Hyperhidrosis–Hypertension–Hypotension in Scorpion Envenoming Syndrome: Insulin–Glucose Infusion Reverses All the Clinical Manifestations Caused by Massive Release of Counter-Regulatory Hormones due to Killer Scorpion (Buthidae family) Stings

Death due to poisonous scorpion (Buthidae family) stings is common in many of the developing countries all over the world. Severe uncontrollable pain at the site of sting (without local oedema) results in autonomic storm, release massive quantities of catecholamines, angiotensin II, ACTH, glucocorticoids, glucagon, ADH, aldosterone, either suppressed insulin secretion/or hyperinsulinemia – insulin resistance causing hyperglycemia and a sudden increase in Free Fatty Acid levels (FFA). The increase in catecholamine and angiotensin II hormonal levels cause hyperhidrosis, initial transient hypertension, hyper salivation, hypotension, mydriasis, miosis, DIC, acute pancreatitis, and many other clinical manifestations. Suddenly increased FFA levels are toxic, produce inactivation of Na+–K+ATPase activities, arrhythmias, conduction defects, myocardial infarction, cardiogenic pulmonary oedema, Acute Respiratory Distress Syndrome (ARDS), multisystem organ failure and death. Hyperhidrosis is harmful and wasteful loss of fluid and electrolytes resulting in peripheral circulatory failure, hypotension and death. Based on our animal experimental studies and treating the scorpion sting victims with insulin glucose infusion, we consider that insulin has a primary metabolic role in preventing and reversing hyperhidrosis, hypertension, hypotension, cardiovascular changes, cardiogenic and non-cardiogenic pulmonary (ARDS) oedema. Treatment: Continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight/hour, for 48–72 hour, supplementation of potassium (if required), and maintenance of acid–base fluid and electrolyte balance.

Suppressed Insulin Secretion, Elevated Mediators of Inflammation, Hyper-Insulinemia-Insulin Resistance: Insulin Administration Reverses Cardiovascular, Metabolic Changes, Pulmonary Edema and All Other Clinical Manifestations in Scorpion Envenoming Syndrome

Death due to poisonous scorpion stings is common in many tropical and sub-tropical countries. Scorpion envenoming syndrome causes stimulation of neuro-endocrine axis resulting in autonomic storm, intense stimulation of sympathetic nervous system, massive release of catecholamines, angiotensin II, suppressed insulin secretion, glucagon, glucocorticoids, increased free fatty acid levels, hyperglycemia, hyper-insulinemia, insulin resistance, acute myocarditis, initial hypertension, hypotension, arrhythmias, conduction defects, ischemia, infarction, acute pancreatitis, CNS damage, motor aphasia, hemiplegia, mydriasis, hyperhidrosis, acute respiratory distress syndrome, disseminated intravascular coagulation, multi system organ failure, shock and death. The scorpion envenoming syndrome also causes stimulation of immuno-pathological axis, systemic and local inflammation, increase in production of proinflammatory cytokines IL-1α, IL-1β, IL-4, IL-6, IL-10, IL-12, TNF-α, IFN-γ and NO and contribute to immunological imbalance, hyperglycemia, hyper-insulinemia, insulin resistance, multi-system organ failure, shock and death. Elevated levels of TNF-α cause impaired glucose tolerance and induce insulin resistance for endogenously secreted insulin. Insulin administration reversed metabolic, respiratory changes, cardiogenic and non-cardiogenic pulmonary edema, electrocardiographic, cardiovascular changes and many other manifestations in our experimental animals and in our scorpion sting victims with scorpion envenoming syndrome. Treatment: Continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1g/kg body weight/h, for 48–72 h, with supplementation of potassium as needed, maintenance of fluid, electrolytes, acidbase balance.

Insight into evolution of a giant congenital nevomelanocytic nevus over 14 years.

Giant congenital nevomelanocytic nevus (GCNN) is a rare variant of congenital melanocytic nevus measuring >20 cm in size that often has a garment-like distribution. Regular follow up is recommended because of a risk of melanoma transformation of 4.6%. We report a 14-year-old boy with gradual regression of giant congenital melanocytic nevus over the left upper limb, chest, back and axilla, whom we have followed-up since birth. At birth, a hyperpigmented jet-black patch without hair was present over the left side of torso and upper limb including palms and nails. Follow up at the ages of 1, 5, 11 and 14 years showed progressive spontaneous regression of the nevus resulting in shiny atrophic skin, diffuse hypopigmentation, lentigo-like macules, nodules and arthrogryphosis of affected areas. Histopathology of the lesions on follow-up revealed absence of pigmented nevus cells in the regressing areas and thickened sclerotic collagen bundles.

Comorbid conditions in patients with physician diagnosed COPD: Data from a tertiary centre in South India.

Background: COPD represents an increasing burden worldwide. COPD is a leading cause of hospitalizations in adults, particularly older adults. Comorbidities are a common cause, or a contributing cause, to many of these hospitalizations. Aims & Objective: To study the comorbid conditions in patients with physician diagnosed COPD in a tertiary centre in South India. Material and Methods: A random sample of 500 patients after taking verbal consent were selected from all COPD patients who attended Dr Pinnamaneni Siddhartha Institute of Medical Sciences and Research Foundation, Chinnaavutapalli, Vijayawada, over a period of 1year in 2012. Personal interview was held to collect data including age, gender, literacy, occupation, comorbidities. Results: The mean age of 500 COPD patients was 61.2. Out of which 47.2% are below 60 years and 52.8% are above 60 years. Males constituted majority of the study population (80.8%). 77% of the total study population gave a history of smoking. Majority of the patients had 2 comorbid illnesses (30%). Among the co morbidities, depression was the commonest comorbid illness (50.4%), followed by anaemia (44%). Conclusion: Knowledge regarding associated comorbidities with COPD in a tertiary care center helps the physician to take the comprehensive management plan. We recommend screening of patients with COPD for possible comorbidities so that appropriate treatment can be initiated at the earliest so as to decrease the cost burden.