Atezolizumab is a monoclonal antibody that targets programmed death ligand-1. Treatments with this drug may cause immune-related adverse events by creating an exaggerated inflammatory response. The most common side effects are fatigue, rash, and gastrointestinal symptoms. Cases of central nervous system toxicity such as encephalitis and encephalopathy are uncommon. We present the case of a 53-year-old female with metastatic squamous cell carcinoma of the cervix who presented to the emergency room 13 days after receiving atezolizumab with altered mental status, headache, and meningeal signs. She was admitted to the intensive care unit. Infectious, anatomical, and neoplastic etiologies were ruled out. Auto-immune meningoencephalitis was diagnosed and treated with high-dose steroids. Within 10 days of the diagnosis, she had clinical, radiological, and laboratory improvement. Given the increasing use of novel immunotherapies and life-threatening side effects associated with them, healthcare providers in the intensive care unit should be aware of their diagnosis and management.

Anthrax is a zoonotic disease and is caused by Bacillus anthracis which is a Gram-positive, nonmotile, spore-forming rod, found in soil. The spores can remain viable for decades. Transmission occurs naturally in humans by direct contact with infected animals or the contaminated animal products. Anthrax is a major health problem in eastern and southern India, with a significant human incidence because the disease is poorly controlled. Here, we discuss such a case of naturally occurring fatal anthrax in North-East India. A 48-year-old man from Assam presented with seizures, hematemesis, and fever. Apart from altered mental status and nonreactive pupils, his cutaneous and systemic examination was unremarkable. Noncontrast computed tomography head showed multiple hemorrhages. Blood and cerebrospinal fluid showed heavy growth of anthrax Bacilli. He was started on specific antibiotics after the reports, but unfortunately, the patient succumbed to infection. Due to high prevalence of anthrax in the endemic regions, a high degree of suspicion is required to clinch the diagnosis. Early initiation of therapy before developing the intracranial hemorrhagic complications might result in a better outcome. Careful history for a possible exposure to animal carcass or a suspected animal death due to anthrax will also help in early diagnosis of the disease and effective therapy.

Patients presenting with acute or chronic hepatopathy can develop altered mental status with psychomotor slowing, most commonly indicating encephalopathy. We present the case of a 56-year-old patient who developed subacute atypical neuropsychiatric symptoms including cognitive and behavioural disorganization, manic-like state, and lateralized parkinsonian syndrome. The sequence of events, complete work-up, and detailed neuropsychiatric examination were not compatible with hepatic encephalopathy or delirium; therefore we extended our differential diagnosis and suggested the pathophysiological process described below.

Ammonium bifluoride is an inorganic, fluoride-containing compound found in glass and metal etching products, as well as wheel cleaners. Fluoride toxicity is a common cause of preventable poisoning and has been reported to cause life-threatening ventricular dysrhythmias. Here, we report a case of recurrent ventricular fibrillation secondary to ingestion of ammonium bifluoride. The patient presented with vomiting and coma. She was intubated for altered mental status and respiratory failure and subsequently had 5 episodes of ventricular fibrillation, each resolving with a single defibrillation. She developed metabolic acidosis and hypocalcemia, which were treated with sodium bicarbonate and calcium gluconate, respectively. During transfer to a tertiary care children's hospital, ventricular fibrillation recurred despite electrolyte correction. Hemodialysis (HD) was initiated emergently. No further dysrhythmia occurred after initiation of HD. The result of a basic urine drug screen was negative, and a comprehensive drug screen (gas chromatography and mass spectroscopy) revealed only a nonsignificant peak for diphenhydramine. Subsequent laboratory evaluation revealed an elevated serum fluoride level. Diagnostic laryngoscopy and upper endoscopy did not reveal evidence of caustic injury. She was successfully extubated on hospital day 2 and discharged from the hospital on day 4 with no neurologic sequelae. With this example, we demonstrate a potential therapeutic approach to this potentially lethal poisoning. Fluoride toxicity is typically treated with calcium. However, dysrhythmia may result from calcium-independent direct myocardial toxicity. The kinetics of fluoride are amenable to HD, and renal clearance is slow. The potential use of HD in cases of fluoride poisoning refractory to other therapies warrants further study.

A 43-year-old man with Hashimoto's thyroiditis and previous thromboembolic events treated with warfarin for 6 months, presented with right flank pain accompanied with vomiting, dizziness, and altered mental status 2 weeks after discontinuation of warfarin. His clinical examination findings were unremarkable. Routine blood work showed lymphopenia, thrombocytopenia, and hypoosmolar hyponatremia. Random serum cortisol level was low (14 nmol/L). Computed tomography scan of the abdomen revealed bilateral bulky heterogeneous suprarenal gland surrounded by fat stranding representing adrenal hemorrhage. He was treated for acute adrenal crisis and subsequently started on hydrocortisone and fludrocortisone, with significant clinical improvement. His diagnosis was secondary antiphospholipid syndrome (APS) to systemic lupus erythematosus (SLE). Bilateral adrenal thrombosis lead to hemorrhage in the adrenals as a paradoxical effect after warfarin cessation and primarily caused by APS. Bilateral adrenal bleeding should lead to the suspicion of thrombophilic disorders, such as APS, with cautious anticoagulation as the treatment of choice.

A 70-year-old woman was adimittetd with subarachnoid haemorrhage. The patient underwent cerebral aneurysm embolization. On hospital day 14, the patient underwent a lumbar subarachnoid continuous drain insertion because of fever and enlarged ventricles were showed on the head computed tomography. On hospital day 19, the patient presented with remittent fever (peak at 39.1 °C) associated with altered mental status. Cerebro-Spinal Fluid (CSF) revealed white blood cell (WBC) count of 53484/mm3 (polymorphonucleocytes,75.4%; monocytes, 24.6 %), red blood cells (RBCs) were +++/HP, glucose was 1.26 mg/dL, and the total proteinwas 14.2 g/dL. The lumbar subarachnoid continunous drain was removed. The patient was started on meropenem 1g intravenous(IV) every 8 h and vancomycin 1g (IV ) every 12h. On hospital day 22, the patient's CSF culture showed that A. baumannii (polymyxin susceptibility was not tested) was susceptible only to tigecycline (MIC ≤1 μg/mL) and cefoperazone sulbatan. The same strain of A. baumannii was isolated from the sputum and blood. With permission, the antimicrobial therapy was changed to intravenous tigecycline (100mg first then 50 mg q12h) and cefoperazone sulbatan (3g q8h). Head computed tomography (CT) demonstrated enlarged ventricles compared with previous studies and an external ventricular drain (EVD) was inserted on hospital day 25. On hospital day 28, the blood culture was negative, however the same strain of A. baumannii was still isolated from the CSF. With permission, tigecycline 2mg intraventricular (IVT) every 12 h was started and lasted for 10 days. On hospital day 38, the patient's CSF culture was negative. On hospital day 104, the patient was discharged. Continued 3-month-follow-up showed no recurrence.