Aim and background: To study the clinical presentation in two cases of poisoning presenting with methemoglobinemia. To review common causes of methemoglobinemia and study differences in their presentation and management. Methemoglobinemia is a common presenting feature among patients presenting to the hospital following deliberate ingestion of various poisons. Case description: We report two patients who had consumed two different groups of toxins and presented with the common manifestation of methemoglobinemia. The first case involves indoxacarb ingestion, whereas the second case presents with consumption of organic fertilizer. Although presenting features and initial management were similar in both patients, the response to therapy, complications, and time to recovery were quite different. Conclusion and clinical significance: In rural backgrounds, suicidal attempts with chemical compounds used for agriculture are common. These compounds are numerous, and it is difficult to have knowledge regarding all of their presentations. Methemoglobinemia is one such presentation, which can easily be missed without a high degree of clinical suspicion. A thorough knowledge of all the toxins capable of causing methemoglobinemia and their unique features is necessary for the appropriate management of these cases.

Importance: Locked-in state, or “coma vigilante,” is a moribund condition where the patient is literally locked inside the body, fully awake and aware of the environment but unable to perform psychomotor responses except for eye winking. The most common cause is ventral pontine stroke. This presentation has also been reported due to peripheral neural and neuromuscular diseases such as Guillain–Barré syndrome, iatrogenic agents, krait bite, etc. However, organophosphate poisoning presenting as a de-efferented state has never been reported before. Aim: To share this observation with the scientific community and disseminate awareness that organophosphate poisoning can cause locked-in state, deceptively masquerading as coma. Design: Prospective observational case series report. Setting and participants: Organophosphate-poisoned patients admitted to the intensive care unit of a government tertiary care hospital. Main outcome: Case series description with supporting video recordings. Results: Four cases of locked-in state were described. All four patients had consumed monocrotophos with intentional self-harm. All patients presented with incomplete variants of locked-in state; three of them expired. Conclusion: Consciousness with absolute unresponsiveness occurs in organophosphate poisoning. It is often mislabeled as coma. This presentation signifies the severity of muscle paralysis and is associated with poor outcomes. Relevance: Intensivists must maintain a high index of suspicion for this presentation to avoid misdiagnosis. Confusing it with coma can have serious consequences for both the patient and the treating physician.

Aim and background: Heavy metal poisoning, including cadmium, can occur with occupational exposure or intake of contaminated food products. The exposed patients may present in the critical care unit with nonspecific symptoms involving multiple organs. The diagnosis may be easily missed in the absence of clinical suspicion, as the presentation may mimic commonly encountered diseases. Case description: We present an unusual case of a 32-year-old woman presenting with a history of intermittent vomiting, loss of appetite, anemia, jaundice, respiratory distress, and decreased urine output. Her sepsis workup, vasculitis profile, antinuclear antibodies (ANA)-18, and investigations for tropical fever were negative. The patient had a tobacco factory at home and was taking weight loss herbal supplements. In view of the clinical history and multiorgan dysfunction of uncertain etiology, heavy metal screening was sent, which revealed high levels of urinary cadmium. The patient was managed in the intensive care unit with supportive treatment, including sustained low-efficiency dialysis (SLED), vasopressors, and mechanical ventilation. However, the patient expired on hospital day 10 due to multiorgan dysfunction. Conclusion: Cadmium toxicity usually occurs with occupational exposure; however, the use of tobacco and ingestion of contaminated food products can be important sources of cadmium exposure. Cadmium toxicity can result in multiorgan dysfunction and shock, which may be difficult to differentiate from other common causes, including sepsis. The management is mainly supportive and involves avoidance of further exposure. Clinical significance: Our case highlights the importance of maintaining a low threshold for suspicion of heavy metal toxicity in patients with unusual presentations and multiorgan dysfunction of uncertain etiology.

Aim and background: Chylothorax and chylous ascites (CA) are often seen after postoperative damage to the thoracic duct, specifically at the cisterna chyli. However, there are rare traumatic causes of the same. This makes it grueling to diagnose and treat. In the present case, we noticed the abovementioned complication after a hyperextension injury of the spine. We believe that shearing forces have a role to play in this scenario. Nonetheless, timely management of such patients can prevent severe morbidity and untimely mortality. Case description: A 40-year-old male presented with a history of a fall and was diagnosed with a hyperextension injury of the spine. He underwent a magnetic resonance imaging (MRI) of the spine to confirm the same. His injuries were managed conservatively, and he was discharged. One month later, he presented with progressive abdominal distension and dyspnea, which revealed an unusual diagnosis of CA. Laparotomy confirmed the source of the leak from the cisterna chyli. Conclusion: CA is a rare complication of hyperextension injury of the spine. When ascites or pleural effusion is noted persistently, injury to the thoracic duct or cisterna chyli must be suspected.

Aim and background: Electrical burn injuries are among the most severe forms of injury due to their high morbidity and mortality rates. They can significantly damage vital organs, with severity influenced by electric voltage, body resistance, and contact duration. In our country, they most commonly affect the extremities and the scalp. Electrical contact injury to the neck is an uncommon presentation and poses a challenge to treat due to critical structures in the neck and cervical region. Case description: A 24-year-old male sustained a high-voltage electrical contact burn to the neck and both feet. He initially presented with normal airway, breathing, and circulation (ABC) and developed severe airway complications after 24 hours. This delayed onset of significant glottic and laryngeal edema underscores the importance of vigilant monitoring and preemptive airway management in patients with electrical contact injuries to the neck. Conclusion: Continuous monitoring and early intervention are crucial in electrical contact injuries to the neck due to the risk of insidious airway edema. Prolonged observation beyond 48 hours is necessary to prevent life-threatening complications. Clinical significance: Direct electrical contact injuries to the neck are uncommon. There is limited literature regarding their management. Contrary to burns to the head and neck leading to inhalational injury, which are common, we have clear-cut guidelines to secure a definitive airway early. A benign-appearing electrical contact injury to the neck with a normal airway examination can subsequently lead to life-threatening airway obstruction.

Aim and background: Bradycardia, renal failure, atrioventricular node blockers, shock, and hyperkalemia (BRASH) syndrome, a pentad of bradycardia, renal failure, atrioventricular (AV) block, shock, and hyperkalemia, was first coined in 2016 by Dr Josh Farkas. It represents a complex interplay between AV nodal block and hyperkalemia, leading to severe bradycardia and shock, often affecting older patients with limited renal reserve. However, it is still underrecognized, as even though there is a history of AV nodal blocker intake, it is not given the same importance as hyperkalemia due to its less ”fear factor.” Case description: We present the management of one such case: a 70-year-old female on amlodipine and atenolol. Her initial potassium level was 5.8 mEq/L and she was in a state of cardiogenic shock. Conclusion: With early intervention, the bradyarrhythmia in BRASH syndrome is reversible. The aim of this case report is to raise awareness of BRASH syndrome, as timely intervention will improve patient outcomes, and the offending agent can be withdrawn.

Aim and background: BRASH syndrome (bradycardia, renal failure, AV-nodal blockade, shock, and hyperkalemia) is a rare and underrecognized clinical entity that poses significant diagnostic and therapeutic challenges. Case description: We report the case of a 75-year-old female with multiple comorbidities presenting with symptomatic bradycardia and shock due to BRASH syndrome, triggered by AV nodal-blocking medications and sepsis-induced hypovolemia. Early recognition, prompt discontinuation of precipitating drugs, correction of hyperkalemia, and hemodynamic stabilization resulted in a favorable outcome. Conclusion: This case underscores the importance of timely diagnosis and comprehensive management to prevent complications, reduce the need for invasive interventions, and improve overall patient outcomes in BRASH syndrome. Clinical significance: In elderly patients with multiple comorbidities, combining calcium channel blockers (CCBs) and beta-blockers should be done with caution. Vigilant monitoring for BRASH features is essential, and even mild hyperkalemia must be treated promptly. Early recognition and tailored management can improve outcomes in BRASH syndrome.

Aim and background: Hyponatremia is a common electrolyte disorder in the setting of neurological disease. Among patients with neurological disorders, syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the common malady, and cerebral salt wasting syndrome (CSWS) is rarely encountered. In SIADH, there is usually increased or normal intravascular volume, and in CSWS, there is central volume depletion. Thus, proper clinical examination of central volume status should be done before making a diagnosis. Case description: A 73-year-old man presented with drowsiness 2 years ago. Serum sodium was low, and he was advised by a physician to take extra salt supplementation. His confusion worsened, he developed gait instability, urinary incontinence, and was diagnosed as having normal pressure hydrocephalus (NPH). A ventriculo peritoneal (VP) shunt was placed. Later in the year, he was again admitted to the hospital with drowsiness. He was diagnosed with SIADH and treated with water restriction and tolvaptan. A year later, he became drowsy and was admitted to this hospital. Serum sodium was low, and he had central volume depletion. He was diagnosed with CSWS. The worsening was due to the change in VP shunt pressure as he walked through a metal detector, which led to excessive drainage of cerebrospinal fluid (CSF). He was treated with hydration, salt supplementation, and shunt pressure adjustment, leading to improvement in his condition. Conclusion: CSWS is a rare metabolic manifestation of NPH. Patients with VP shunts should be cautioned against walking through a metal detector with a potential electromagnetic field. Clinical significance: Clinical assessment of jugular venous pressure (JVP) is important in order to differentiate between SIADH and CSWS.

Aim and background: Metformin and clonazepam mixed-drug poisoning is rare and life-threatening. Early diagnosis, aggressive treatment, and careful monitoring are essential for improving patient outcomes. Case description: A 36-year-old man with bipolar disorder attempted suicide by ingesting 45 gm of metformin and 30 gm of clonazepam. He developed central nervous system depression, severe lactic acidosis, acute kidney injury (AKI), and liver injury. The patient suffered cardiac arrest with ventricular fibrillation and required defibrillation and mechanical ventilation. The primary goals of therapy were prompt removal of metformin and clonazepam, restoration of acid-base balance, and management of AKI. Treatment included consistent sodium bicarbonate infusion, prompt initiation of hemodialysis, an aggressive antibiotic regimen, mechanical ventilation, flumazenil treatment to manage clonazepam toxicity, and long-term supportive care. Despite a poor prognosis, the patient survived and was discharged after a hospital stay of 50 days. The patient has recovered completely and is routinely following up with his consulting physician. Conclusion: Despite severe acidosis, metformin-induced lactic acidosis warrants immediate treatment with renal replacement therapy and sodium bicarbonate. Clinical significance: Emergency physicians and intensivists should be aware of the need for a multifaceted intervention approach involving sustained low-efficiency dialysis, extracorporeal therapy, hemodynamic support, and meticulous acid-base balance management, which are crucial for the survival of patients presenting with severe lactic acidosis.