Rhino orbital cerebral mucormycosis: A life-threatening complication of coronavirus diseases 2019 in an uncontrolled diabetic patient.

Mucormycosis is a progressive and life-threatening disease that has been increasingly reported in patients infected by coronavirus diseases 2019 (COVID-19). We describe a case of rhino-orbital mucormycosis with central nervous system involvement resulting in bilateral blindness and intracranial extension in a patient with uncontrolled diabetes mellitus (DM) and mild COVID-19 infection. A 35-year-old obese male, recently diagnosed with DM, presented to the emergency department suffering from dizziness, headache, speech difficulty, and facial weakness. His glycosylated hemoglobin was 10.4% and his reverse transcriptase-polymerase chain reaction (PCR) test came positive for COVID-19. Ocular examination revealed left eye proptosis, ophthalmoplegia, and lid edema with no ocular movement. Imaging studies showed pansinusitis and periorbital and orbital cellulitis with intracranial involvement. Histopathology and biopsy examination confirmed mucormycosis. Medical management included glucose control and liposomal amphotericin B therapy. Septoplasty and functional endoscopic sinus surgery was performed as emergency procedures. The patient survived with bilateral blindness. In this case, we described the importance of considering mucormycosis in COVID-19 patients with uncontrolled diabetes, particularly those presenting with sinusitis, headache, and orbital edema symptoms. Despite intensive antifungal therapy and surgical intervention, it is a serious opportunistic fungal infection associated with long-term complications.

Neurological Sequelae After Acute Carbon Monoxide Poisoning.

Carbon monoxide poisoning (COP) is a common cause of death due to poisoning. After COP, a significant number of patients may develop a distinct type of neurological dysfunction called delayed neurological sequel (DNS). Recently, we came across a disaster of COP cases after a fire in a shared accommodation. The hostel was overcrowded and had a faulty air-conditioning/exhaust system. A total of five patients with loss of consciousness and shock were brought to us. They were diagnosed with acute COP based on their history of exposure to carbon monoxide (CO) and elevated carboxyhemoglobin levels in blood gas measurements. All patients were intubated and mechanically ventilated. Standard intensive care management was given to them, which included oxygenation, sedation, fluid resuscitation, and vasopressors. Their carboxyhemoglobin was rapidly reversed with normobaric oxygen therapy (NBO2). Three patients showed good response and neurological recovery after NBO2. Unfortunately, two patients developed DNS. DNS is a neuropsychological condition that may have cognitive, psychiatric, vestibulocochlear, motor, sensory, or diffuse demyelinating effects after COP. DNS is diagnosed in patients with a typical history of exposure to CO and a constellation of signs and symptoms. Neuroimaging, specifically magnetic resonance imaging of the brain with gadolinium contrast, is the method of choice for diagnosis. Treatment of DNS after COP begins with anticipation. All patients should receive appropriate oxygen therapy to bring down carboxyhemoglobin as soon as possible. Hyperbaric oxygen therapy (HBO2) for the treatment of COP and prevention of DNS is still debatable. In the available medical literature, there are conflicting recommendations regarding the use of HBO2 in COP/DNS. Moreover, apart from a lack of consensus, there is also a lack of clarity about optimum timing, duration, atmospheric pressure, and number of sessions of HBO2 in preventing DNS after COP. The development of DNS after COP is not directly responsible for mortality, but recovery sometimes takes a long time, which can contribute to increased morbidity and costs of treatment.

Epidemiology and outcome of an acute kidney injuries in the polytrauma victims admitted at the apex trauma center in Dubai.

BACKGROUND: Polytrauma from road accidents is a common cause of hospital admissions and deaths, frequently leading to acute kidney injury (AKI) and impacting patient outcomes. METHODS: This retrospective, single-center study included polytrauma victims with an Injury Severity Score (ISS) >25 at a tertiary healthcare center in Dubai. RESULTS: The incidence of AKI in polytrauma victims is 30.5%, associated with higher Carlson comorbidity index (P=0.021) and ISS (P=0.001). Logistic regression shows a significant relationship between ISS and AKI (odds ratio [OR], 1.191; 95% confidence interval [CI], 1.150-1.233; P<0.05). The main causes of trauma-induced AKI are hemorrhagic shock (P=0.001), need for massive transfusion (P<0.001), rhabdomyolysis (P=0.001), and abdominal compartment syndrome (ACS; P<0.001). On multivariate logistic regression AKI can be predicated by higher ISS (OR, 1.08; 95% CI, 1.00-1.17; P=0.05) and low mixed venous oxygen saturation (OR, 1.13; 95% CI, 1.05-1.22; P<0.001). The development of AKI after polytrauma increases length of stay (LOS)-hospital (P=0.006), LOS-intensive care unit (ICU; P=0.003), need for mechanical ventilation (MV) (P<0.001), ventilator days (P=0.001), and mortality (P<0.001). CONCLUSIONS: After polytrauma, the occurrence of AKI leads to prolonged hospital and ICU stays, increased need for mechanical ventilation, more ventilator days, and a higher mortality rate. AKI could significantly impact their prognosis.

What should an intensivist know about pneumocephalus and tension pneumocephalus?

Collection of air in the cranial cavity is called pneumocephalus. Although simple pneumocephalus is a benign condition, accompanying increased intracranial pressure can produce a life-threatening condition comparable to tension pneumothorax, which is termed tension pneumocephalus. We report a case of tension pneumocephalus after drainage of a cerebrospinal fluid hygroma. The tension pneumocephalus was treated with decompression craniotomy, but the patient later died due to the complications related to critical care. Traumatic brain injury and neurosurgical intervention are the most common causes of pneumocephalus. Pneumocephalus and tension pneumocephalus are neurosurgical emergencies, and anesthetics and intensive care management like the use of nitrous oxide during anesthesia and positive pressure ventilation have important implications in their development and progress. Clinically, patients can present with various nonspecific neurological manifestations that are indistinguishable from a those of a primary neurological condition. If the diagnosis is questionable, patients should be investigated using computed tomography of the brain. Immediate neurosurgical consultation with decompression is the treatment of choice.

Paget-Schroetter syndrome: An unfamiliar cause of upper-limb deep venous thrombosis.

Paget-Schroetter syndrome (PSS), which is also called "effort thrombosis," is a venous variant of thoracic outlet syndrome. We report a rare case of upper-limb deep venous thrombosis (ULDVT) in a young patient who was later diagnosed as PSS. PSS is a rare cause of ULDVT, and it is usually seen in young adults who are involved in strenuous physical activity. PSS is either due to anatomical abnormality of the thoracic outlet or due to repeated microtrauma to the endothelium of the subclavian/axillary vein. Clinically, the patient usually presents with signs and symptoms of ULDVT. Noninvasive Doppler ultrasonography is the initial investigation of choice, but computerized tomography and digital subtraction angiography are the gold standards for diagnosis. Treatment consists of therapeutic anticoagulation, catheter-directed thrombolysis, first rib resection, and postoperative oral anticoagulation. Although the PSS less likely causes pulmonary embolism, it can contribute to postthrombotic syndrome. PSS is a rare and distinct clinical entity, and most emergency care or primary care physicians are unaware of this condition. PSS requires rapid diagnosis, timely thrombolysis, and prompt referral to a vascular and thoracic surgeon.

Acute kidney injury in ventilated patients with coronavirus disease-2019 pneumonia: A single-center retrospective study.

BACKGROUND: Acute kidney injury (AKI) is repeatedly observed in ventilated critically ill patients with coronavirus disease-2019 (COVID-19) pneumonia. This study aimed to determine the incidence, risk factors, and consequences of AKI in the ventilated critically ill adult patients with COVID-19 pneumonia. METHODS: This retrospective study included all the ventilated critically ill adult patients with COVID-19 pneumonia from March 1, 2020, to June 1, 2020. Data were collected from the electronic medical system. AKI was diagnosed using the Kidney Disease: Improving Global Outcomes 2012 Clinical Practice definition. Patients were followed 90 days from the intensive care unit (ICU) admission time or to the date when they were discharged from the hospital. RESULTS: AKI occurred in 65.1% of patients, with 26.6% of these started on continuous renal replacement therapy (CRRT). Patients with AKI had higher comorbidity and illness severity scores (P < 0.001). Age and the vasopressor requirements were predictors of AKI (P= 0.016 and P = 0.041) and hypertension predicted AKI (P = 0.099) and its progression (P = 0.05). The renal recovery rate was 86.7% and was associated with the mean arterial pressure on ICU admission in the no-CRRT group (P = 0.014) and the hypoxic index in the CRRT group (P = 0.019). AKI was associated with higher mortality (P = 0.017) and significantly longer ICU length-of-stay (P = 0.001). Additionally, AKI patients were more often discharged to a long-term skilled nursing facility (P = 0.005). CONCLUSION: COVID-19-associated AKI was common and associated with poor outcome, with the specific mechanisms being the main driving factors.

Upregulation of oxidative stress gene markers during SARS-COV-2 viral infection.

Severe viral infections, including SARS-COV-2, could trigger disruption of the balance between pro-oxidant and antioxidant mediators; the magnitude of which could reflect the severity of infection and lung injury. Using publicly available COVID-19 transcriptomic datasets, we conducted an in-silico analyses to evaluate the expression levels of 125 oxidative stress genes, including 37 pro-oxidant genes, 32 oxidative-responsive genes, and 56 antioxidant genes. Seven oxidative stress genes were found to be upregulated in whole blood and lung autopsies (MPO, S100A8, S100A9, SRXN1, GCLM, SESN2, and TXN); these genes were higher in severe versus non-severe COVID-19 leucocytes. Oxidative genes were upregulated in inflammatory cells comprising macrophages and CD8+ T cells isolated from bronchioalveolar fluid (BALF), and neutrophils isolated from peripheral blood. MPO, S100A8, and S100A9 were top most upregulated oxidative markers within COVID-19's lung autopsies, whole blood, leucocytes, BALF derived macrophages and circulating neutrophils. The calprotectin's, S100A8 and S100A9 were upregulated in SARS-COV-2 infected human lung epithelium. To validate our in-silico analysis, we conducted qRT-PCR to measure MPO and calprotectin's levels in blood and saliva samples. Relative to uninfected donor controls, MPO, S100A8 and S100A9 were significantly higher in blood and saliva of severe versus asymptomatic COVID-19 patients. Compared to other different viral respiratory infections, coronavirus infection showed a prominent upregulation in oxidative stress genes with MPO and calprotectin at the top of the list. In conclusion, SARS-COV-2 induce the expression of oxidative stress genes via both immune as well as lung structural cells. The observed correlation between oxidative stress genes dysregulation and COVID-19 disease severity deserve more attention. Mechanistical studies are required to confirm the correlation between oxidative stress gene dysregulation, COVID-19 severity, and the net oxidative stress balance.