ME IN 2014

7th December 2015

Dr Kelly Hamill

North Bellingen Medical Centre

58 Wheatley Street

Bellingen NSW 2454

Dear Dr Hamill,

RE: LYNNE SANDERS-BRAITHWAITE

MRN: 130 02 61

DOB: 19/10/1949

BACKGROUND:

  1. Chronic liver disease secondary to chronic hepatitis C (CHC) and previous excessive alcohol consumption.  Child Pugh score A5, previous episode of decreased level of consciousness and peripheral oedema, chronic hypoalbuminaemia 26 g/L, mild elevation bilirubin 22 umol/L.  INR 1.4, platelets 48 x 109/L (chronic suppression), normal bone marrow biopsy previously.  Dr John Gibson, RPAH.  Ongoing moderate hepatitis ALT 56 U/L.

1.1            Chronic hepatitis C (CHC) genotype 1A, viral load 5.6 log IU/mL likely contracted through intravenous drug use in 1972, treated in 1997, no ongoing injecting drug use or Opioid substitution therapy.

1.2            Previous excessive alcohol use until 9/1997 now resolved.  No ongoing alcohol use.

1.3            Hepatitis B core antibody positive, hepatitis B surface antigen negative.  Hepatitis B surface antibody 54 IU/ml consistent with previous exposure with ongoing immunocompetency.

1.4            Hepatocellular carcinoma screening, November 2015; cirrhotic liver with splenomegaly, no liver lesions., organs otherwise unremarkable.  November 2015 alpha-fetoprotein 13 ug/L.

1.5            No previous bone mineral density.

1.6            No previous dietician reviewed albumin 26 g/L for nocturnal protein supplementation.

  1. Previous cardiomegaly with no specific diagnosis.  Echocardiography November 2015 normal LV size and systolic function, mild to moderate dilatation of left atrium, mild pulmonary hypertension, ejection fraction 64%.
  2. Morbid obesity.  Weight 100 kg.  Height 152 cm.  BMI is 42.8.  No previous dietetic intervention.

MEDICATIONS: Frusemide 20 mg daily, Spironolactone 50 mg daily and Salbutamol prn ALLERGIES: No known.

Thank you for referring Lynne to clinic regarding her chronic liver disease secondary to chronic hepatitis C (CHC) and resolved alcohol excess. She is a 66-year-old woman living independently in Urunga with significant history of bereavement and health crisis during 2014, which nearly resulted in death.  Since that time she has improved significantly and been able to resume home life independently. She has not previously had specialist liver review.  She is known of CHC for many years and nominates intravenous drug use from 1972 onwards as the likely source of infection.  During the period 1972 through 1987 she consumed alcohol and used intravenous drugs and was able to control substance abuse initially with IV substitution therapy and eventually through Narcotics Anonymous to avoid all ongoing issues with drug and alcohol since that time.  She has not previously had therapy for CHC. 

Lynne’s health issues in 2014 were described as decompensation of her cirrhosis in the setting of severe pneumonia which resulted in loss of consciousness and ICU care for several weeks and involved significant fluid overload. Since that time, her fluid overload has mostly resolved and she has no ongoing features of encephalopathy that previously troubled her.  Her other health issues relate to dyspnoea and morbid obesity; I believe these to be linked.  She is morbidly obese with BMI of 42.8 and has significant difficulty moving with this weight.  She has not undertaken exercise or diet programs and has no previous referral for bariatric surgery. She was previously described as having cardiomyopathy with dilatation of the cardiac changes, however her most recent echo does not demonstrate features of cardiomegaly and has normal left ventricular size and systolic function. Her echo shows mild pulmonary hypertension which may contribute to breathlessness, however I feel that her muscle bulk is likely to be quite modest in her body which is requiring significant exertion and I believe her breathlessness relates to both her liver disease and her obesity rather than cardiac or respiratory function.  She is not previously known to have ischaemic heart disease.

On examination, Lynne is obese with a soft abdomen and no evidence of ascites. She has splenomegaly and otherwise unremarkable abdomen with minimal tenderness. She has very mild peripheral oedema and few other stigmata of chronic liver disease. Her respiratory examination is unremarkable without crepitation at the bases. She had dual heart sounds which were faint. She had no signs of encephalopathy. Blood testing from November 2015 shows moderate elevation in ALT 56 U/L with other enzymes elevated, deranged liver synthetic function with albumin 25 g/L, bilirubin 22 umol/L, INR 1.4. She had profound thrombocytopenia 39 x 109/L with normal haemoglobin and normal iron studies. She has recent testing for HCV infection with genotype IA, viral load 5.6 log IU/mL and evidence of previous exposure to chronic hepatitis B with HBc antibody positive in the absence of other markers of ongoing infection. Ultrasound of the abdomen performed in November 2015 shows a cirrhotic liver with no evidence of hepatic lesions, splenomegaly and no note of ascites present. Her alpha-fetoprotein was marginally elevated consistent with her level of elevation in ALT. She has not previously had gastroscopy and has never had upper GI haemorrhage.

Lynne is reluctant to have antiviral therapy for her CHC and is unsure where she would like to be treated should this became available. The standard of care in 2016 for genotype IA infection would be three months of oral antiviral therapy using either Viekira Pak or Harvoni both of which are due to became available through the PBS over the coming months.  Liverpool Hospital treatment team consist mainly of nursing and medical staff with significant experience that are dealing with advanced liver disease and this would be an appropriate environment for Lynne.  This is a long way from home and presents significant logistics complications.  I am happy to work with local services in Coffs Harbour or in the Bega area where her son lives should treating physician be available.  In the meantime, I have asked her to alter her diet to involve high protein supplementation nocturnally (for instance, Sustagen in milk prior to sleep), a low salt diet low in other carbohydrates to try to reduce her weight.  I will seek advice on diet solution for Lynne by involving the dietician from the Royal Prince Alfred Liver Unit who has specific skills in this area. Certainly, salt free diet will benefit her with respect to fluid overload and to this end I have introduced Spironolactone 50 mg daily to assist in loss of fluid.  I would recommend water based exercise such as walking around the shallow swimming pool to assist with weight loss. I think that prophylactic banding of varices should they be present would be ideal.  However organising gastroscopy may be complex and I have not addressed this as yet. Lynne needs bone mineral density study and should have vitamin D supplementation with or without osteoporosis care if indicated. I frequently use Zoledronic acid annually and for osteoporosis care. I think that Lynne has intermediate prognosis from her cirrhosis and may benefit from control of her viral infection, however with the current profile of obesity she may struggle to overcome her significant health issues. She requires ultrasound of the abdomen every six months to assess for new lesions related to hepatocellular carcinoma and six monthly alpha-fetoprotein as a standard of care. I will be happy to see her on ongoing basis and/or provide support to treating physician who may review her regularly.

Yours sincerely,

Dr Scott Davison

Staff Specialist, Gastroenterology and Hepatology

Liverpool Hospital

cc              Clinical Information, Liverpool Hospital

cc              Gastro file

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