Yellow discolouration

Saturday, August 21, 2010

The pathologist reported

Sections show fragments of gastric mucosa with sheets and nests and occasional glands of malignant epithelial cells invading the stroma. The tumour cells are pleomorphic, have increased N/C ratio, vesiculer nuclei and eosinophilic cytoplasm. Abundant mitotic figures are seen.

Impression: Adenocarcinoma, poorly differentiated, infiltrating
This is an elderly woman in her seventies, who was warded 4 months ago with the chief compliant of yellow discoloration of her eyes and skin. I remember this particular patient vividly as she gave the medical team a hard time figuring out what is wrong with her.

When she was admitted, she was grossly jaundice. It wouldn't be difficult to spot her in a sea of people. The semester one student nurses were pretty curious with her presentation and some of them asked me what's wrong with her.

It's pretty simple when you have a patient presenting to you with jaundice which is actually yellow discolouration of the mucous membrane and skin due to excessive bilirubin deposition. In our Malaysian setting, an underlying liver pathology/gall stone disease is usually the culprit.

However, upon detailed history taking, we couldn't elicit anything related to an underlying chronic liver disease. No weight loss, appetite was fine either. Crepitations at both lung bases were picked up and the legs were minimally edematous as well. She has no risk factors of viral hepatitis infection but of course a full jaundice workup was done including hepatitis serology.

An ultrasound was subsequently ordered to look for evidence of liver cirrhosis that could explain her presentation. I scratched my head when the report came back, everything was fine other than the enlarged lymph nodes compressing the porta hepatis. Liver was homogenous in terms of echogenicity, no evidence of cirrhosis.

To cut the long story short, a full battery of investigations were performed and we finally hit the jackpot when an OGDS found a fungating mass at the body of the stomach. A biopsy was taken and the result as mentioned above. Bile flow was obstructed due to external compression by the enlarged lymph nodes. Prognosis was not good. Management was then to relieve the obstruction by stenting, the rest are just palliative.

I followed her up for almost two and a half weeks, trying to understand the disease progression. Every afternoon before lunch time, she'll definitely ask me whether I've had my lunch. And if I say no or later, she will start lecturing me on how I should take care of my own health, and how eating late is bad for health. She was a very cheerful lady and even the student nurses enjoyed chit-chatting with her. They call her "po po"(grandma). After the stent was put in, she was allowed to be discharged

Today while I was doing my groceries in Giant, I bumped into her daughter. We started talking and I asked about po po. "She passed away 2 weeks ago, in peace, without any pain" her daughter said. " Thanks for asking doc" she added.

I can't remember her exact full name. But other than that, I can remember every single thing she told me before she passed away. I spent quite some time telling stories, listening to stories, laughing with a woman who would not survive the year.

I do hope she's doing fine up there, surrounded by lovely people!

A good cry

Saturday, August 7, 2010

She looked outside the window and started crying. Her tears welled up in her eyes, rolled down her chicks and then subsequently she broke into a full out sob. She tried to suppress the urge to cry, wiping away the tears with her tudung.

I excused myself from the team of doctors doing round, went over and gave her a gentle tap at her back and said:" I'm sorry Mak Cik, is there anything else we could do for you?". I knew she had no choice, your mind overrides any effort to suppress the need to cry, I told her it's fine to let it all out, because i know when you hold your tears back, you are only amplifying the emotions your body is trying to release through crying. She took a deep breath and said: Thanks for the pineapple cake young doc, and asked me how I became a doctor at such young age.

Her husband is a 65 year old malay gentleman with a known history of type 2 diabetes mellitus under the follow up of one of the district clinic. He presented with the chief complaint of dysphagia(difficulty swallowing) that was progressively getting worse. It started off with solid food especially bolus of rice and subsequently followed by fluid. Prior to admission this time, he could only tolerate 3 spoons of whatever food before regurgitating. Vomitus was free from billous substances and the fact that he could pin point the level of obstruction above the nipple line strongly suggest a mechanical obstruction at the distal oesophagus. With the significant weight loss of 20kgs in one month with anorexia, any sound reasonable competent doctor will give the the provisional diagnosis of a malignant space occupying lesion anywhere along the oesophagus causing the above symptoms. And yes, the was the provisional diagnosis of adenocarcinoma of the lower oesophagus was agreed by the specialists and the rest of the MOs and HOs. The plan of management at that time was to get an urgent OGDS for diagnosis and probably a tissue biopsy of histopathological evaluation.

Looking at him, he was lying on his bed, propped up with the wife and a wheel chair beside him. He has not been ambulating well according to the wife, and probably it is due to his poor oral intake i said to myself. A quick glance at him reveals a man in his 60s, emanciated with temporal wasting looking quite pale probably with a haemoglobin level of 8 or 9. He's not in pain, comfortable under room air without any oxygen supplementation. Did a quick examination on him and found nail bed, conjunctival pallor, distended abdomen with positive fluid thrill and bilateral pedal edema up to the mid shin. From auscultation, there was reduced air entry bilaterally with bronchial breathing just above it suggesting some degree of pleural effusion. After palpating the abdomen quickly, I concluded that his physical findings were consistent with the provisional and probably there is liver metastasis to the liver causing a hypoproteinemic state.

When I went back to the ward after class that day, I was confused as the OGDS did not show any intraluminal obstruction, but instead 4 large oesophageal varices occupying more than 1/3 of the oesophageal lumen with red cherry spots indicating stigmata of recent hemorrhage. Something was not right, from the history itself, there was nothing to suggest an underlying liver disease. No previous history of jaundice, distension, tea coloured urine and pruritus. Stool was normal as well. I traced his liver function test and found myself even more confused with the LFT being relatively normal. Serum albumin was on the lowish side, serum bilirubin and the other liver enzymes were normal. Nothing at all that suggest a primary liver pathology. Coagulation profile was not prolonged as well. I doubted my skills in history taking at that point, did I make a mistake? But I am very sure that the patient's complaint upon admission was "Susah nak telan".

During the A.M round the next day, an abdominal ultrasound was done and serological investigations to detect Hep B/Hep C infection were dispatched. The report from the radiologist came back stunning all of us- a large heterogenous hypoechoic lesion over the left lobe of the liver suggesting hepatocellular carcinoma! The liver was mildly cirrhotic and there is no clear fat plane between the mass between the body of pancreas, suggesting local infiltration. This is not a good news at all, his wife asked me about the radiological report, I said I am not in a position to give any comments and the consultant will be a better person to talk to. To cut the long story short, a 3 phase liver CECT was done and subsequently found multicentric lesions over the liver with invasion into the main and right hepatic veins and distortion of the IVC. Everything make sense now, the portal hypertension was not due to cirrhosis of the liver, but instead thrombosis in the main hepatic veins with anatomical distortion of the IVC. Budd-Chiari syndrome.

I put the CT films down and rush to the patient, I asked for permission to examine him. By then, the abdomen is grossly distended with the umbilicus everted. Shifting dullness cannot be any more clear, even with such an amount of fluid in the abdomen, when I laid my hands over the epigastrium, I noted a firm mass with an irregular boarder, covering half of the epigastrium. HOW CAN I MISS THAT from the initial physical examination? I flipped open the case file and found out that it was missed by the HO who first examined him as well. This is a retrospective finding, nothing to be proud, but definitely something to be ashamed off. All my tutors were right, even the consultant was right, medicine is still an art that cannot be replaced even by the advent of sophisticated imaging technology.

She looked outside the window and started crying. I asked whether I could do more although I do know that as a student, I can do nothing. The wife and the family members decided to bring him back. There's nothing that can be done here in HSAJB for him, only palliative management. I spent some time talking about a few things that could possibly go wrong after discharge, asking him to come back if ever he finds himself passing black stool or experiencing any symptoms of anemia from UGIB. The ascites will only get worse, and I reminded him to come back for a peritoneal tap if he finds himself having difficulty breathing from all the fluids in his lungs and the restrictive effect imposed on the lungs by the large abdomen. I thanked both of them for all the teachings and bid goodbye.

HCC without the background of cirrhosis, alcohol binging and chronic hepatitis infections. Something different from the pathology that I've learnt previously. Looked up the patho textbook that night itself, and found that a variant of HCC can occur without cirrhosis/ hepatotrophic viral infection- Fibrolamelar carcinoma of the liver. I hope that the mass could be a benign one like an adenoma or focal nodular hyperplasia. But from the aggressiveness of the mass as reported, and the fact that is has infiltrated the major hepatic vessels and distorted the IVC, its unlikely that it is benign, a tissue biopsy is still mandatory for confirmation.

Too bad, I've lost all the notes that I've taken for this patient. Must have misplaced it. From the history, daily reviews and even investigations, all gone. Ahh, what a waste, but he taught me so much throughout his stay in the hospital that I can still remember that his serum bilirubin level-it was only 29.