Diagnostic Assessment — Cholelithiasis
Example 1 of 1 · fictitious patient (Veteran CG)
Diagnostic Assessment
Cholelithiasis
BOP Code: 70 of 2025 (Gallstone Disease (Cholelithiasis))
RH Code: 69 of 2025 (Gallstone Disease (Cholelithiasis))
ADF History
Veteran CG, date of birth 06 April 1970, Australian Army, Nursing Officer (Registered Nurse, later Major), enlisted 15 January 1990, medically discharged 19 December 2013. Operational service: Cambodia, 10 November 1992 to 25 June 1993 (peacekeeping); Rwanda, 18 February 1995 to 22 August 1995 (peacekeeping); East Timor, 20 September 1999 to 15 February 2000 (warlike); Afghanistan, 05 March 2011 to 14 September 2011 (warlike).
Occupational History
As an Army nursing officer the veteran worked in field hospitals, health centres and deployed surgical facilities, cannulating, suturing and handling blood and body fluids, often in austere conditions where needle-stick and splash injuries were common. Shift work, irregular meals and long periods of standing alternated with sedentary administrative postings.
On peacekeeping and warlike deployments she lived and worked alongside local communities, ate local food and drank locally sourced water, and was exposed to endemic parasitic, bacterial and viral infections. Road moves in protected vehicles carried a risk of rollover and blast injury, and deployed personnel with chronic conditions had limited access to elective surgery and specialist follow-up.
History
Veteran CG, an Army nursing officer, developed gallstone disease on 20 July 2009, ten weeks after the birth of her child and two weeks after a month of parenteral nutrition for a Crohn flare, on a background of an ileal resection, obesity, type 2 diabetes, steatotic liver disease, chronic hepatitis C from a needle-stick injury in Rwanda and a haemolytic crisis of hereditary spherocytosis. The disease worsened on 20 October 2016 with stones throughout the biliary tree, cholangitis and pancreatitis, after a spinal cord injury in Afghanistan, a vagotomy, fluke infestation from Cambodia, a somatostatinoma and a year on a very low-calorie diet, during seven years in which cholecystectomy could not be obtained.
Timeline
- 14 May 1995 — During peacekeeping service in Rwanda the veteran sustained a needle-stick injury from a used cannula while resuscitating a casualty in a field hospital. Hepatitis C antibody and RNA were positive on testing in September 1995, genotype 1a. Interferon treatment in 2003 failed and the infection remained chronic. "needle-stick, hepatitis C seroconversion"
- 22 Mar 2001 — After bloody diarrhoea that began with bacterial gastroenteritis on warlike service in East Timor in December 1999, Crohn disease of the terminal ileum was diagnosed in July 2000. A stricture caused obstruction and she had an ileocaecal resection removing 25 centimetres of terminal ileum. She needed several prednisolone courses over the following years and her BMI rose to 31.4 by June 2004. "ileocaecal resection, 25 cm ileum"
- 03 Sep 2008 — Ultrasound of the abdomen, requested for abnormal liver function tests, showed diffuse hepatic steatosis. The gallbladder was thin-walled with no stones or sludge and the bile ducts were normal. Type 2 diabetes had been diagnosed in June 2007. A hepatologist recorded steatotic liver disease with chronic hepatitis C. "steatosis, gallbladder normal, no stones"
- 14 Jan 2009 — At 22 weeks of pregnancy the veteran, who has mild hereditary spherocytosis, had a haemolytic crisis with parvovirus B19 infection: haemoglobin 72 grams per litre, reticulocytes 14 per cent and bilirubin 68 micromoles per litre. She was transfused two units. She was delivered by caesarean section on 10 May 2009. "haemolytic crisis, Hb 72"
- 21 Jul 2009 — Ten weeks after the caesarean delivery, and two weeks after completing 28 days of total parenteral nutrition for a Crohn flare with subacute small bowel obstruction, the veteran presented with severe right upper quadrant pain radiating to the back after an evening meal the day before, with vomiting. Ultrasound showed multiple gallstones up to 9 millimetres with sludge and a normal common bile duct. Cholecystectomy was recommended. "biliary colic, multiple gallstones"
- 14 Sep 2011 — During warlike service in Afghanistan, where she had had three attacks of biliary colic since June managed only with analgesia, the veteran's protected vehicle rolled over. She sustained a T11 burst fracture with an incomplete spinal cord injury and was evacuated. On 26 October 2011 she had an emergency truncal vagotomy and antrectomy for a perforated duodenal stress ulcer. She remained paraplegic. "T11 fracture, incomplete paraplegia"
- 12 Mar 2016 — Admitted with cholangitis, the veteran had ERCP showing pus, intrahepatic pigment stones and a hilar stricture, and a plastic biliary stent was placed. Bile grew Escherichia coli and Klebsiella. On 18 March, during ceftriaxone treatment, she developed immune haemolytic anaemia with a positive direct antiglobulin test. She was on fenofibrate, transdermal oestradiol and a 600 to 750 kilocalorie diet, and cirrhosis had been confirmed in May 2015. "cholangitis, stent, immune haemolysis"
- 20 Oct 2016 — The veteran was admitted with fever, rigors, jaundice and severe epigastric pain. Lipase was 2,400 units per litre. MRCP showed numerous gallbladder stones, a 12 millimetre common bile duct stone and left-sided intrahepatic stones with an occluded stent, and CT showed a 24 millimetre pancreatic head mass, later confirmed as a somatostatinoma. Her weight had fallen from 111 to 86 kilograms over the previous year. "cholangitis, pancreatitis, duct stones"
- 24 Oct 2016 — At ERCP the occluded stent was exchanged, the duct stone and debris cleared, and adult Opisthorchis flukes were extracted. Bile PCR was positive for Helicobacter pylori. A hepatobiliary surgeon recorded marked worsening of the gallstone disease with recurrent pyogenic cholangitis. She had open cholecystectomy, left lateral sectionectomy and hepaticojejunostomy with enucleation of the somatostatinoma on 15 March 2017. "flukes extracted, worsening confirmed"
Symptoms
At onset the veteran had episodes of severe, constant right upper quadrant and epigastric pain radiating to the back, lasting two to six hours, usually after meals, with nausea and vomiting. Between attacks she had fatty food intolerance and bloating.
From October 2016 she had fever, rigors and jaundice with cholangitis and pancreatitis, recurrent attacks requiring admission, and marked weight loss. She now reports intermittent right upper quadrant discomfort, fat intolerance and diarrhoea, and she has had two episodes of cholangitis of the hepaticojejunostomy since surgery.
Imaging
- 03 Sep 2008 — Ultrasound abdomen: "Diffuse increased hepatic echogenicity in keeping with steatosis. Thin-walled gallbladder without calculi or sludge. Common bile duct 4 millimetres."
- 21 Jul 2009 — Ultrasound abdomen: "Multiple mobile echogenic calculi with acoustic shadowing within the gallbladder, the largest 9 millimetres, with sludge. No wall thickening. Common bile duct 5 millimetres. Hepatic steatosis."
- 12 Mar 2016 — ERCP cholangiogram: "Stricture at the hilum involving the left hepatic duct with multiple filling defects in the left intrahepatic ducts in keeping with stones. Purulent bile. Plastic stent placed. Multiple gallbladder calculi."
- 21 Oct 2016 — MRCP and CT abdomen: "Numerous gallbladder calculi. 12 millimetre calculus in the distal common bile duct with duct dilatation. Intrahepatic calculi and ductal dilatation in the left lobe. Occluded biliary stent. Nodular cirrhotic liver with splenomegaly. 24 millimetre enhancing mass in the head of the pancreas."
Onset Date
The most likely date of onset of this condition is 20 Jul 2009.
At that date the veteran was serving full time as a nursing officer, on maternity leave after the caesarean delivery of her child on 10 May 2009. She had completed 28 days of total parenteral nutrition for a Crohn flare on 06 July 2009, and that evening she had her first attack of biliary colic.
This date is appropriate because ultrasound on 03 September 2008 showed a normal gallbladder with no stones or sludge, and she presented the next day, 21 July 2009, with typical biliary pain and ultrasound showing multiple gallstones with sludge. It falls within uninterrupted full-time service.
For the onset factors, the 3 months before onset run from 20 Apr 2009 to 20 Jul 2009 and the 6 months from 20 Jan 2009 to 20 Jul 2009; she was pregnant until 10 May 2009. The 1 year before onset runs from 20 Jul 2008 to 20 Jul 2009 and contains the haemolytic crisis of 14 January 2009. Parenteral nutrition ran continuously from 08 Jun 2009 to 06 Jul 2009, 28 days, and ceased 14 days before onset. The 5 years before onset run from 20 Jul 2004 to 20 Jul 2009, throughout which her BMI was 30 or more. The 25 years before onset run from 20 Jul 1984 to 20 Jul 2009 and contain the ileal resection of 22 March 2001. Type 2 diabetes, steatotic liver disease, hepatitis C and Crohn disease were each present on 20 July 2009.
For the worsening factors, the documented clinical worsening occurred on 20 Oct 2016, with stones in the common bile duct and intrahepatic ducts, cholangitis and pancreatitis. The 5 years before the worsening run from 20 Oct 2011 to 20 Oct 2016; she was paraplegic and unable to exceed 3 METs throughout, and the vagotomy of 26 October 2011 falls within them. The 1 year before the worsening runs from 20 Oct 2015 to 20 Oct 2016 and contains the immune haemolysis of 18 March 2016, the very low-calorie diet throughout and the loss of 22.5 per cent of body mass from 20 October 2015 to 20 April 2016. Fenofibrate from 10 February 2014 and oestradiol from 12 August 2013 were each taken continuously for more than 6 months to the worsening. The biliary stent was placed on 12 March 2016, before the worsening, and spinal cord injury, opisthorchiasis, bacterial and Helicobacter pylori biliary infection, recurrent pyogenic cholangitis, cirrhosis and the somatostatinoma were each present on 20 October 2016.
1. What is the formal diagnosis of the condition claimed above?
The formal diagnosis is Gallstone Disease (Cholelithiasis) (ICD-10 K80.2), later complicated by choledocholithiasis, intrahepatic stones, cholangitis and gallstone pancreatitis, under the Statements of Principles concerning gallstone disease (cholelithiasis), Balance of Probabilities No. 70 of 2025 and Reasonable Hypothesis No. 69 of 2025.
Gallstone disease is the presence of one or more stones larger than 2 millimetres in the gallbladder or the bile ducts, formed by the aggregation of bile constituents. Cholesterol stones form when bile is supersaturated with cholesterol or the gallbladder empties poorly, as in obesity, pregnancy, oestrogen therapy, rapid weight loss, parenteral nutrition, ileal resection, vagotomy and spinal cord injury. Pigment stones form from excess bilirubin in haemolysis and cirrhosis, and from bacterial and parasitic infection of the bile ducts. Stones cause biliary colic and can pass into or form in the bile ducts, causing obstruction, cholangitis and pancreatitis.
The condition began on 20 July 2009, confirmed on ultrasound the next day, and worsened on 20 October 2016 with stones throughout the biliary tree, cholangitis and pancreatitis.
2. For each diagnosis identified, please also provide the following dates:
When did the veteran first experience symptoms attributable to this condition?
20 July 2009.
When did the veteran first present to a health / medical provider for this condition?
21 July 2009.
When was the condition confirmed / formally diagnosed?
21 July 2009.
When did the veteran first present to you (or your practice) for this condition?
30 July 2025.
3. How was this diagnosis confirmed? i.e. what were the key symptoms and signs, investigation results, specialist opinions?
The diagnosis was made on ultrasound on 21 July 2009, which showed multiple mobile, shadowing calculi in the gallbladder up to 9 millimetres with sludge, in a patient presenting with typical biliary colic. The stones exceed 2 millimetres and lie in the gallbladder, meeting the Statement of Principles definition of gallstone disease. The normal gallbladder on ultrasound of 03 September 2008 confirms that the stones formed after that date.
The worsening was confirmed by MRCP and CT on 21 October 2016, showing numerous gallbladder stones, a 12 millimetre common bile duct stone and intrahepatic stones, by ERCP on 24 October 2016 with duct clearance and extraction of flukes, and by the clinical picture of cholangitis and pancreatitis with a lipase of 2,400 units per litre. A hepatobiliary surgeon recorded the worsening and performed cholecystectomy, left lateral sectionectomy and hepaticojejunostomy on 15 March 2017.
4. What do you consider to be the cause(s) of the condition in this veteran? Give consideration to constitutional and common risk factors, pre-existing injuries or diseases, and occupational or lifestyle risks, as well as direct causative mechanisms.
Legislation: the clinical onset of this condition was on 20 July 2009, after 1 July 2004, during continuous full-time service. This is a Military Rehabilitation and Compensation Act 2004 (MRCA) claim and the Statements of Principles apply. The Balance of Probabilities instrument applies to peacetime service. The Reasonable Hypothesis instrument applies to the veteran's operational service: her peacekeeping service in Cambodia in 1992 to 1993, where she acquired the liver fluke infection, and in Rwanda in 1995, where she acquired hepatitis C, and her warlike service in East Timor in 1999 to 2000, where the gastroenteritis that preceded her Crohn disease occurred, and in Afghanistan in 2011, where she sustained the spinal cord injury. In each instrument every factor applies to either the clinical onset or the clinical worsening, and the analysis below identifies which.
Each factor must be related to the person's relevant service. Under the beneficial approach required by the legislation, the absence of documentation does not mean that an event or exposure did not occur: lack of evidence is not evidence of lack.
Balance of Probabilities — Statement of Principles concerning Gallstone Disease (Cholelithiasis), No. 70 of 2025
Causative and worsening factors (each applies to clinical onset or clinical worsening)
Factor 9(1): having a spinal cord injury at the time of clinical onset or clinical worsening; — MET
- The veteran sustained an incomplete spinal cord injury with paraplegia from a T11 burst fracture in a vehicle rollover on 14 September 2011, in the course of her duties during continuous full-time service. It was present at the worsening on 20 October 2016, and paraplegia causes gallbladder hypomotility and bile stasis.
Factor 9(2): having a foreign body in the biliary tract, or a mechanical obstruction of the biliary tract, before clinical onset or clinical worsening; — MET
- A plastic biliary stent was placed across a hilar stricture at ERCP on 12 March 2016 by a gastroenterologist and was found occluded with sludge and stone debris at the worsening on 20 October 2016. The stent is a foreign body in the biliary tract and the stricture a mechanical obstruction of it, both before the worsening.
Factor 9(3): having an ileal resection or ileal bypass within the 25 years before clinical onset or clinical worsening; — MET
- The ileocaecal resection of 22 March 2001, removing 25 centimetres of terminal ileum for Crohn disease diagnosed during her service, was within the 25 years before onset on 20 July 2009 and before the worsening.
Factor 9(4): having a gastric or oesophageal resection, or another operation that includes a vagotomy, within the 5 years before clinical onset or clinical worsening; — MET
- The truncal vagotomy and antrectomy of 26 October 2011, for a perforated duodenal stress ulcer during her in-service hospitalisation for spinal cord injury, were within the 5 years before the worsening, from 20 October 2011 to 20 October 2016.
Factor 9(5): having one of the following parasitic diseases of the biliary tract at the time of clinical onset or clinical worsening: (a) ascariasis; (b) clonorchiasis; (c) fascioliasis; (d) opisthorchiasis; — MET
- Adult Opisthorchis flukes were extracted from the bile ducts at ERCP on 24 October 2016 and eggs were found in bile and stool, confirming opisthorchiasis of the biliary tract at the worsening on 20 October 2016. The infection was acquired from food eaten while she was serving overseas.
Factor 9(6): having Helicobacter pylori infection of the biliary tract at the time of clinical onset or clinical worsening; — MET
- Helicobacter pylori DNA was detected in bile at ERCP on 24 October 2016 and in gallbladder mucosa at cholecystectomy, confirming infection of the biliary tract at the worsening on 20 October 2016.
Factor 9(7): having cholangiohepatitis or recurrent pyogenic cholangitis at the time of clinical onset or clinical worsening; — MET
- Recurrent pyogenic cholangitis with intrahepatic pigment stones and left-sided ductal strictures was diagnosed by a hepatobiliary surgeon in March 2016 and was present, with acute cholangitis, at the worsening on 20 October 2016.
Factor 9(8): having an acquired haemolytic disease, characterised by red cell defects and breakdown with bilirubin overproduction, within the 1 year before clinical onset or clinical worsening; — MET
- Ceftriaxone given for cholangitis caused drug-induced immune haemolytic anaemia on 18 March 2016, with haemoglobin 68 grams per litre, a positive direct antiglobulin test and bilirubin 96 micromoles per litre. This was within the 1 year before the worsening, from 20 October 2015 to 20 October 2016.
Factor 9(9): having worsening of an inherited haemolytic disease, characterised by red cell defects and breakdown with bilirubin overproduction, within the 1 year before clinical onset or clinical worsening; — MET
- Her hereditary spherocytosis worsened on 14 January 2009 with a parvovirus-associated haemolytic crisis requiring transfusion (haemoglobin 72 grams per litre, reticulocytes 14 per cent), within the 1 year before onset, from 20 July 2008 to 20 July 2009, while she was serving full time.
Factor 9(10): having a somatostatinoma at the time of clinical onset or clinical worsening; — MET
- A 24 millimetre pancreatic somatostatinoma was shown on CT on 21 October 2016 and confirmed on endoscopic ultrasound biopsy, with a markedly raised plasma somatostatin, and was present at the worsening on 20 October 2016.
Factor 9(11): being pregnant within the 3 months before clinical onset or clinical worsening; — MET
- The veteran was pregnant until her caesarean delivery on 10 May 2009, during continuous full-time service, within the 3 months before onset, from 20 April 2009 to 20 July 2009.
Factor 9(12): for males, being obese for at least the 5 years before clinical onset or clinical worsening; — MET
- The veteran's BMI was 30 or more at every recorded health examination from 15 June 2004 to onset, so she was obese throughout the 5 years before onset, from 20 July 2004 to 20 July 2009. Factor 9(12) is expressed for males and she is female, so the same documented obesity is relied on directly under factor 9(13). The weight gain followed corticosteroid treatment of Crohn disease diagnosed during service.
Factor 9(13): for females, being overweight or obese for at least the 5 years before clinical onset or clinical worsening; — MET
- With a BMI of 30 or more at every health examination from 15 June 2004, the veteran was overweight or obese throughout the 5 years before onset, from 20 July 2004 to 20 July 2009. The weight gain followed corticosteroid courses for Crohn disease diagnosed during her service.
Factor 9(14): having rapid and extreme weight loss, involving a reduction of body mass by at least 15 percent: (a) within a continuous 6 month period; or (b) at an average rate of at least 1.5 kilograms per week, and within the 1 year before clinical onset or clinical worsening; — MET
- Under a supervised very low-calorie diet her weight fell from 111 to 86 kilograms between 20 October 2015 and 20 April 2016, a 22.5 per cent loss within a continuous 6 month period, within the 1 year before the worsening, from 20 October 2015 to 20 October 2016. The diet was prescribed for obesity caused by the immobility of her service-related paraplegia.
Factor 9(15): having a very low-calorie diet, with an energy intake of less than 800 kilocalories per day, for the 1 year before clinical onset or clinical worsening; — MET
- The veteran followed a supervised diet of 600 to 750 kilocalories per day from 12 October 2015 continuously to the worsening, so it covered the whole of the 1 year before the worsening, from 20 October 2015 to 20 October 2016.
Factor 9(16): having type 2 diabetes mellitus at the time of clinical onset or clinical worsening; — MET
- Type 2 diabetes mellitus, diagnosed on 12 June 2007 with an HbA1c of 7.6 per cent, was present at onset on 20 July 2009.
Factor 9(17): having cirrhosis of the liver at the time of clinical onset or clinical worsening; — MET
- Cirrhosis was confirmed by elastography (19.8 kilopascals) and biopsy on 18 May 2015 and was present at the worsening on 20 October 2016. It resulted from hepatitis C acquired from a needle-stick injury in the course of her nursing duties, and steatotic liver disease.
Factor 9(18): having Crohn disease at the time of clinical onset or clinical worsening; — MET
- Crohn disease of the terminal ileum, diagnosed on 18 July 2000 during her service, was active at onset on 20 July 2009, having flared after childbirth with subacute obstruction requiring parenteral nutrition.
Factor 9(19): taking any of the following medications for a continuous period of at least 6 months before clinical onset or clinical worsening, and where treatment has ceased, clinical onset or clinical worsening occurred within 3 months of cessation: (a) atazanavir; (b) cyclosporine A; (c) fibrates; (d) somatostatin analogues; (e) tamoxifen; — MET
- The veteran took fenofibrate 145 milligrams daily continuously from 10 February 2014 to and beyond the worsening on 20 October 2016, a continuous period of more than 2 years, prescribed by Defence-funded and later DVA-funded doctors for hypertriglyceridaemia.
Factor 9(20): having oestrogen therapy for a continuous period of at least 6 months before clinical onset or clinical worsening, and where oestrogen therapy has ceased, clinical onset or clinical worsening occurred within 3 months of cessation; — MET
- Transdermal oestradiol 50 micrograms daily was taken continuously from 12 August 2013, after surgical menopause, to the worsening on 20 October 2016, a period of more than 3 years.
Factor 9(21): having total parenteral nutrition for a continuous period of at least 3 weeks before clinical onset or clinical worsening, and where total parenteral nutrition has ceased, clinical onset or clinical worsening occurred within 30 days of cessation; — MET
- Total parenteral nutrition was given continuously from 08 June 2009 to 06 July 2009, 28 days, for a Crohn flare with subacute obstruction, and onset on 20 July 2009 was 14 days after it ceased.
Factor 9(22): inability to undertake any physical activity greater than 3 METs for at least the 5 years before clinical onset or clinical worsening; — MET
- Since her spinal cord injury in the course of her duties on 14 September 2011 the veteran has been paraplegic and unable to undertake any activity above about 2 METs, throughout the 5 years before the worsening, from 20 October 2011 to 20 October 2016.
Factor 9(23): inability to obtain appropriate clinical management for gallstone disease (cholelithiasis) before clinical worsening; — MET
- Cholecystectomy recommended in July 2009 was deferred by Defence health providers for her Crohn flare and her deployment, and after her spinal cord injury for rehabilitation and cirrhosis, followed by a public waiting list from 2014. The disease went untreated for seven years before the worsening on 20 October 2016. Under Brew v Repatriation Commission (1999) this is an inability to obtain appropriate clinical management.
Reasonable Hypothesis — Statement of Principles concerning Gallstone Disease (Cholelithiasis), No. 69 of 2025
Causative and worsening factors (each applies to clinical onset or clinical worsening)
Factor 9(1): having a spinal cord injury at the time of clinical onset or clinical worsening; — MET
- On 14 September 2011, during warlike service in Afghanistan, the veteran's protected vehicle rolled over on a road move and she sustained a T11 burst fracture with an incomplete spinal cord injury, leaving her paraplegic and a full-time wheelchair user. The spinal cord injury was present at the clinical worsening on 20 October 2016. Spinal cord injury causes gallbladder hypomotility and bile stasis.
Factor 9(2): having a foreign body in the biliary tract, or a mechanical obstruction of the biliary tract, before clinical onset or clinical worsening; — MET
- At ERCP on 12 March 2016 a plastic biliary stent was placed across a hilar stricture caused by recurrent pyogenic cholangitis arising from opisthorchiasis acquired on peacekeeping service in Cambodia. The stent remained in place, occluded with sludge and stone debris, until the worsening on 20 October 2016. A biliary stent is a foreign body in the biliary tract, and the stricture is a mechanical obstruction of it.
Factor 9(3): having an ileal resection or ileal bypass within the 25 years before clinical onset or clinical worsening; — MET
- On 22 March 2001 the veteran had an ileocaecal resection, removing 25 centimetres of terminal ileum, for Crohn disease that followed bacterial gastroenteritis on warlike service in East Timor in December 1999. The resection was within the 25 years before onset on 20 July 2009 and before the worsening on 20 October 2016. Loss of the terminal ileum interrupts bile salt reabsorption and makes bile lithogenic.
Factor 9(4): having a gastric or oesophageal resection, or another operation that includes a vagotomy, within the 5 years before clinical onset or clinical worsening; — MET
- On 26 October 2011 the veteran had an emergency truncal vagotomy and antrectomy for a perforated stress ulcer of the duodenum that developed after her spinal cord injury on warlike service in Afghanistan. The operation was within the 5 years before the worsening, which run from 20 October 2011 to 20 October 2016. Vagotomy reduces gallbladder contraction and promotes stasis.
Factor 9(5): having one of the following parasitic diseases of the biliary tract at the time of clinical onset or clinical worsening: (a) ascariasis; (b) clonorchiasis; (c) dicrocoeliasis; (d) fascioliasis; (e) opisthorchiasis; (f) trypanosomiasis; — MET
- During peacekeeping service in Cambodia from November 1992 to June 1993 the veteran ate raw and fermented freshwater fish in villages while working with local communities, and a marked eosinophilia on her return screening was not followed up. At ERCP on 24 October 2016 adult Opisthorchis flukes were extracted from the bile ducts and eggs were found in bile and stool. Opisthorchiasis of the biliary tract was present at the worsening on 20 October 2016.
Factor 9(6): having bacterial infection of the biliary tract at the time of clinical onset or clinical worsening; — MET
- Bile cultures at ERCP on 12 March 2016 and 24 October 2016 grew Escherichia coli and Klebsiella pneumoniae, and on 20 October 2016 she was admitted with acute ascending cholangitis, fever, rigors and jaundice. Bacterial infection of the biliary tract, secondary to the fluke infestation and stricture arising from her peacekeeping service in Cambodia, was present at the worsening. Bacterial enzymes deconjugate bilirubin and form pigment stones.
Factor 9(7): having Helicobacter pylori infection of the biliary tract at the time of clinical onset or clinical worsening; — MET
- Bile aspirated at ERCP on 24 October 2016 was positive for Helicobacter pylori DNA on PCR, and the gallbladder mucosa at cholecystectomy in 2017 was positive on immunostaining. Helicobacter pylori infection of the biliary tract was present at the worsening on 20 October 2016, having colonised the biliary tree after the antrectomy and vagotomy that followed her spinal cord injury on warlike service.
Factor 9(8): having cholangiohepatitis or recurrent pyogenic cholangitis at the time of clinical onset or clinical worsening; — MET
- A hepatobiliary surgeon diagnosed recurrent pyogenic cholangitis in March 2016 after three episodes of cholangitis since 2015, with intrahepatic pigment stones and strictures of the left ductal system on cholangiography. It arose from chronic opisthorchiasis acquired on peacekeeping service in Cambodia and was present at the worsening on 20 October 2016.
Factor 9(9): having an acquired haemolytic disease, characterised by red cell defects and breakdown with bilirubin overproduction, within the 1 year before clinical onset or clinical worsening; — MET
- On 18 March 2016, during ceftriaxone treatment for cholangitis, the veteran developed drug-induced immune haemolytic anaemia: haemoglobin fell from 118 to 68 grams per litre, the direct antiglobulin test was positive, bilirubin rose to 96 micromoles per litre and haptoglobin was undetectable. This was within the 1 year before the worsening, from 20 October 2015 to 20 October 2016. The cholangitis being treated arose from her peacekeeping service in Cambodia.
Factor 9(10): having worsening of an inherited haemolytic disease, characterised by red cell defects and breakdown with bilirubin overproduction, within the 1 year before clinical onset or clinical worsening; — MET
- The veteran has hereditary spherocytosis, mild and compensated before 2009. On 14 January 2009, at 22 weeks of pregnancy, she had a haemolytic crisis with parvovirus B19 infection: haemoglobin 72 grams per litre, reticulocytes 14 per cent and bilirubin 68 micromoles per litre, requiring transfusion. This worsening of the inherited haemolytic disease was within the 1 year before onset, from 20 July 2008 to 20 July 2009, and it was contracted while she was serving.
Factor 9(11): having a somatostatinoma at the time of clinical onset or clinical worsening; — MET
- CT on 21 October 2016 showed a 24 millimetre mass in the head of the pancreas, and endoscopic ultrasound biopsy on 27 October 2016 confirmed a well-differentiated neuroendocrine tumour staining for somatostatin, with a fasting plasma somatostatin many times the upper limit of normal. The somatostatinoma was present at the worsening on 20 October 2016. Somatostatin inhibits gallbladder contraction.
Factor 9(12): being pregnant within the 6 months before clinical onset or clinical worsening; — MET
- The veteran was pregnant until 10 May 2009, when she was delivered by caesarean section while serving full time as a nursing officer. This was within the 6 months before onset, from 20 January 2009 to 20 July 2009. Pregnancy raises oestrogen and progesterone levels, which make bile lithogenic and slow gallbladder emptying.
Factor 9(13): for males, being obese for at least the 2 years before clinical onset or clinical worsening; — MET
- The veteran's BMI was 31.4 on 15 June 2004 and was recorded at 30 or more at every health examination to onset, 33.2 before pregnancy, so she was obese throughout the 2 years before onset, from 20 July 2007 to 20 July 2009. Factor 9(13) is expressed for males and she is female, so the same documented obesity is relied on directly under factor 9(14). Her weight gain followed repeated prednisolone courses for Crohn disease that began after gastroenteritis on warlike service in East Timor.
Factor 9(14): for females, being overweight or obese for at least the 2 years before clinical onset or clinical worsening; — MET
- The veteran was obese, with a BMI of 30 or more, at every recorded health examination from 15 June 2004 to onset, well above the overweight threshold, so she was overweight or obese throughout the 2 years before onset, from 20 July 2007 to 20 July 2009. The weight gain followed corticosteroid treatment of Crohn disease that arose after gastroenteritis on warlike service in East Timor.
Factor 9(15): having rapid and extreme weight loss, involving a reduction of body mass by at least 15 percent: (a) within a continuous 6 month period; or (b) at an average rate of at least 1.5 kilograms per week, and within the 2 years before clinical onset or clinical worsening; — MET
- Under a supervised very low-calorie diet the veteran's weight fell from 111 kilograms on 20 October 2015 to 86 kilograms on 20 April 2016, a loss of 22.5 per cent of body mass within a continuous 6 month period, recorded by the bariatric dietitian. This was within the 2 years before the worsening on 20 October 2016. The diet was prescribed for obesity caused by the immobility of her paraplegia from the spinal cord injury on warlike service in Afghanistan.
Factor 9(16): having a very low-calorie diet, with an energy intake of less than 800 kilocalories per day, for the 6 months before clinical onset or clinical worsening; — MET
- From 12 October 2015 the veteran followed a supervised meal-replacement diet of 600 to 750 kilocalories per day, continued to the worsening, so it covered the whole 6 months before the worsening, from 20 April 2016 to 20 October 2016. It was prescribed for obesity arising from paraplegia caused by her spinal cord injury on warlike service in Afghanistan.
Factor 9(17): having type 2 diabetes mellitus at the time of clinical onset or clinical worsening; — MET
- Type 2 diabetes mellitus was diagnosed on 12 June 2007 with an HbA1c of 7.6 per cent and fasting glucose of 9.1 millimoles per litre, and treated with metformin. It was present at onset on 20 July 2009. It developed from the obesity that followed corticosteroid treatment of Crohn disease arising from her warlike service in East Timor.
Factor 9(18): having cirrhosis of the liver at the time of clinical onset or clinical worsening; — MET
- Transient elastography on 18 May 2015 showed liver stiffness of 19.8 kilopascals and liver biopsy confirmed cirrhosis, caused by chronic hepatitis C acquired on peacekeeping service in Rwanda together with steatotic liver disease. The cirrhosis was present at the worsening on 20 October 2016, with splenomegaly and thrombocytopenia.
Factor 9(19): having metabolic dysfunction-associated steatotic liver disease at the time of clinical onset or clinical worsening; — MET
- Ultrasound on 03 September 2008 showed diffuse hepatic steatosis with normal gallbladder and ducts, and a hepatologist diagnosed metabolic dysfunction-associated steatotic liver disease in the setting of obesity and type 2 diabetes. It was present at onset on 20 July 2009. The underlying obesity and diabetes followed corticosteroid treatment of Crohn disease arising from warlike service in East Timor.
Factor 9(20): having hepatitis C virus infection at the time of clinical onset or clinical worsening; — MET
- On 14 May 1995, during peacekeeping service in Rwanda, the veteran sustained a needle-stick injury while cannulating a casualty in a field hospital. Hepatitis C antibody and RNA became positive in September 1995 (genotype 1a), interferon treatment in 2003 failed, and RNA remained positive until direct-acting antiviral treatment in 2017. Hepatitis C infection was present at onset on 20 July 2009.
Factor 9(21): having Crohn disease or ulcerative colitis at the time of clinical onset or clinical worsening; — MET
- Crohn disease of the terminal ileum was diagnosed on 18 July 2000 after bacterial gastroenteritis on warlike service in East Timor in December 1999. It flared after childbirth in June 2009, with subacute small bowel obstruction requiring parenteral nutrition, and was active at onset on 20 July 2009.
Factor 9(22): taking any of the following medications for a continuous period of at least 3 months before clinical onset or clinical worsening, and where treatment has ceased, clinical onset or clinical worsening occurred within 3 months of cessation: (a) atazanavir; (b) cyclosporine A; (c) fibrates; (d) somatostatin analogues; (e) tamoxifen; — MET
- The veteran took fenofibrate 145 milligrams daily from 10 February 2014 for severe hypertriglyceridaemia (triglycerides 9.8 millimoles per litre) related to her diabetes, continuously to and beyond the worsening on 20 October 2016, a period of more than 2 years. Fibrates increase cholesterol secretion into bile.
Factor 9(23): having oestrogen therapy for a continuous period of at least 3 months before clinical onset or clinical worsening, and where oestrogen therapy has ceased, clinical onset or clinical worsening occurred within 6 months of cessation; — MET
- After a total hysterectomy and bilateral salpingo-oophorectomy on 05 August 2013 for a large benign ovarian mass, the veteran was prescribed transdermal oestradiol 50 micrograms daily from 12 August 2013, continued without interruption to the worsening on 20 October 2016, more than 3 years. Oestrogen increases biliary cholesterol saturation.
Factor 9(24): having total parenteral nutrition for a continuous period of at least 3 weeks before clinical onset or clinical worsening, and where total parenteral nutrition has ceased, clinical onset or clinical worsening occurred within 30 days of cessation; — MET
- After the caesarean delivery the veteran's Crohn disease flared with subacute small bowel obstruction, and she received total parenteral nutrition through a central line from 08 June 2009 to 06 July 2009, a continuous period of 28 days. Onset on 20 July 2009 was 14 days after it ceased, within the 30 days the factor allows. Parenteral nutrition removes the stimulus for gallbladder contraction and causes sludge and stones. The Crohn disease arose from her warlike service in East Timor.
Factor 9(25): inability to undertake any physical activity greater than 3 METs for at least the 5 years before clinical onset or clinical worsening; — MET
- Since her spinal cord injury on warlike service in Afghanistan on 14 September 2011 the veteran has been paraplegic and unable to stand or walk, and her rehabilitation physician recorded that she cannot undertake any activity above about 2 METs. This inability covered the whole 5 years before the worsening, from 20 October 2011 to 20 October 2016.
Factor 9(26): inability to obtain appropriate clinical management for gallstone disease (cholelithiasis) before clinical worsening; — MET
- Cholecystectomy was recommended after onset in July 2009 but was deferred because of her Crohn flare and then her deployment to Afghanistan, where she had three attacks of biliary colic between June and August 2011 that could only be managed with analgesia. After her spinal cord injury the operation was deferred again during rehabilitation and for cirrhosis, and she remained on a public waiting list from 2014. The gallstone disease therefore went untreated for seven years before the worsening on 20 October 2016. Under Brew v Repatriation Commission (1999) this is an inability to obtain appropriate clinical management.
The % contribution of the causes is 100% and significant.
Sequelae
The gallstone disease is a sequela of the veteran's accepted conditions: the Crohn disease and ileal resection that followed gastroenteritis in East Timor, the obesity and type 2 diabetes that followed its corticosteroid treatment, chronic hepatitis C and cirrhosis from the needle-stick injury in Rwanda, opisthorchiasis and recurrent pyogenic cholangitis from Cambodia, and the spinal cord injury and vagotomy from Afghanistan. It has in turn caused cholangitis, gallstone pancreatitis and the need for liver resection and biliary bypass.
Unintended Consequence
Met. The total parenteral nutrition of June and July 2009, the vagotomy and antrectomy of October 2011, the ceftriaxone that caused immune haemolysis in March 2016, the biliary stent, the fenofibrate and the oestradiol were each treatments provided and paid for by the Commonwealth (section 6A of the DRCA and the equivalent provisions of the MRCA), and each contributed to the formation of stones or to the worsening.
Inability to Attain Appropriate Medical Management
MET. Cholecystectomy was recommended in July 2009 but was deferred for her Crohn flare, could not be obtained during her deployment to Afghanistan, where three attacks of biliary colic were managed only with analgesia, and was deferred again after her spinal cord injury for rehabilitation and cirrhosis, after which she waited on a public list from 2014. Her known gallstone disease therefore went untreated for more than seven years and progressed to stones throughout the biliary tree with cholangitis and pancreatitis. Applying the objective and subjective tests in Brew v Repatriation Commission (Full Federal Court, 10 September 1999, Merkel J), this amounted to an inability to obtain appropriate clinical management.
5. Please provide a Health Summary and a medication / prescribing history.
See attached report.
References
- 14 May 1995, Field hospital incident record, Rwanda, and hepatitis serology September 1995, Pathologist
- 22 Mar 2001, Operation report and histology, Colorectal surgeon and Pathologist
- 12 Jun 2007, Outpatient health record, Medical Officer, Garrison health centre
- 03 Sep 2008, Ultrasound abdomen report and hepatology consultation, Radiologist and Hepatologist
- 14 Jan 2009, Obstetric and haematology admission record, Obstetrician and Haematologist
- 08 Jun 2009, Gastroenterology admission and parenteral nutrition record, Gastroenterologist
- 21 Jul 2009, Emergency department record and ultrasound abdomen report, Emergency physician and Radiologist
- 14 Sep 2011, Aeromedical evacuation and spinal injury unit records, Spinal surgeon
- 26 Oct 2011, Operation report, General surgeon
- 18 May 2015, Transient elastography and liver biopsy report, Hepatologist and Pathologist
- 12 Mar 2016, ERCP report, bile culture and haematology record, Gastroenterologist and Haematologist
- 20 Oct 2016, Hospital admission record, MRCP and CT abdomen reports, General physician and Radiologist
- 24 Oct 2016, ERCP report and bile PCR, Gastroenterologist and Microbiologist
- 27 Oct 2016, Endoscopic ultrasound biopsy report, Gastroenterologist and Pathologist
- 15 Mar 2017, Operation report, Hepatobiliary surgeon
- Statement of Principles concerning Gallstone Disease (Cholelithiasis) (Balance of Probabilities) No. 70 of 2025, Repatriation Medical Authority
- Statement of Principles concerning Gallstone Disease (Cholelithiasis) (Reasonable Hypothesis) No. 69 of 2025, Repatriation Medical Authority
