Description

● Case Overview:
➣ Patient Profile: 78-year-old female patient taking several cardiovascular drugs, such as statins and antiplatelets, for ischaemic heart disease and hypertension.
➣ Duration/Complaints presented: nausea, vomiting, chills without a temperature, and excruciating epigastric pain that radiates to the back (worst while supine).

● Clinical Examination Results:
➣ At admission, the patient appeared ill and was afebrile; vital signs were initially stable (HR 80 bpm, BP 130/80 mmHg, SpO₂ 94% on room air).
➣ Severe epigastric discomfort spreading to the back and a soft abdomen.

● Results from the laboratory:
➣ Serum lipase: 230 U/L ↑ (initial) → peaked at 1450 U/L.
➣ Serum amylase: 185 U/L ↑ (initial) → peaked at 1200 U/L.
➣ Mild thrombocytopenia (149 ×10³/µL); BUN 22 mg/dL; creatinine 1.4 mg/dL (reasonable baseline renal function); unremarkable lipid and ➣ electrolyte profiles (no hypertriglyceridemia); no gallstones were seen on ultrasound.

● Radiological Findings:
➣ Abdominal ultrasound: No gallstones or biliary blockage; enlarged, heterogeneous pancreas indicative of severe pancreatitis.
➣ Follow-up CT: Development of bilateral ground-glass alterations and imaging characteristics consistent with necrotising pancreatitis. Chest CT (day 2): Bilateral peripheral ground-glass opacities suggestive of COVID-19.

● Differential Diagnosis:
➣ Drug-induced pancreatitis (drugs not usual culprits; lipids normal);
➣ Hypertriglyceridemia;
➣ Viral pancreatitis (including SARS-CoV-2)
➣ Ischemic/metabolic causes (less likely);
➣ Gallstone pancreatitis (ruled out by imaging);

● Verification of the diagnosis:
➣ Nasopharyngeal/Oropharyngeal swab rRT-PCR: Positive for SARS-CoV-2 ➣ The most likely cause, after ruling out common aetiologies and temporal associations, was COVID-19-associated pancreatitis.

● Discussion & Clinical Significance:
➣ Because pancreatic tissue contains ACE2 receptors, there is a biologically reasonable explanation for how SARS-CoV-2 can cause pancreatic damage by direct viral invasion or indirect mechanisms such hypoxia, microvascular thrombosis, and systemic inflammatory response.
➣ The connection with COVID-19 was strengthened in this patient by excluding out typical causes of pancreatitis, such as gallstones, alcohol, and hypertriglyceridemia.
➣ Pancreatitis caused by COVID-19 can be severe and proceed quickly, leading to necrosis and multi-organ failure. Although it is crucial, early detection does not always change the course of serious disease.

Protocol

● Clinical Course & Treatment:
➣ Initial management: IV crystalloids, analgesia, bowel rest, and oxygen supplementation as required.
➣ Day 4: intubation and ICU admission for mechanical ventilation due to increasing hypoxia (SpO₂ 89% on nasal cannula)
➣ Antiviral/immunomodulatory treatment: Interferon Beta-1b (8 million IU SC every other day) and Remdesivir (200 mg IV loading, followed by 100 mg IV daily) were given.
➣ The patient's pancreatitis worsened despite vigorous treatment, resulting in oliguria, hypotension, multiorgan failure, refractory shock, and a substantial increase in enzymes. On the seventh day of admission, there was cardiac arrest; resuscitation was unsuccessful.

Notes

For more details visit https://pmc.ncbi.nlm.nih.gov/articles/PMC7682978/