The Impact of SARS-Cov-2 Virus Infection on the Endocrine System.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has spread across the globe rapidly causing an unprecedented pandemic. Because of the novelty of the disease, the possible impact on the endocrine system is not clear. To compile a mini-review describing possible endocrine consequences of SARS-CoV-2 infection, we performed a literature survey using the key words Covid-19, Coronavirus, SARS CoV-1, SARS Cov-2, Endocrine, and related terms in medical databases including PubMed, Google Scholar, and MedARXiv from the year 2000. Additional references were identified through manual screening of bibliographies and via citations in the selected articles. The literature review is current until April 28, 2020. In light of the literature, we discuss SARS-CoV-2 and explore the endocrine consequences based on the experience with structurally-similar SARS-CoV-1. Studies from the SARS -CoV-1 epidemic have reported variable changes in the endocrine organs. SARS-CoV-2 attaches to the ACE2 system in the pancreas causing perturbation of insulin production resulting in hyperglycemic emergencies. In patients with preexisting endocrine disorders who develop COVID-19, several factors warrant management decisions. Hydrocortisone dose adjustments are required in patients with adrenal insufficiency. Identification and management of critical illness-related corticosteroid insufficiency is crucial. Patients with Cushing syndrome may have poorer outcomes because of the associated immunodeficiency and coagulopathy. Vitamin D deficiency appears to be associated with increased susceptibility or severity to SARS-CoV-2 infection, and replacement may improve outcomes. Robust strategies required for the optimal management of endocrinopathies in COVID-19 are discussed extensively in this mini-review.

Prevention and management of COVID-19 among patients with diabetes: an appraisal of the literature.

The coronavirus disease 2019 (COVID-19) pandemic has emerged as one of the greatest challenges faced by humankind in the recent past. People with diabetes and related comorbidities are at increased risk of its complications and of COVID-19-related death. Older age, multi-morbidity, hyperglycaemia, cardiac injury and severe inflammatory response are predictors of poor outcome. The complex interplay between COVID-19, diabetes and the effects of related therapies is being explored. Most patients experience a mild illness with COVID-19, while people with diabetes are at increased risk of severe disease. Optimising glycaemic control and adopting measures to prevent disease spread are critical aspects. The management of mild disease is supportive, while very many immunomodulatory and antiviral therapies are being investigated for the treatment of severe disease. Several of these agents have specific considerations for use in people with diabetes. Since mass population lockdowns are considered a key step in controlling disease spread, it follows that, in addition to the direct vulnerability to severe COVID-19, people with diabetes can be affected by limited access to healthcare, insulin, other medications and blood glucose monitoring equipment. Measures to prevent disease spread at the individual and community level are the key to mitigating the rapidly escalating pandemic, while agents for chemoprophylaxis and vaccines are being explored. People with diabetes should be recognised as a vulnerable group for complicated disease and are at risk during times of disturbed social systems. Strategies are needed to safeguard the health of patients with diabetes during the pandemic. This review summarises the current knowledge and perceived challenges for prevention and management of COVID-19 in people with diabetes.

A patient with neurofibromatosis type 1 presenting with bilateral frontal lobe infarctions following anterior communicating artery aneurysm rupture.

Neurofibromatosis is a neurocutaneous genetic condition with dysplasia of the mesodermal and ectodermal tissues. Vascular abnormalities are well recognized in neurofibromatosis and cerebral aneurysms are rarely reported in literature. Here, we present a 20-year-old Sri Lankan female presented with headache, altered personality, disinhibited behaviour, and urinary incontinence. On imaging, she was found to have infarctions of both frontal lobes and evidence of a ruptured anterior communicating artery aneurysm with a small subarachnoid haemorrhage. Another small middle cerebral artery aneurysm was also seen in the angiogram. She was managed conservatively and gradually recovered. Because aneurysms in neurofibromatosis are usually asymptomatic and as rupture of such an aneurysm is rare, regular vascular screening is not recommended to all patients with neurofibromatosis. This is the first case report in literature in which a patient with neurofibromatosis presented with infarctions of both frontal lobes due to rupture of an anterior communicating artery aneurysm.

A case of anterior spinal cord syndrome in a patient with unruptured thoracic aortic aneurysm with a mural thrombus.

BACKGROUND: Spinal cord infarction is an uncommon condition. Anterior cord syndrome present with paraparesis or quadriparesis with sparing of vibration and proprioceptive senses. The common causes of anterior cord syndrome are aortic dissection and aortic surgical interventions. Spontaneous unruptured nondissected aortic aneurysms with intramural thrombus can rarely cause anterior cord infarctions. CASE PRESENTATION: We report a case of anterior spinal cord syndrome due to aneurysm of the thoracic aorta with a mural thrombus. A 64 year old male presented with sudden onset paraparesis with a sensory level at T1 with preserved sense of proprioception and vibration. The MRI panspine revealed increased T2 intensity in the anterior portion of the spinal cord from C5 to T10 level with characteristic 'owl eye' appearance on axial imaging. The CT aortogram detected aneurysmal dilatation of the ascending aortic, arch and descending thoracic aorta with significant intimal irregularities, calcified atherosclerotic plaques and a small mural thrombus. CONCLUSION: The possible mechanisms postulated are occlusion of ostia of radicular arteries by the atherosclerotic plaques and mural thrombus or thromboembolism to the anterior spinal artery. Nondissected atherosclerotic aortic aneurysms should be considered in patients presenting with spinal cord infarctions especially in the presence of vascular risk factors and smoking.

A case report of zinc phosphide poisoning: complicated by acute renal failure and tubulo interstitial nephritis.

BACKGROUND: Run Rat® is a rodenticide widely used against small mammals. It comprises of a minimum of 32% zinc phosphide which is highly toxic in acute exposures to humans. It may be consumed accidentally or intentionally. It enters the body via skin, respiratory and gastrointestinal tracts. Zinc phosphide is hydrolyzed by the gastric acid and is transformed into phosphine gas. Phosphine is a respiratory toxin that inhibits cytochrome C oxidase system resulting in renal failure and liver failure. CASE PRESENTATION: A 35 year old Sri Lankan female presented following ingestion of 2.5 g of Run Rat®, which is a branded preparation of zinc phosphide, resulting in 61 mg/kg poison load. She developed severe acute kidney injury with acute tubular necrosis, subnephrotic ranged proteinuria and tubulointerstitial nephritis for which she underwent haemodialysis three times along with other measures of resuscitation. She also developed elevated liver enzymes with hyperblirubinaemia, hypoalbuminaemia, acute pancreatitis and mild myocarditis. She improved with supportive therapy over a period of 3 weeks. CONCLUSION: Run Rat® is a commonly used rodenticide and the toxic effects are mediated through conversion of phosphide to phosphine gas. The majority of the deaths had occurred in the first 12 to 24 h and the main causes identified are refractory hypotension and arrhythmias. The late deaths (beyond 24 h) had been commonly due to adult respiratory distress syndrome, liver and renal failure. The outcome is poorer with delayed presentation, development of coagulopathy, hyperglycaemia and multiorgan failure with elevated liver enzymes. In our patient, Zinc phosphide poisoning caused severe acute kidney injury, abnormal liver profile, pancreatitis and possible myocarditis. The patient improved with repeated haemodialysis. The renal biopsy revealed acute tubulointerstitial nephritis with acute tubular necrosis. In tropical countries, the rural population engaged in agriculture has easier access to the compound, as it is available at a lower cost. Furthermore, the lack of an antidote and advanced resuscitative measures such as inotropic supportive therapy and renal replacement facilities at most of the peripheral hospitals pose a major challenge in providing timely interventions to prevent deaths.

Electrocardiographic changes mimicking acute coronary syndrome in a large intracranial tumour: A diagnostic dilemma.

BACKGROUND: ST elevation Myocardial infarction is a medical emergency. A variety of noncardiac conditions had been known to mimic the ECG changes that are seen in acute coronary syndrome. Although the common ECG changes that are documented with raised intracranial pressure are T inversions, prolongation of QT interval and sinus bradycardia, ST elevation or depression, arrhythmias and prominent U waves have also been recognized. However, ST elevations in association with primary intracranial tumours are rarely reported. CASE PRESENTATION: A 68-year-old female patient with a large left sided frontoparietal sphenoidal ridge meningioma with mass effect developed sudden onset shortness of breath while awaiting surgery. Her ECG showed ST segment elevations in the inferior leads along with reciprocal T inversions in anterior leads. The patient was treated with dual antiplatelet therapy and unfractionated heparin. The ST elevations in the ECG remained static and the cardiac Troponin assay was repeatedly negative. 2D ECHO, coronary angiogram and CT pulmonary angiography were normal. The repeat noncontract CT scan of the brain revealed two small areas of haemorrhage in the tumour. CONCLUSION: The two mechanisms for ECG changes described in subarachnoid haemorrhage are the neurogenic stunned myocardium due to the catecholamine surge on the myocytes and stress cardiomyopathy. The same mechanisms could be the reasons for the ECG changes seen in intracranial tumours. These ECG changes could be easily misdiagnosed as acute coronary syndrome. This case emphasizes the importance of the cardiac biomarkers, 2D ECHO and coronary angiogram when confronted with such a diagnostic dilemma. Thus a more holistic analysis should be practiced in diagnosing acute coronary events in patients with intracranial pathologies to obviate a myriad of unnecessary investigations, interventions, costly treatment strategies which may well be detrimental to the patient.

Amitraz poisoning: A case report of an unusual pesticide poisoning in Sri Lanka and literature review.

BACKGROUND: Amitraz is a pesticide used worldwide on animals and in agriculture. It contains triazapentadiene, which is a centrally acting alpha-2 adrenergic agonist. Amitraz poisoning is fairly uncommon in humans and occurs via oral, dermal or inhalational routes. Only a limited number of case reports of human intoxication have been published and most of them are of accidental ingestion by children. CASE PRESENTATION: A twenty-year-old Sri Lankan female presented following self-ingestion of 20 ml of amitraz resulting in 37.8 mg/ kg of amitraz poisoning. She lost consciousness after 20 min of ingestion, developed bradycardia and hypotension, which needed intravenous fluid resuscitation and dobutamine. Gastric lavage was performed. Her bradycardia persisted for 36 h and she was drowsy for 48 h. She did not develop respiratory depression, convulsions or hypothermia and the urine output was normal. Arterial blood gas revealed mild respiratory alkalosis. She recovered fully within 48 h and was discharged on day 3. CONCLUSION: The clinical manifestations of amitraz (impaired consciousness, drowsiness, vomiting, disorientation, miosis, mydriasis, hypotension, bradycardia, respiratory depression, hypothermia, generalized seizures, hyperglycemia and glycosuria) can be explained by the agonist action of amitraz on α1 and α2 receptors. Management of amitraz poisoning is still considered to be supportive and symptomatic with monitoring of nervous system, cardiovascular and respiratory systems. Activated charcoal may still be considered for treatment and the place for gastric lavage is controversial. Atropine is effective for symptomatic bradycardia and inotropic support is needed for hypotension that does not respond to fluid resuscitation. Diazepam or Lorazepam is used for convulsions and some patients may require intubation and ICU care. Several α2 adrenergic antagonists like yohimbine have been tried on animals, which have successfully reversed the effects of amitraz. Since the majority of amitraz poisoning cases are due to accidental ingestion, manufactures, regulatory authorities and national poisons control centers have a significant role to play in minimizing its occurrence.