Well done Paul for your detailed reasoning and suggesting doing a serum lipase which is not available in our lab, but would have been very high.

 

Remarkably, he was not volume contracted neither by clinical examination nor by UEs as he kept drinking fluids of whatever type.

 

I agree the hypocalcaemia is one of the features that we commonly see in severe acute pancreatitis due to calcium salt deposition in the peritoneum, the CT scan did show peritoneal calcifications in keeping with acute pancreatitis.

 

The massive fluid amylase has one explanation really, that it is pancreatic fluid and you could disregard other causes like ruptured oesophagus and malignancy.

 

BW,

 

Mohammad

 

 

 

Thank you for sharing this interesting case. My thoughts and reasons for suggesting lipase are below.

 

The pleural fluid analysis is in keeping with an exudative process (elevated LDH indicates exudate, regardless of fluid protein based on Light's criteria). Exudative pleural effusions are usually unilateral, so the bilateral effusions in this case make pneumonia/abscess/neoplasia/pulmonary embolism less likely causes. The differential based on the pleural fluid analysis therefore includes diagnoses such as pancreatitis, connective tissue disorders, and ruptured oesophagus. There was nothing in the history to suggest connective tissue disease, and he would be unlikely to survive 5 days with a ruptured oesophagus. The fact that he is a heavy drinker was also in support of acute pancreatitis as the cause.

 

In relation to the other tests, I would argue that the hyponatraemia is likely to be due to effective circulating volume depletion. He has lost considerable fluid into his abdominal and pleural cavities. The low urinary sodium is an appropriate response to dehydration and the relatively high urine osmolality is in keeping with appropriate ADH action.

 

The mildly cholestatic LFTs suggest something irritating the biliary system. The low albumin with relatively normal INR and bilirubin suggests sepsis, rather than liver failure, and the high white cell count and CRP support this.

 

The blood gas analysis shows respiratory alkalosis, presumably due to hyperventilation due to the chest disease. I presume the pO2 is venous. The hypocalcaemia possibly reflects the formation of intra-abdominal soaps, a typical finding in acute pancreatitis.

 

The most specific test for diagnosing acute pancreatitis is the serum lipase. A very high amylase will of course also point to the diagnosis but is much less specific. Of note, a pleural fluid amylase can also be seen with a ruptured oesophagus.

 

Thanks again for sharing this great case.

Best wishes,

Paul

 

 

 

Solving the case, learning points and conclusion:

 

I have simply added pleural fluid amylase and the result was phenomenal >100,000 U/L.

 

I have seen many cases of pleural effusions associated with acute pancreatitis and also in alcoholic liver disease with tense ascites. My reasoning is that heavy alcohol drinking frequently targets the liver and the pancreas.

 

Serum amylase was measured on admission sample and it was >3000 U/L.

 

CT scan of the abdomen was later performed on my advice which showed acute pancreatitis with small pancreatic pseudocyst formation.

 

The patient gave a history of grumbling abdominal discomfort over past 10 days but not severe enough abdominal pain characteristic of acute pancreatitis to make him seek medical help. It was until he experienced severe dyspnoea due to massive bilateral pleural effusions that he presented to the emergency department.

 

This represents a case of painless acute pancreatitis started 10 days prior to admission and evolved to pancreatic pseudocyst that has ruptured into the pleural space allowing for its natural drainage.

 

I would argue that the pseudocyst was larger than CT has detected but has reduced in size due to its natural drainage into the pleura.

 

The pleural effusions were not merely reactionary to acute pancreatitis but they were actual pseudocyst amylase rich fluid hence the massive fluid amylase detected.

 

The left chest drain is still draining pleural fluid 5 days after admission, the right side has stopped draining so the chest tube has been removed on this side.

 

The hyponatraemia was merely due to excessive fluid intake combined with inappropriate ADH production due to the chest pathology.

 

Conclusion: In an alcoholic patient presenting with bilateral or unilateral pleural effusion, consider acute pancreatitis even if abdominal pain is not a conspicuous feature.

Measuring serum and fluid amylase should be undertaken in such cases.

 

I hope you enjoyed the case as I did.

 

BW,

 

Mohammad

 

 

 

 

I like your wild guesses Ali, keep them coming.

 

Hint: although the diagnosis is a significant disease, it is not a malignant one.

 

BW,

 

Mohammad

 

 

Supportive of dilutional/appropriate  hyponatraemia and U&E – very likely CA lung –  probably the low urine Na is due to long term salt wastage driven by excess ethanol intake. What is the HCO3/Anion gap/ADH/Aldo!

 

 

Dear mailbase members,

 

You may find this case interesting.

 

 

A 40 year old man presented with severe dyspnea of 5 days duration. CXR showed massive bilateral pleural effusions and biochemistry showed:

 

Sodium     - 108 mmol/L     

Potassium    4.8         

GGT        + 69

Urea         3.1         

ALT          35

Creatinine - 30          

ALP        + 173

Bilirubin    14

CRP        + 266         

Albumin    - 23

Cortisol   + 1000 nmol/L        

S.Osmolal  - 223

EGFR        >90         

TSH          1.87

TnI     <10 ng/L

 

FBC: WC 31.5 mainly neutrophils, HB162 g/L, platelets 345

INR: 1.2

D-dimer: >5000

 

Urine biochemistry:

Ur.Osmolal   673

Ur.Sodium    <5

Ur.Potas     61

Ur.Creat     9.85 mmol/L

 

Pleural fluid biochemistry:

Visual appearance: serosanguinous

Glucose      2.7

Fluid LDH    919

Protein      22

Albumin      12

Sodium       107

Potassium    3.6

Urea         3.7

 

The patient was a heavy drinker.

 

Could you suggest further biochemical tests in order to arrive at the final diagnosis?

 

Reply directly to the mailbase please for a better collective interaction and reasoning.

 

Regards,

 

Mohammad

       

Dr. M. A. Al-Jubouri

MBChB, FRCP Edin, FRCPath

Consultant Chemical Pathologist

Clinical Director of Pathology

St. Helens & Knowsley Teaching Hospitals

 

 

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