The case is reported of a 39-year-old severely obese woman who developed acute metabolic disorders after the administration of a short course of intravenous amiodarone. The main biological features were hypertriglyceridemia, hypoglycaemia, hyperlactatemia and hyperammonemia; all were reversible after amiodarone discontinuation. There was an associated rise in liver enzymes. However, the influence of co-factors on these metabolic disorders, such as acquired carnitine deficiency, severe obesity, a long-term course of pancreatitis, and abdominal infections, could not be excluded.
Levodopa is a dopamine precursor and a mainstay treatment in the management of Parkinson’s disease. Its side effects induce dyskinesia, nausea, vomiting, and orthostatic hypotension. Acute levodopa acute poisoning is uncommon, with only a few reported cases in the medical literature. Treatment of poisoning by levodopa is mainly supportive. The case of a child admitted to a hospital for acute levodopa poisoning is presented in this report.
Background: The systemic inflammatory response syndrome (SIRS) is a complex immune response which can be precipitated by non-infectious aetiologies such as trauma, burns or pancreatitis. Addressing the underlying cause is crucial because it can be associated with increased mortality. Although the current literature associates chronic heart failure with SIRS, acute right ventricular dysfunction has not previously been reported to trigger SIRS. This case report describes the presentation of acute right ventricular dysfunction that triggered SIRS and mimicked septic shock.
Case presentation: A 70-year-old male presented to the Intensive Care Unit (ICU) with elevated inflammatory markers and refractory hypotension after a robotic-assisted laparoscopic radical choledochectomy with pancreaticoduodenectomy. Septic shock was misdiagnosed, and he was later found to have a pulmonary embolus. Thrombectomy and antimicrobials had no significant effect on lowering the elevated inflammatory markers or improving the persistent hypotension. Through Point of Care Ultrasound (POCUS), right ventricular dysfunction was diagnosed. Treatment with intravenous milrinone improved blood pressure, normalised inflammatory markers and led to a prompt discharge from the ICU.
Conclusion: Acute right ventricular dysfunction can trigger SIRS, which may mimic septic shock and delay appropriate treatment.
Introduction: Organophosphorus poisoning is the most common poison used for suicidal attempt in Nepal. Diabetes insipidus is unusual and rare in this poisoning. This is the second case report of Diabetes insipidus developing in organophosphorus poisoning. Management of diabetes insipidus includes desmopressin and adequate fluid management.
Case presentation: A 34-year-old female patient accompanied by her father presented at the Emergency department with an alleged history of ingestion of unknown amount of chlorpyrifos, cypermethrin and quinalphos. On admission, she had a Glasgow Coma Scale (GCS) of 7/15. Her blood pressure was 110/60 mm Hg, pulse 54/min, respiratory rate 45/min and saturation 35% on room air, pinpoint pupil reactive to light and bilateral crepitations. She was immediately resuscitated with two litres of normal saline and intubated with a 7 mm endotracheal tube. Atropinisation was done, and pralidoxime was started. She developed a urine output of 250-350 ml per hour with rising sodium and serum osmolality. The urine examination showed low sodium and urine specific gravity. A diagnosis of diabetes insipidus was made. There was no immediate improvement in her GCS. She was managed with 5% dextrose and subcutaneous desmopressin and was transferred out of the intensive care unit on the sixth day and was discharged from hospital on the fifteenth day.
Conclusion: Diabetes insipidus is a rare transient complication in organophosphorus poisoning that requires careful observation and early management with desmopressin and adequate fluid balance to improve patient outcome.
Introduction: Hungry bone syndrome (HBS) refers to the rapid, profound, and prolonged hypocalcaemia associated with hypophosphatemia and hypomagnesaemia, and is exacerbated by suppressed parathyroid hormone (PTH) levels, which follows parathyroidectomy in patients with severe primary hyperparathyroidism (PHPT) and preoperative high bone turnover. 
Case report: This report concerns a dialysed patient who underwent surgical treatment for secondary refractory hyperparathyroidism. Haemodialysis was carried out pre-operatively, and subsequently, a total parathyroidectomy with auto-transplantation of parathyroid tissue in the sternocleidomastoid muscle (SCM) was performed. Rapid and progressive hypocalcaemia symptoms developed during the second day postoperatively. Acute cardiac symptoms with tachyarrhythmia, haemodynamic instability and finally asystole occurred, which required cardiopulmonary resuscitation (CPR). The ionic calcium level was 2.2 mg/dL being consistent with a diagnosis of HBS. A second cardiac arrest unresponsive to CPR followed an initial period of normal sinus rhythm. Death ensued shortly after. Before death, the ionic calcium was 3.1 mg/dL.
Conclusion: HBS, after parathyroidectomy in patients with secondary hyperparathyroidism (SHPT), may be severe, prolonged and sometimes fatal. Generally, HBS symptomatology is that of a mild hypocalcaemia. It can, however, include heart rhythm disturbances with haemodynamic alterations requiring intensive care measurements and even cardiopulmonary resuscitation. A close clinical and laboratory post-parathyroidectomy monitoring of dialysed patients is of the utmost importance.
Introduction: As chronic HIV infection is prone to co-infections more than any other infectious condition, many severely immune-depressed patients require advanced diagnostic investigations and complex treatment.
Case report: The case of a 30-year-old severely immune-depressed patient with AIDS, who developed neurological impairment and was diagnosed with encephalitis is presented. Multiple diagnostic approaches had to be used in order to identify the etiologic agents responsible for the clinical, immunological and biological evolution. Despite using advanced laboratory investigations and complex treatment, the patient developed multiple organ dysfunction syndromes that led to a fatal outcome.
Conclusions: Establishing etiologic relations and treatment priorities in patients with severe immunodeficiency and co-infections can prove difficult, underlining the need of rapid syndromic testing.
Introduction: The current lack of clear guidelines on how to manage cases of brain-dead pregnant patients makes this topic controversial and extremely difficult to deal with for both medical and ethical reasons. This report deals with such a situation.
Case presentation: A twenty-seven years old woman, thirteen weeks pregnant, with a ruptured brain aneurysm was admitted to an Intensive Care Unit. She presented with loss of all brain functions, but somatic support was sustained to enable the delivery of her baby.
Conclusion: The case report gives a detailed account of the management of the mother before the successful delivery of her baby. It indicates the need for ongoing contributions to the debate on this delicate subject area to establish guidelines on how to manage brain-dead pregnant patients.
Introduction: Vertebrobasilar occlusion poses difficult diagnostic issues and even when properly diagnosed has a poor prognosis. Newer studies highlight a better outcome when thrombectomy was carried out between six and twenty-four hours after an initial diagnosis of stroke. This paper reports a case where a patient suffered a vertebrobasilar stroke secondary to a traumatic bilateral vertebral arteries dissection was treated with late thrombectomy.
Case presentation: A 34-year-old woman was manipulated on the cervical spinal column by a chiropractor. Following three weeks of cervical pain, she presented with severe aphasia and quadriplegia (NIHSS = 28). An MRI scan indicated ischemia of the vertebrobasilar system. Thirty-one hours after the onset of these symptoms, a thrombectomy was performed. After one month, the patient could move her head and the proximal part of her limbs but remained confined to bed (NIHSS = 13).
Conclusion: The current case illustrates the benefit of late mechanical thrombectomy for a posterior cerebral circulation infarct. Although there was a delay in treatment, partial recovery ensued.
Introduction: Human brucellosis, the most prevalent zoonotic disease worldwide, is a systemic infection which can involve several organs. Among musculoskeletal complaints, spondylitis is the most frequent complication of brucellosis and primarily affects the lumbar and thoracic vertebrae. The involvement of the cervical spine is infrequent.
Case report: This case report concerns an unusual case of cervical spine spondylitis with an epidural abscess due to Brucella in a 43-year-old man. The diagnosis was based on the patient being domiciled in an endemic region, his symptoms and his occupation. Clinical outcomes improved following antimicrobial therapy of rifampin, doxycycline, and gentamycin, and were confirmed radiologically.
Conclusion: Early diagnosis and treatment are crucial for these patients. The timely commencement of medical treatment can help prevent surgery.
Pyruvate dehydrogenase complex deficiency (PDCD) is a rare neurodegenerative disorder associated with abnormal mitochondrial metabolism. Structural brain abnormalities are common in PDCD. A case of a patient with PDCD with an unusual presentation is described. A 20-month-old boy with hypotonia and developmental delay, presented with hypoxia and respiratory distress due to bronchiolitis. During hospitalisation, he was prescribed PediaSure® feeds. Two days after starting these feeds, he developed respiratory arrest requiring intubation. His blood gas before arrest revealed lactate of 8.9 mmol/L despite normal haemodynamics. After stabilisation and a period of compulsory fasting, subsequent feeding with PediaSure® resulted in the recurrence of lactic acidosis. A metabolic workup revealed an elevated serum pyruvate level. Brain MRI was normal. Skeletal muscle biopsy confirmed PDCD. The most common cause of PDCD is a mutation in the X-linked PDHA1 gene. The severity of PDCD can range from neonatal death to more delayed onset of symptoms as in our index case. Normal brain MRI is reported in only 2% of patients with PDCD. There is no effective treatment for PDCD. In patients with proximal muscle weakness and feeding intolerance with glucose-containing feeds, the presence of lactic acidosis should raise the suspicion of PDCD irrespective of the patient’s age and normal MRI.