scholarly journals An Atypical Presentation of Hyperosmolar Hyperglycemic State Induced by SARS CoV 2

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A366-A367
Author(s):  
Ivan Augusto Rivera Nazario ◽  
Arnaldo Nieves Ortiz ◽  
Jose Ayala Rivera ◽  
Kyomara Hernandez Moya ◽  
Arnaldo Rojas ◽  
...  

Abstract Hyperglycemic emergencies such as Diabetic Ketoacidosis (DKA) or Hyperosmolar Hyperglycemic State (HHS) are commonly precipitated by infectious processes. Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) is a novel infectious process prompting hyperglycemic crisis. SARS-CoV-2 at the level of the lungs affects ACE2 functioning which in turns decrease the B cells proliferation at the pancreas and hinders insulin secretion. Advanced age and comorbidities such as hypertension, cardiovascular disease and diabetes mellitus are considered to be a risk factors for severe illness and mortality between patients with SARS-CoV-2. We present the case of a 39-year-old woman with medical history of uterine fibroma, who presented with complains of general malaise, polyuria and polydipsia of one week evolution, associated with sore throat, subjective fever, dry cough, abdominal pain, nausea and vomiting. Physical examination remarkable for dry oral mucosa, decreased skin turgor, and prolonged capillary refills. Vital signs significant for hypertension, tachycardia, and tachypnea. Laboratory work up remarkable for glucose of 1321 mg/dL, HCO3- of 16 mEq/L, serum osmolality of 333 mOsm/kg, serum ketones positive and HbA1C of 15%. ABG’s showed pH of 7.33, PCO2 of 29.8 and a PAO2 of 158.5 mmHg for a high anion gap metabolic acidosis (AG of 15.3 mEq/L), non-anion gap metabolic acidosis with respiratory alkalosis. Chest X-ray revealed bilateral perihilar, peribronchial cuffing. SARS-CoV-2 PCR testing was positive. Clinical and laboratory workup met criteria for diagnosis of HHS and Diabetes Mellitus de Novo most likely secondary to SARS-CoV-2 infection. Patient was treated with aggressive IV hydration and insulin infusion with resolution of hyperglycemia, ketonemia and symptoms. SARS-CoV-2 infection can precipitate acute metabolic complications in patients with diabetes or unknown diagnosis of diabetes. The effect of the virus could be direct effect on β-cell function. To our knowledge, there are only a few cases reported of HHS precipitated by SARS-CoV-2 infection therefore medical awareness is important for early diagnosis of possible triggering factors such as COVID-19 and early management of patients presenting with new onset hyperglycemic emergencies.

2021 ◽  
Vol 14 (2) ◽  
pp. e223668
Author(s):  
Dileep Kumar ◽  
Muhammad Zubair Nasim ◽  
Bilal Ahmad Shoukat ◽  
Syed Shabahat Ali Shah

Diabetic ketoacidosis (DKA) is one of the most serious acute metabolic complications of diabetes mellitus. It is characterised by the biochemical triad of hyperglycaemia, ketonemia/ketonuria, and an increased anion gap metabolic acidosis. In this case, a 40-year-old male patient presented to the emergency department, with vomiting, nausea, polydipsia, polyuria and weight loss. He was found to have an elevated plasma glucose, despite having no known history of diabetes mellitus. His medical history was significant for spina bifida and ileal neobladder reconstruction. The plasma glucose level was 38 mmol/L. Blood gas analysis showed normal anion gap metabolic acidosis with high chloride and low bicarbonate. His plasma ketone level was 4.5 mmol/L. No significant reason for hyperchloraemia was identified. On initiation of DKA regimen, his condition improved and serum ketones normalised. Due to persistent hyperchloraemic metabolic acidosis, bicarbonate infusion was administered and his metabolic acidosis resolved.


Author(s):  
Vsevolod Skvortsov ◽  
Ekaterina Skvortsova ◽  
Georgiy Malyakin ◽  
Elina Goliyeva

Lactic acidosis is a metabolic acidosis with a large anion gap (> 10 mmol/L) and a level of lactic acid in the blood > 4 mmol/L (according to some definitions, more than 2 mmol/L). This is a critical pathological condition of the body, accompanied by acute or chronic hypoxia, and even coma. The prognosis for the development of this condition is always severe, mortality is 50–80 %. Clear criteria for the diagnosis and treatment of this pathological condition are defined at the moment. This article focuses on the main issues that endocrinologists and resuscitators may encounter when identifying this complex of symptoms.


Author(s):  
Ali A Zaied ◽  
Halis K Akturk ◽  
Richard W Joseph ◽  
Augustine S Lee

Summary Nivolumab, a monoclonal antibody against programmed cell death-1 receptor, is increasingly used in advanced cancers. While nivolumab use enhances cancer therapy, it is associated with increased immune-related adverse events. We describe an elderly man who presented in ketoacidosis after receiving nivolumab for metastatic renal cell carcinoma. On presentation, he was hyperpneic and laboratory analyses showed hyperglycemia and anion-gapped metabolic acidosis consistent with diabetic ketoacidosis. No other precipitating factors, besides nivolumab, were identified. Pre-nivolumab blood glucose levels were normal. The patient responded to treatment with intravenous fluids, insulin and electrolyte replacement. He was diagnosed with insulin-dependent autoimmune diabetes mellitus secondary to nivolumab. Although nivolumab was stopped, he continued to require multiple insulin injection therapy till his last follow-up 7 months after presentation. Clinicians need to be alerted to the development of diabetes mellitus and diabetic ketoacidosis in patients receiving nivolumab. Learning points: Diabetic ketoacidosis should be considered in the differential of patients presenting with metabolic acidosis following treatment with antibodies to programmed cell death-1 receptor (anti-PD-1). Autoimmune islet cell damage is the presumed mechanism for how insulin requiring diabetes mellitus can develop de novo following administration of anti-PD-1. Because anti-PD-1 works by the activation of T-cells and reduction of ‘self-tolerance’, other autoimmune disorders are likely to be increasingly recognized with increased use of these agents.


2021 ◽  
Vol 19 (3) ◽  
pp. 263-269
Author(s):  
L. V. Nikonova ◽  
◽  
S. V. Tishkovskiy ◽  
O. N. Martinkevich ◽  
О. А. Shidlovskaya ◽  
...  

Since the first outbreak of SARS-Cov-2 in China, much attention has been paid by the medical community to people with diabetes, as it is well known that diabetes increases the risk of developing various infectious diseases. The reason for this is multifactorial: age, gender, ethnicity, concomitant diseases such as hypertension and cardiovascular diseases, obesity, as well as pro-inflammatory and procoagulatory conditions – all these factors contribute to a more severe course of SARS-Cov-2 in patients with diabetes mellitus. Moreover, severe SARS-Cov-2 infection itself may be a worsening factor for people with diabetes, as it can cause acute metabolic complications through direct negative effects on beta-cell function. This review is intended to provide a systematic assessment of potential prognostic factors and mutual effects in patients with diabetes mellitus, obesity and SARS-Cov-2.


2019 ◽  
Author(s):  
Awad Magbri ◽  
Eusera El-Magbri ◽  
Mariam El-Magbri ◽  
Brar Balhinder ◽  
Shauket Rashid

The case is that of 58 year-male with type 2 diabetes mellitusfor 7 years, hypertension, hypercholesterolemia, who was admittedto the hospital with left lower limb cellulitis over the past 8 days.On work-up he was found to have high anion-gap metabolic acidosis(AGMA) with anion gap of 25, his lactate levels were normal (Dand L-lactate). He denies overdosing with any medications and histoxicology screen for methanol, ethanol, aspirin, and ethylene glycolwere negative. He has no psychiatric history of note. He denies usingover the counter medications like acetaminophen. No bowel surgerycould be elicited. He felt dehydrated and nauseous but otherwisefine.His medications includes; carvedalol 25mg twice daily,hydrochlothiazide 25 mg daily, Lipitor 20 mg daily, insulin, aspirin81 mg daily, and was started on canagliflozoin 300 mg daily 4 weeksago to control his blood sugar level and A1C.Physical examination of the patient revealed, slightly dehydratedbut well-nourished man, his vital signs; heart rate of 78 BPM andregular, BP 143/85 mmHg, temperature 98.7 F, and his oxygensaturation while breathing room air was 92%. Examination of theheart, abdomen, and chest were unremarkable. He had left lower legcellulitis but no edema or tenderness.His work-up including chemistry-7 which showed sodium of142 mmol/L, potassium of 4.3 mmol/L, chloride of 102 mmol/L,bicarbonate of 13 mmol/L, BUN and creatinine of 18 mg/L and 0.78mg/L respectively. His blood glucose level was 178 mg/L with A1Cof 8.2. His serum osmolality was 312 mosm/L, and his arterial bloodpH was 7.2 with a carbon dioxide in blood gas analysis (Pco2) of32mmHg. His calculated anion gap was 25 given his normal albuminlevel. His investigation also showed positive ketones in the serumand urine. His urine PH was 5.5 and the urine contain >800 mg ofglucose


1979 ◽  
Vol 25 (7) ◽  
pp. 1329-1330 ◽  
Author(s):  
J Koett ◽  
J Howell ◽  
S Steinberg ◽  
P Wolf

Abstract The usual metabolic derangement in uncontrolled diabetes mellitus is metabolic acidosis, with an increase in the anion gap because of increased ketoacids and lactate. However, diabetic ketoalkalosis may occasionally be encountered, the prominent clinical feature of which is vomiting, with depletion of potassium, chloride, and hydrogen ions. Self-medication with absorbabe alkali may also contribute to the alkalosis. It would be dangerous to treat hyperlgycemic patients with alkali if their condition is ketoalkalosis instead of ketoacidosis.


2019 ◽  
Author(s):  
Awad Magbri ◽  
Eusera El-Magbri ◽  
Mariam El-Magbri ◽  
Brar Balhinder ◽  
Shauket Rashid

7 years, hypertension, hypercholesterolemia, who was admitted to the hospital with left lower limb cellulitis over the past 8 days. On work-up he was found to have high anion-gap metabolic acidosis (AGMA) with anion gap of 25, his lactate levels were normal (D and L-lactate). He denies overdosing with any medications and his toxicology screen for methanol, ethanol, aspirin, and ethylene glycol were negative. He has no psychiatric history of note. He denies using over the counter medications like acetaminophen. No bowel surgery could be elicited. He felt dehydrated and nauseous but otherwise fine. His medications includes; carvedalol 25mg twice daily, hydrochlothiazide 25 mg daily, Lipitor 20 mg daily, insulin, aspirin 81 mg daily, and was started on canagliflozoin 300 mg daily 4 weeks ago to control his blood sugar level and A1C. Physical examination of the patient revealed, slightly dehydrated but well-nourished man, his vital signs; heart rate of 78 BPM and regular, BP 143/85 mmHg, temperature 98.7 F, and his oxygen saturation while breathing room air was 92%. Examination of the heart, abdomen, and chest were unremarkable. He had left lower leg cellulitis but no edema or tenderness. His work-up including chemistry-7 which showed sodium of 142 mmol/L, potassium of 4.3 mmol/L, chloride of 102 mmol/L, bicarbonate of 13 mmol/L, BUN and creatinine of 18 mg/L and 0.78 mg/L respectively. His blood glucose level was 178 mg/L with A1C of 8.2. His serum osmolality was 312 mosm/L, and his arterial blood pH was 7.2 with a carbon dioxide in blood gas analysis (Pco2) of 32mmHg. His calculated anion gap was 25 given his normal albumin level. His investigation also showed positive ketones in the serum and urine. His urine PH was 5.5 and the urine contain >800 mg of glucose.


Children ◽  
2021 ◽  
Vol 8 (12) ◽  
pp. 1155
Author(s):  
Moon-Bae Ahn ◽  
Seul-Ki Kim ◽  
Shin-Hee Kim ◽  
Won-Kyoung Cho ◽  
Jin-Soon Suh ◽  
...  

Fetuin-A and adiponectin are inflammatory cytokines associated with obesity and insulin resistance. This study aimed to examine the fetuin-A-to-adiponectin ratio (FAR) in diabetic children and to determine the role of FAR. A total of 54 children and adolescents with diabetes mellitus (DM) and 44 controls aged 9–16 years were included in this study. Clinical characteristics, including plasma fetuin-A and adiponectin levels, were compared with respect to body mass index (BMI) and diabetes type. Of 98 children, 54.1% were obese, whereas 18.4% were obese and diabetic. FAR was higher in obese children with DM than in non-obese children and also in type 2 DM children than in type 1. FAR showed a stronger association with BMI than with fetuin-A and adiponectin individually, and its association was more prominent in diabetic children than in controls. BMI was a risk factor for increased FAR. Plasma fetuin-A was elevated in obese children, and its association with insulin resistance and β cell function seemed more prominent in diabetic children after adjustment for adiponectin. Thus, FAR could be a useful surrogate for the early detection of childhood metabolic complications in diabetic children, particularly those who are obese.


2019 ◽  
Author(s):  
Awad Magbri ◽  
Eusera El-Magbri ◽  
Mariam El-Magbri ◽  
Brar Balhinder ◽  
Shauket Rashid

The case is that of 58 year-male with type 2 diabetes mellitus for 7 years, hypertension, hypercholesterolemia, who was admitted to the hospital with left lower limb cellulitis over the past 8 days. On work-up he was found to have high aniongap metabolic acidosis (AGMA) with anion gap of 25, his lactate levels were normal (D and L-lactate). He denies overdosing with any medications and his toxicology screen for methanol, ethanol, aspirin, and ethylene glycol were negative. He has no psychiatric history of note. He denies using over the counter medications like acetaminophen. No bowel surgery could be elicited. He felt dehydrated and nauseous but otherwise fine. His medications includes; carvedalol 25mg twice daily, hydrochlothiazide 25 mg daily, Lipitor 20 mg daily, insulin, aspirin 81 mg daily, and was started on canagliflozoin 300 mg daily 4 weeks ago to control his blood sugar level and A1C. Physical examination of the patient revealed, slightly dehydrated but well-nourished man, his vital signs; heart rate of 78 BPM and regular, BP 143/85 mmHg, temperature 98.7 F, and his oxygen saturation while breathing room air was 92%. Examination of the heart, abdomen, and chest were unremarkable. He had left lower leg cellulitis but no edema or tenderness. His work-up including chemistry-7 which showed sodium of 142 mmol/L, potassium of 4.3 mmol/L, chloride of 102 mmol/L, bicarbonate of 13 mmol/L, BUN and creatinine of 18 mg/L and 0.78 mg/L respectively. His blood glucose level was 178 mg/L with A1C of 8.2. His serum osmolality was 312 mosm/L, and his arterial blood pH was 7.2 with a carbon dioxide in blood gas analysis (Pco2) of 32mmHg. His calculated anion gap was 25 given his normal albumin level. His investigation also showed positive ketones in the serum and urine. His urine PH was 5.5 and the urine contain >800 mg of glucose.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Disha K Narang ◽  
Pick Anthony ◽  
Zegrean Anca ◽  
Simona Balu ◽  
Tole Mateo

Abstract Background: We describe the case of a patient with euglycemic diabetic ketoacidosis (euDKA), in the setting of sodium-glucose cotransporter-2 (SGLT2) inhibitor use, complicated by non-anion gap metabolic acidosis and low-carbohydrate diet leading to admission. Presentation: A 43-year-old woman with a history of type 2 diabetes mellitus treated with Metformin, with no prior history of DKA, was admitted with progressive dizziness, nausea, vomiting, malaise, palpitations, and dyspnea starting 3 days prior to admission. Her other history includes anemia due to uterine fibroids, hypertension, and hyperlipidemia. Hemoglobin A1C was 6.7%, however in the setting of anemia. She denied polyuria and polydipsia, and alcohol and drug use. She was started on a low-dose SGLT2i and pioglitazone 1 week prior to admission. Labs revealed mild hyperglycemia (blood glucose 145 mg/dL), with mixed anion-gap and non-anion-gap metabolic acidosis, and respiratory alkalosis [arterial pH 6.97 (rr7.35-7.45), PCO2 <13.0 mmHg (rr 32-45 mmHg), bicarbonate 5mm/dL (rr 24-33 mg/dL), anion gap 22, B-hydroxybutyrate 12.52 mmol/L (rr 0-0.3 mmol/L), and chloride 108 mEq/L (rr 98-109 mEq/L)], with normal renal function, hepatic function, and lactate. Infectious work-up was negative, including chest x-ray and urinalysis. She was diagnosed with euDKA due to SGLT2i. The SGLT2i was stopped and she was treated with insulin drip, intravenous fluids, and temporary bicarbonate drip given combined acidoses and severely low bicarbonate level, until her acidosis cleared. The patient noted that she had lately been eating a very low-carbohydrate diet in order to improve her glycemic control and promote weight loss. Discussion: In this case, DKA was likely precipitated by ketogenesis from low-carbohydrate diet for 1 week while taking a low-dose SGLT2i. Additionally, the dual anti-hyperglycemic therapy with Metformin and SGLT2i contributed to high anion-gap metabolic acidosis, along with the presence of a non-anion-gap metabolic acidosis. The patient was successfully transitioned to Metformin and pioglitazone upon discharge. As the use of SGLT2i is becoming widespread across multiple disciplines, recognizing euDKA in the setting of profound acidemia and very low carbohydrate diet in patients who are overall lower risk is particularly important.


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