Acute Esophageal Necrosis: A Cause or Effect of Diabetic Ketoacidosis (DKA)?

Thuluvath, Avesh J.; Moore, D J; Alghanim, Fahid

doi:10.14309/00000434-201710001-01650

Cited by 2 publications

(7 citation statements)

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“…Patients with diabetes can present with severe hyperglycemia-induced hypovolemia that can exacerbate the ischemia in the lower third of the esophagus [ 19 ]. A case study by Thuluvath et al followed a 30-year-old female patient with a history of type 2 diabetes presenting to the emergency department with symptoms of UGB [ 20 ]. On admission, the patient was incoherent, and her status was rapidly deteriorating [ 20 ].…”

Section: Reviewmentioning

confidence: 99%

“…A case study by Thuluvath et al followed a 30-year-old female patient with a history of type 2 diabetes presenting to the emergency department with symptoms of UGB [ 20 ]. On admission, the patient was incoherent, and her status was rapidly deteriorating [ 20 ]. The patient was hypotensive (90/50 mmHg), tachycardic (132 bpm), and tachypneic (32/min) with Kussmaul breathing, and complained of abdominal pain on physical examination [ 20 ].…”

Section: Reviewmentioning

confidence: 99%

“…On admission, the patient was incoherent, and her status was rapidly deteriorating [ 20 ]. The patient was hypotensive (90/50 mmHg), tachycardic (132 bpm), and tachypneic (32/min) with Kussmaul breathing, and complained of abdominal pain on physical examination [ 20 ]. Laboratory findings revealed a significant leukocytosis with a white blood cell (WBC) count of 45 K/cu mm (normal: 4.5-11 K/cu mm), hyperglycemia with a blood glucose of 1294 mg/dL (normal: < 140 mg/dL) [ 20 ].…”

Section: Reviewmentioning

confidence: 99%

“…The patient was hypotensive (90/50 mmHg), tachycardic (132 bpm), and tachypneic (32/min) with Kussmaul breathing, and complained of abdominal pain on physical examination [ 20 ]. Laboratory findings revealed a significant leukocytosis with a white blood cell (WBC) count of 45 K/cu mm (normal: 4.5-11 K/cu mm), hyperglycemia with a blood glucose of 1294 mg/dL (normal: < 140 mg/dL) [ 20 ]. Additionally, her findings were consistent with anion gap metabolic acidosis with the bicarbonate level of 4 mmol/L (normal: 23-30 mmol/L), anion gap of 32 mmol/L (normal: <10 mmol/L), and venous blood pH <6.8 (normal: 7.31-7.41) [ 20 ].…”

Section: Reviewmentioning

confidence: 99%

“…Laboratory findings revealed a significant leukocytosis with a white blood cell (WBC) count of 45 K/cu mm (normal: 4.5-11 K/cu mm), hyperglycemia with a blood glucose of 1294 mg/dL (normal: < 140 mg/dL) [ 20 ]. Additionally, her findings were consistent with anion gap metabolic acidosis with the bicarbonate level of 4 mmol/L (normal: 23-30 mmol/L), anion gap of 32 mmol/L (normal: <10 mmol/L), and venous blood pH <6.8 (normal: 7.31-7.41) [ 20 ]. This patient was diagnosed with DKA and, on EGD, revealed necrosis with black-colored esophageal mucosa at the distal esophagus [ 20 ].…”

Section: Reviewmentioning

confidence: 99%

See 4 more Smart Citations

Epidemiology, Pathogenesis, and Clinical Manifestations of Acute Esophageal Necrosis in Adults

Rehman¹,

Jaferi²,

Padda³

et al. 2021

Cureus

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Acute esophageal necrosis (AEN), also termed "black esophagus," is a unique and uncommon occurrence observed in severely sick patients. Other terminologies include acute necrotizing esophagitis and Gurvits syndrome. This condition is described as a darkened distal third of the esophagus observed on endoscopy and presents as an upper gastrointestinal (GI) bleed, difficulty swallowing, abdominal pain, fever, syncope, nausea, and vomiting. The etiology of AEN has been linked to several possibilities, such as excessive gastric acid reflux, hypoperfusion, and ischemia due to impaired vascular supply and hemodynamic instability. Risk factors include increased age, sex (male), heart disease, hemodynamic insufficiency, alcohol use, gastric outlet obstruction, diabetic ketoacidosis (DKA), malnutrition, renal disease, and trauma which also have the propensity to complicate disease course. An esophageal biopsy is not warranted. Treatment of AEN is comprised of supportive management with intravenous fluids, proton pump inhibitors (PPI), sucralfate, parenteral nutrition, and antacids. Management of preexisting comorbidities associated with AEN is crucial to prevent exacerbation of the disease course that could result in a poor prognosis and increased mortality rates. This literature review article comprises epidemiology, etiology, pathogenesis, diagnosis, and management of AEN.

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Section: Reviewmentioning

confidence: 99%