Download Diabetic Myonecrosis in the Setting of Chronic Pancreatitis

Nambi Nallasamy, HMS III
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Our Patient
Imaging Chronic Pancreatitis
Lab Findings
Imaging Acute Pancreatitis
Imaging of Our Patient
Putting it all Together
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Bob is a 39 yo M with a h/o:
 chronic pancreatitis s/p distal pancreatectomy & splenectomy
 pancreatic pseudocyst
 past EtOH abuse
 HTN, DM, and hypercholesterolemia
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He presented to the ED with:
 new back pain, confusion, fatigue, weakness, abd
discomfort, and fever
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Extensive past EtOH use (started drinking in 7th
grade, 30 beers/night in his 20s)
 Has been abstinent since 2001 per his record
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Alcoholic pancreatitis, s/p distal pancreatectomy
10 yrs ago
ARDS with hx tracheostomy
Splenic hematoma  splenectomy
 Chronic abd pain since splenectomy, on methadone and oxycodone
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Portal vein thrombosis with partial occlusion
Asthma
Depression
 Our Patient
 Imaging Chronic Pancreatitis
 Lab Findings
 Imaging Acute Pancreatitis
 Imaging of Our Patient
 Putting it all Together
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Alcohol abuse
Cigarette smoking
Hereditary Pancreatitis (AD, 80% penetrance)
 Onset before 20, often before 5
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Ductal obstruction
 Strictures 2/2 trauma, pseudocysts, calcific
stones, or tumors
Tropical pancreatitis (possible SPINK1 mutation relation)
 CF gene mutation
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Chronic inflammation of the pancreas leads to:
 Destruction of pancreatic acini  fibrosis
 Pancreatic duct dilation and irregularity 2/2 formation of intraductal protein plugs and calcifications
▪ Protein plugs serve as nidus for calcification within inter‐ and intra‐lobular ducts
▪ Ductal epithelial lesions result  scarring and obstruction of ducts  inflammatory changes and cell loss
▪ Protein plugs consist primarily of GP2, a glycosyl
phsphatidylinositol anchored protein that is cleaved from the zymogen granule membrane and secreted into pancreatic juice
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Abdominal pain
 Typically epigastric, radiating to the back
 Worse 15‐30 minutes after eating
 May become continuous as course progresses
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Pacreatic insufficiency
 Fat malabsorption
 Diabetes
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Normal serum amylase and lipase concentrations
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ERCP
 Dilated, beaded, and tortuous pancreatic duct
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Abd Plain Film
 Punctate calcific densities scattered throughout pancreas
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Abd CT
 Punctate calcifications throughout pancreas (found in 30‐60% of pts)
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MRI
 Irregularity of the pancreatic duct
 Atrophic pancreas
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MRCP
 Tortuosity of the pancreatic duct  Irregularity in caliber of the pancreatic duct
Note the punctate
calcifications throughout the calcifications pancreas
Axial C‐ Abd CT
Lieberman’s eRadiology
http://eradiology.bidmc.harvard.edu
Bob’s abdominal CT does not demonstrate the punctate
calcifications commonly seen in chronic pancreatitis
It does, however demonstrate a different finding, which shall different finding
be discussed later
Axial C‐ Abd CT
BIDMC PACS
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Pancreatic pseudocyst formation
Renal cyst formation
Bile duct or duodenal obstruction
Pancreatic ascites or pleural effusion
Splenic vein thrombosis
Pseudoaneurysms
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US
 Anechoic fluid collection within the head of the pancreas with enhanced through transmission
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Abd CT
 Homogeneous fluid density collection in the head of the pancreas
 Collection does not enhance with contrast
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MRI
 Homogeneous water intensity mass
Area of decreased attenuation corresponding to pancreatic pseudocyst on non‐contrast CT
No evidence of intracystic
hemorrhage
Axial C‐ Abd CT
BIDMC PACS
Area of increased attenuation corresponding to pancreatic pseudocyst that does not enhance with contrast.
No air pockets seen to indicate infection of the pseudocyst.
Axial C+ Abd CT
BIDMC PACS
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Pseudocyst
Abscess
True cyst
Benign cystic neoplasm
Malignant primary cystic neoplasm
Liver metastasis
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Pseudocyst vs. True Cyst:
 Pseudocyst is technically not a cyst – the wall consists of granulation and/or fibrous tissue (2/2 inflammation)
 Pancreatic pseudocyst results from passage of inflammatory fluid into the omental bursa
 True cyst has a wall that consists of a clearly defined epithelial cell layer
Renal Cyst (likely 2/2 chronic Renal Cyst pancreatitis) measuring 42.17 mm in diameter.
Sagittal FRFSE T2‐Weighted L‐
Spine MRI
(FRFSE, FR‐FSE) Fast Relaxation Fast Spin Echo sequence provides high signal intensity of fluids, even with short TR.
BIDMC PACS
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Acute on Chronic Pancreatitis
Acute cholecystitis
Muscle strain
Pyomyositis
Myonecrosis
Perforated duodenal ulcer
Bowel obstruction
Bowel infarction
Aortic dissection
Renal Colic
Appendicitis
 Our Patient
 Imaging Chronic Pancreatitis
 Lab Findings
 Imaging Acute Pancreatitis
 Imaging of Our Patient
 Putting it all Together
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Elevated LFTs, AST > ALT (787 : 285)
 Indicative of acute pancreatitis 2/2 EtOH use
 Points to relapse of EtOH use, which patient denies
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CK > 22,000
Leukocytosis
 Concern for epidural abscess given urinary retention, intermittent complaints of saddle anesthesia
 Our Patient
 Imaging Chronic Pancreatitis
 Lab Findings
 Imaging Acute Pancreatitis
 Imaging of Our Patient
 Putting it all Together
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Gallstones
Ethanol
Trauma
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Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidemia
Drugs (azothioprine, diuretics)
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Sensitization of acinar cells to CCK‐induced premature activation of zymogens
Potentiation of the effect of CCK on the activation of transcription factors, NF‐kappa B and activating protein‐1
Generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters
Activation of pancreatic stellate cells by acetaldehyde and oxidative stress  increased production of collagen and other matrix proteins
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RUQ Abdominal pain
 Can last for days
 Can occur 1‐3 days after an alcohol binge
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Fever
Tachycardia
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Elevated serum amylase
 Rises within 6‐12 hours of onset
 Often elevated for 3‐5 days
 First serum amylase in this patient obtained 3 days after admission and was normal
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Abd Plain Film
 “splenic cut off sign” – paucity of air in the colon distal to the splenic flexure due to functional spasm of the descending colon 2/2 spread of pancreatic inflammation to the area
 Sentinel loop in LUQ
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Abd CT
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Edema of pancreas
Fat stranding surrounding the pancreas
Fluid collection(s) within pancreas
Gas in the pancreas or retroperitoneum
MRI
 Offers ability to delineate fluid collections as acute, necrotic, abscess, hemorrhage, or pseudocyst
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Focal fluid collections and ascites
Pseudocyst formation
Pancreatic abscess
Pancreatic necrosis
Peripancreatic hemorrhage
Biliary obstruction
Pseudoaneurysm formation
Portal Vein Thrombosis
Abberant Air
 Our Patient
 Imaging Chronic Pancreatitis
 Lab Findings
 Imaging Acute Pancreatitis
 Imaging of Our Patient
 Putting it all Together
Non‐enhancing region within portal vein on CT indicating likely portal vein thrombosis
Axial C+ Abd CT
BIDMC PACS
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Acute on Chronic Pancreatitis
Acute cholecystitis
Muscle strain
Pyomyositis
Myonecrosis
Perforated duodenal ulcer
Bowel obstruction
Bowel infarction
Aortic dissection
Renal Colic
Appendicitis
Dessication of the L4‐L5 intervertebral disc
Sagittal L‐Spine T1‐weighted MRI
BIDMC PACS
Increased signal seen in the multfidus and quadratus
lumborum muscles
Axial T2‐Weighted L‐Spine MRI
BIDMC PACS
Increased signal seen in the multfidus and quadratus
lumborum muscles
Axial T1‐Weighted MRI with Post‐Processing
BIDMC PACS
Edema of paraspinal
musculature extending from T12 to L4/5.
Dependent edema in deep Dependent edema dorsal subcutaneous soft tissues – can be seen in supine patients
Sagittal STIR (Short Tau Inversion Recovery) L Spine MRI
BIDMC PACS
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Reason for study:  Evaluation for epidural abscess, pyomyositis, myonecrosis, discitis, vertebral osteomyelitis
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Reason for IV contrast:
 To evaluate for enhancing abscess walls, hypervascular masses, hyperemia
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Findings:
 Increased STIR signal within R paraspinal musculature
 With contrast, patchy enhancement of R multifidus, longissimus, and quadratus luborum muscles
 Normal signal within bone
 Normal vertebral body height, signal and sagittal alignment
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Impression:
 No evidence of osteomyelitis, discitis, septic arthritis, or epidural abscess
 No drainable fluid collection
 Findings indicate myonecrosis vs. pyomyositis without frank abscess formation
 Our Patient
 Imaging Chronic Pancreatitis
 Lab Findings
 Imaging Acute Pancreatitis
 Imaging of Our Patient
 Putting it all Together
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Acute‐onset damage of the right paraspinal muscle (indicated by elevated CK at admission) with subsequent dramatic symptomatic improvement and normalization of CK
Abn signal in paraspinal muscles on MR concerning for pyomyositis vs. myonecrosis
 No fluid collections or abscess formation seen
 Initially treated empirically with abx, but clinical course pointed away from infection
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No evidence of inflammatory myositis per Rheumatology
Possibile etiologies of his myonecrosis:
 Myonecrosis in setting of diabetes
 Rhabomyolysis in setting of pramipexole use
 Trauma
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Epidemiology
 Usually affects patients with long‐standing poorly controlled DM with pre‐
existing microvascular complications (e.g. retinopathy, nephropathy, or neuropathy)
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Lab Findings
 Elevated CK
 Can be accompanied by leukocytosis (35%)
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MRI Features
 High intensity of the involved muscle (on T2‐weighted sequences)
 Subcutaneous edema
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DDx
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Pyomyositis (S. aureus)
Spontaneous gangrenous myositis (Strep)
Clostridial myonecrosis
DVT
Intramuscular hematoma
Neoplasm
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This patient is a particularly poor historian.
 Even when not acutely ill, is taken care of by his mother
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The patient’s past tendencies raised clinical suspicion of EtOH relapse given lab values indicative of acute pancreatitis
Imaging allowed team to overcome these limitations, and point toward myonecrosis
rather than infection
 Shortened the patient’s hospital stay
 Reduced antibiotic usage
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