Diagnostic Assessment — Hypoparathyroidism
Example 1 of 1 · fictitious patient (Veteran CD)
Diagnostic Assessment
Hypoparathyroidism
No Statement of Principles applies to this condition (non-SOP claim).
ADF History
Veteran CD, date of birth 08 September 1980, Australian Army, Infantry Soldier (Rifleman, Corporal), enlisted 20 January 1999, medically discharged 11 October 2019. Operational service: Iraq, 05 June 2006 to 10 December 2006 (warlike); Afghanistan, 01 February 2013 to 15 August 2013 (warlike).
Occupational History
As an infantry soldier the veteran conducted foot and vehicle patrols in protected vehicles, with a high risk of blast and fragment injury to the head and neck, haemorrhage and the large-volume blood transfusion used to treat it. Deployed soldiers are exposed to contaminated food and water, with frequent gastrointestinal infections such as giardiasis.
Infantry soldiers commonly take anti-inflammatory medication for musculoskeletal injuries, with gastric protection, and the service culture of the period normalised heavy alcohol use after operational deployments, particularly in those with deployment-related posttraumatic stress.
History
Veteran CD, an infantry soldier in the Australian Army, sustained a penetrating fragment injury to the left neck requiring surgical exploration and massive transfusion in Iraq in 2006, and later had radioactive iodine for Graves' disease and a total thyroidectomy for thyroid cancer. He developed hypoparathyroidism in June 2014, with hypomagnesaemia from proton pump inhibitor use, alcohol and post-giardial diarrhoea, which worsened after a neck dissection in March 2017.
Timeline
- 23 Oct 2006 — On warlike service in Iraq an improvised explosive device detonated beside the veteran's vehicle and a fragment penetrated the left side of his neck. He had a large haematoma and haemorrhagic shock. At the role 3 hospital the neck was surgically explored and the inferior thyroid artery ligated, with tissue around the lower pole of the left thyroid lobe debrided. He received 28 units of red cells and blood products. "penetrating neck injury, 28 units transfused"
- 03 Aug 2009 — An endocrinologist had diagnosed Graves' disease on 14 May 2009, with suppressed TSH, raised free T4 and positive TSH receptor antibodies. Radioactive iodine (I-131, 555 MBq) was given on 03 August 2009 and he became hypothyroid, starting thyroxine. In February 2010 pantoprazole 40 mg daily was started for reflux and anti-inflammatory gastropathy from his service injuries, and it continued without interruption. "Graves' disease, I-131 555 MBq"
- 15 Mar 2011 — A 1.8 cm thyroid nodule was found to be papillary thyroid carcinoma and a surgeon performed a total thyroidectomy. Dense scarring from the 2006 neck exploration was recorded, and one devascularised parathyroid gland was autotransplanted into the sternocleidomastoid. Transient post-operative hypocalcaemia settled within a week. At six weeks the PTH was 3.1 pmol/L and calcium was normal. "total thyroidectomy, parathyroid autotransplanted"
- 22 Apr 2013 — On warlike service in Afghanistan the veteran developed watery diarrhoea and Giardia lamblia was found on stool testing. Despite treatment he had persistent loose stools four to five times a day from then on, recorded as post-infectious diarrhoea. His alcohol intake was recorded at about 70 grams a day, having been at that level since 2007 after his Iraq deployment. "giardiasis, persistent diarrhoea, alcohol 70g"
- 14 Nov 2013 — Routine blood tests showed corrected calcium 2.31 mmol/L, PTH 2.4 pmol/L and magnesium 0.71 mmol/L, all within normal limits. Serum ferritin was 2,400 micrograms/L with transferrin saturation of 62 per cent, and MRI showed moderate hepatic iron overload. A haematologist attributed this to the massive transfusion of 2006, alcohol and HFE C282Y heterozygosity. "calcium normal, ferritin 2,400"
- 05 Jun 2014 — The veteran presented to the garrison health centre with three days of tingling around the mouth and in the fingers and painful cramps in the hands and calves. Chvostek's sign was positive. Corrected calcium was 1.82 mmol/L, phosphate 1.78 mmol/L, PTH 0.8 pmol/L and magnesium 0.42 mmol/L. He was admitted for intravenous calcium and magnesium. "perioral tingling, calcium 1.82, PTH low"
- 18 Jun 2014 — After magnesium had been corrected to 0.82 mmol/L, PTH remained inappropriately low at 0.9 pmol/L with corrected calcium 1.94 mmol/L. An endocrinologist diagnosed permanent hypoparathyroidism, attributed to the 2006 neck injury and 2011 thyroidectomy with contributions from hypomagnesaemia, iron overload and autoimmunity; calcium-sensing receptor antibodies were positive. Calcitriol and calcium carbonate were commenced. "permanent hypoparathyroidism, calcitriol commenced"
- 20 Mar 2017 — Eleven days after a left lateral neck dissection for recurrent thyroid cancer nodes on 09 March 2017, the veteran presented with carpopedal spasm. Corrected calcium was 1.68 mmol/L and magnesium 0.48 mmol/L. During a posting to a remote northern base from April 2016 he had had no endocrinology review or calcium and magnesium monitoring for nine months. His calcitriol requirement doubled to 1 microgram daily and the endocrinologist recorded worsening hypoparathyroidism. "carpopedal spasm, calcium 1.68"
Symptoms
At onset the veteran had tingling around the mouth and in the fingers and toes, painful muscle cramps and spasms of the hands and calves, fatigue and irritability. Chvostek's sign was positive.
After onset he had recurrent paraesthesiae and cramps whenever calcium fell, and at the worsening in March 2017 he developed carpopedal spasm. He now reports daily fatigue, intermittent paraesthesiae and cramps, poor concentration and memory, and dependence on calcitriol, calcium and magnesium supplements with frequent blood tests; CT in 2018 showed basal ganglia calcification.
Imaging
- 23 Oct 2006 — CT angiogram neck: "Metallic fragment in the left lower neck adjacent to the inferior pole of the left thyroid lobe, with surrounding haematoma. No carotid injury."
- 15 Feb 2011 — Ultrasound thyroid: "1.8 cm hypoechoic nodule in the right lobe with microcalcifications. Scarring adjacent to the left lower pole."
- 14 Nov 2013 — MRI liver iron quantification: "Moderate hepatic iron overload, liver iron concentration 9.8 mg/g dry weight."
- 12 Sep 2018 — CT brain: "Bilateral symmetrical basal ganglia calcification."
Onset Date
The most likely date of onset of this condition is 02 Jun 2014.
At that date the veteran was a serving Army corporal with an infantry battalion in Australia. He had been taking pantoprazole daily for four years, was drinking about 70 grams of alcohol a day and had had persistent diarrhoea since his giardiasis in Afghanistan. From that day he had perioral and digital tingling and cramps.
This date is appropriate because blood tests on 14 November 2013 showed normal calcium, PTH and magnesium, and he presented on 05 June 2014 with three days of symptoms and confirmed hypocalcaemia with low PTH. The endocrinologist confirmed on 18 June 2014 that the hypoparathyroidism persisted after magnesium correction. The date falls within continuous full-time service.
For the neck surgery, neck trauma and radiation causes, the neck exploration of 23 October 2006, the radioactive iodine of 03 August 2009 and the thyroidectomy of 15 March 2011 all occurred before onset. For the proton pump inhibitor cause, the year before onset runs from 02 Jun 2013 to 02 Jun 2014, during which he took pantoprazole daily. For alcohol, he drank about 70 grams a day throughout that year. For chronic diarrhoea, the 3 months before onset run from 02 Mar 2014 to 02 Jun 2014, during which he had loose stools four to five times a day. Hypomagnesaemia, iron overload and calcium-sensing receptor autoimmunity were present at onset.
For the worsening causes, the documented worsening was on 20 Mar 2017. The neck dissection was on 09 Mar 2017. The year before the worsening runs from 20 Mar 2016 to 20 Mar 2017, during which he took pantoprazole and drank about 60 grams of alcohol a day, and magnesium was 0.48 mmol/L at the worsening. His endocrine monitoring lapsed from April 2016 to January 2017.
1. What is the formal diagnosis of the condition claimed above?
The formal diagnosis is Hypoparathyroidism (ICD-10-AM E89.2, postprocedural hypoparathyroidism), with contributions from hypomagnesaemia, iron overload and parathyroid autoimmunity.
Hypoparathyroidism is deficient secretion or action of parathyroid hormone, producing low serum calcium, raised phosphate and an inappropriately low or undetectable PTH. Low calcium causes neuromuscular irritability with perioral and digital paraesthesiae, muscle cramps, carpopedal spasm, laryngospasm and seizures, as well as fatigue, cognitive symptoms, cataract and basal ganglia calcification. The commonest cause is damage to or removal of the parathyroid glands during neck surgery; other causes include neck trauma, radiation, autoimmune destruction or calcium-sensing receptor activation, infiltration by iron, and magnesium deficiency, which impairs PTH secretion and action.
The diagnosis followed a penetrating neck injury with surgical exploration and massive transfusion in 2006, radioactive iodine in 2009 and a total thyroidectomy in 2011. It began on 02 June 2014, was confirmed by an endocrinologist on 18 June 2014 and worsened after neck dissection in March 2017.
2. For each diagnosis identified, please also provide the following dates:
When did the veteran first experience symptoms attributable to this condition?
02 June 2014.
When did the veteran first present to a health / medical provider for this condition?
05 June 2014.
When was the condition confirmed / formally diagnosed?
18 June 2014.
When did the veteran first present to you (or your practice) for this condition?
14 August 2025.
3. How was this diagnosis confirmed? i.e. what were the key symptoms and signs, investigation results, specialist opinions?
The diagnosis was confirmed by an endocrinologist on 18 June 2014. Corrected calcium was 1.82 mmol/L with raised phosphate of 1.78 mmol/L and an inappropriately low PTH of 0.8 pmol/L on 05 June 2014, and after magnesium had been corrected PTH remained low at 0.9 pmol/L with persistent hypocalcaemia, confirming true hypoparathyroidism rather than a purely functional effect of magnesium deficiency. Vitamin D, renal function and albumin were normal.
The clinical picture was consistent: perioral and digital paraesthesiae, cramps and a positive Chvostek's sign, with a history of neck trauma, neck surgery with parathyroid autotransplantation and radioactive iodine. The continuing need for calcitriol and calcium, and basal ganglia calcification on CT in 2018, confirm its permanence. The worsening was confirmed on 20 March 2017 by carpopedal spasm, corrected calcium of 1.68 mmol/L and a doubling of the calcitriol dose.
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.
No Statement of Principles has been determined by the Repatriation Medical Authority for hypoparathyroidism. The claim is therefore decided on the sound medical-scientific evidence of what causes and worsens the condition, without the limits a Statement of Principles would impose. The recognised causes below are drawn from the endocrinology literature.
Legislation: the clinical onset of this condition was on 02 June 2014, after 1 July 2004, during continuous full-time service. This is a Military Rehabilitation and Compensation Act 2004 (MRCA) claim. The veteran's warlike service in Iraq in 2006, where the neck injury and transfusion occurred, and in Afghanistan in 2013, where the giardiasis occurred, is operational service; his service in Australia, including the thyroid treatment, is peacetime service. Each cause must be related to 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.
Recognised causes on the medical-scientific evidence (no Statement of Principles)
Causative factors
Cause 1: having undergone surgery to the thyroid gland, parathyroid glands or anterior neck before the clinical onset of hypoparathyroidism; — MET
- The veteran underwent a total thyroidectomy on 15 March 2011, during which one devascularised parathyroid gland was autotransplanted, and surgical exploration of the left neck on 23 October 2006 with ligation of the inferior thyroid artery, the main blood supply of the inferior parathyroid glands. Both preceded onset on 02 June 2014. Neck surgery is the commonest cause of hypoparathyroidism, and parathyroid reserve after surgery can fail later.
Cause 2: having a penetrating injury or other significant trauma to the anterior neck before the clinical onset of hypoparathyroidism; — MET
- On warlike service in Iraq on 23 October 2006 a fragment penetrated the left lower neck beside the inferior pole of the left thyroid lobe, the usual site of the left inferior parathyroid gland, with haematoma and debridement of the surrounding tissue.
Cause 3: having received radioactive iodine therapy or external beam radiation to the neck before the clinical onset of hypoparathyroidism; — MET
- The veteran received 555 MBq of I-131 on 03 August 2009 for Graves' disease, nearly five years before onset. Radiation to the thyroid bed can damage the adjacent parathyroid glands.
Cause 4: having an autoimmune disease affecting the endocrine glands, or antibodies against the calcium-sensing receptor or parathyroid tissue, at the time of the clinical onset of hypoparathyroidism; — MET
- The veteran had Graves' disease, an autoimmune endocrine disease, from May 2009, and calcium-sensing receptor antibodies were positive in June 2014, at onset. Activating calcium-sensing receptor antibodies suppress PTH secretion and are a recognised cause of acquired hypoparathyroidism.
Cause 5: having iron overload, including iron overload following multiple blood transfusions, before the clinical onset of hypoparathyroidism; — MET
- The veteran received 28 units of blood and blood products for haemorrhagic shock on warlike service on 23 October 2006. Ferritin was 2,400 micrograms/L and MRI showed moderate hepatic iron overload on 14 November 2013, before onset. Iron deposition in the parathyroid glands is a recognised cause of hypoparathyroidism.
Cause 6: having hypomagnesaemia, with a serum magnesium below 0.5 mmol/L, at the time of the clinical onset of hypoparathyroidism; — MET
- Serum magnesium was 0.42 mmol/L on 05 June 2014, three days after onset. Severe magnesium deficiency impairs PTH secretion and causes end-organ resistance to PTH, unmasking reduced parathyroid reserve.
Cause 7: taking a proton pump inhibitor for at least the one year before the clinical onset of hypoparathyroidism; — MET
- The veteran took pantoprazole 40 mg daily continuously from February 2010, prescribed for reflux and gastropathy from anti-inflammatory treatment of his service injuries. He took it throughout the year before onset, from 02 June 2013 to 02 June 2014. Long-term proton pump inhibitor use causes hypomagnesaemia by impairing intestinal magnesium absorption.
Cause 8: consuming an average of at least 60 grams of alcohol per day for at least the one year before the clinical onset of hypoparathyroidism; — MET
- His alcohol intake was recorded at about 70 grams a day from 2007, after his warlike service in Iraq, including throughout the year before onset. Chronic heavy alcohol use causes renal magnesium wasting and directly suppresses PTH secretion.
Cause 9: having chronic diarrhoea or malabsorption for at least the 3 months before the clinical onset of hypoparathyroidism; — MET
- After giardiasis on warlike service in Afghanistan on 22 April 2013 the veteran had loose stools four to five times a day, which continued throughout the 3 months before onset, from 02 March 2014 to 02 June 2014. Chronic diarrhoea causes gastrointestinal magnesium loss.
Worsening factors
Worsening 1: having undergone further surgery to the thyroid bed, parathyroid glands or neck within the 3 months before the clinical worsening of hypoparathyroidism; — MET
- A left lateral neck dissection for recurrent thyroid cancer nodes was performed on 09 March 2017, eleven days before the documented worsening on 20 March 2017, with carpopedal spasm, corrected calcium of 1.68 mmol/L and a doubled calcitriol requirement.
Worsening 2: having hypomagnesaemia, with a serum magnesium below 0.5 mmol/L, at the time of the clinical worsening of hypoparathyroidism; — MET
- Serum magnesium was 0.48 mmol/L on 20 March 2017, at the worsening.
Worsening 3: taking a proton pump inhibitor for at least the one year before the clinical worsening of hypoparathyroidism; — MET
- Pantoprazole continued daily throughout the year before the worsening, from 20 March 2016 to 20 March 2017.
Worsening 4: consuming an average of at least 60 grams of alcohol per day for at least the one year before the clinical worsening of hypoparathyroidism; — MET
- His alcohol intake was recorded at about 60 grams a day throughout the year before the worsening.
Worsening 5: inability to obtain appropriate clinical management for hypoparathyroidism. — MET
- During his posting to a remote northern base from April 2016 to January 2017 the veteran had no access to endocrinology review and no calcium or magnesium monitoring for nine months, so his hypomagnesaemia and under-treatment were not detected before the neck dissection. 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 hypoparathyroidism is a sequela of the veteran's accepted conditions: the penetrating neck injury sustained on warlike service in Iraq in 2006 and its surgical treatment, the iron overload from the massive transfusion given for that injury, the alcohol use disorder that followed his deployment, and the post-giardial diarrhoea from Afghanistan. It has in turn caused basal ganglia calcification and recurrent symptomatic hypocalcaemia, which should be considered as sequelae.
Unintended Consequence
Met. The hypoparathyroidism is in part an unintended consequence of medical treatment provided by or paid for by the Commonwealth while the veteran was serving: the neck exploration of 2006, the radioactive iodine of 2009, the total thyroidectomy of 2011 and long-term pantoprazole (section 6A of the DRCA and the equivalent provisions of the MRCA).
Inability to Attain Appropriate Medical Management
MET. From April 2016 to January 2017 the veteran was posted to a remote northern base with no endocrinology service, and his calcium and magnesium were not monitored for nine months. His hypomagnesaemia and inadequate calcitriol dosing went undetected before the neck dissection of March 2017, after which he developed carpopedal spasm and his calcitriol requirement doubled. Applying the objective and subjective tests in Brew v Repatriation Commission (Full Federal Court, 10 September 1999, Merkel J), the absence of the specialist monitoring this condition requires, because of a service posting, amounts to an inability to obtain appropriate clinical management.
5. Please provide a Health Summary and a medication / prescribing history.
See attached report.
References
- 23 Oct 2006, Trauma admission, CT angiogram and operation report, Role 3 hospital, Iraq
- 14 May 2009, Endocrinology consultation, Endocrinologist
- 03 Aug 2009, Radioactive iodine treatment record, Nuclear medicine physician
- 12 Feb 2010, Outpatient health record, Medical Officer, Garrison health centre
- 15 Mar 2011, Operation report and histopathology, Endocrine surgeon
- 22 Apr 2013, Role 2 treatment record and stool microscopy, Medical Officer, Afghanistan
- 14 Nov 2013, Pathology results and MRI liver, Haematologist
- 05 Jun 2014, Outpatient health record and admission, Medical Officer, Garrison health centre
- 18 Jun 2014, Endocrinology consultation, Endocrinologist
- 09 Mar 2017, Operation report, Endocrine surgeon
- 20 Mar 2017, Endocrinology review, Endocrinologist
- 12 Sep 2018, CT brain, Radiologist
- Recognised causes of hypoparathyroidism, endocrinology literature (no Statement of Principles)
