Dr Ryan Agnew
A 50 y.o. lady presented from an aid outpost about a day’s walk away, however she was flown into Kompiam, PNG, as she was unable to walk the distance. Her main complaint was abdominal pain for 3 months, and more recently had not been able to walk secondary to shortness of breath and global oedema. She reported that her oedema had only started 2 weeks previously, she had been given a litre of IV fluids at the aid outpost. By the time I saw her the abdominal pain had resolved, after only paracetamol. She was also given a penicillin class antibiotic and albendazole. She was not particularly concerned regarding the oedema, only being thankful that we had alleviated her pain.
On examination she was saturating at 97%, HR in the 90s, BP 88/48, normal respiratory rate and afebrile. She appeared comfortable but was grossly fluid overloaded with severe pitting oedema, ascites and even swollen breasts and forearms. She had pale palmar creases and pale sclera. She had an ejection systolic murmur. She had good air entry with fine crackles in the bilateral bases, percussion note resonant. Sacral oedema was present. On abdominal examination an enlarged liver edge was palpated, approximately 5cm below the costal margin. It was difficult to get the texture of the liver due to the ascites. The pitting oedema was well up her thighs. No lymph nodes were palpable. A chest XR showed an enlarged heart, pleural effusions and some signs of pulmonary oedema.
The clinical suspicion initially was of either liver or kidney origin protein wasting/production issue with accompanying anaemia. A finger prick Hb, rapid Hep B/C/HIV/malaria strips and urine dipstick were complete. The deceptive electrolyte/liver function test machine was fired up. Her Hb was 19 g/L, she was Hep B and C positive, albumin was 10 and she had proteinuria on the dipstick. The LFTs were either normal or failed to produce a result on our machine.
I suspected she had synthetic disruption of her liver resulting in the gross oedematous state and potentially contributing to her anaemia. I suspected that the liver failure was secondary to chronic viral hepatitis B/C and potentially a hepatocellular carcinoma. Despite no history of bleeding I suspected chronic blood loss secondary to decrease in clotting factors. Once the experienced SMO reviewed the patient, he felt that all the symptoms are likely to be secondary to severe anaemia and would resolve with blood transfusions. As we are unable to treat either hepatitis B or C, our only available treatment is to top her up with red cells.