, liver, kidneys, and muscles. In the case report presented, the patient was a 40-year-old man who developed severe HS. His condition rapidly deteriorated, and he developed multi-organ failure, involving the brain, liver, kidneys, muscles, and hematological system. The patient was admitted to the intensive care unit (ICU) and intubated, despite aggressive treatment. After an 18-day stay in the ICU, the patient achieved full recovery except for myopathy, which necessitated physiotherapy.

BACKGROUND: Thyroid storm can be complicated by liver dysfunction, which may occasionally progress to acute liver failure. We herein report a case of acute liver failure following thyroid storm that was treated with living donor liver transplantation after resuscitation from cardiopulmonary arrest.
METHODS: The patient was a woman in her 40 s who had been diagnosed with an abnormal thyroid function. She suffered from fatigue and vomiting, and was found to have consciousness disorder, a fever, and tachycardia with a neck mass. She was diagnosed with thyroid storm and was referred to our hospital. After arrival, she went into cardiopulmonary arrest and veno-arterial extracorporeal membrane oxygenation was initiated. In addition to treatment for thyroid storm with antithyroid drugs, steroids, and plasma exchange, extracorporeal life support was required for 5 days. However, despite improvements in her thyroid function, her liver function deteriorated. We planned living donor liver transplantation for acute liver failure after ensuring the recovery and control of the thyroid function following total thyroidectomy. The donor was her husband who donated the right lobe of his liver. Although she experienced acute cellular rejection after surgery, and other complications-including intra-abdominal hemorrhaging and ischemic changes in the intestine-her liver function and general condition gradually improved. One year after living donor liver transplantation, the patient was in a good condition with a normal liver function.
CONCLUSIONS: To our knowledge, this is the first report of living donor liver transplantation in a patient with acute liver failure following thyroid storm. Liver transplantation should be recognized as an effective treatment for acute liver failure following thyroid storm.