Milk alkali syndrome case presentation

This is a case of a 28-year-old female with a history of restrictive anorexia

nervosa.

She initially presented to JHC Emergency Department this year following a fall with
two facial lacerations. Her blood calcium (corrected level) was found to be 2.64
mmol/L (2.20-2.55).

The patient’s family and partner reported weight loss of 11 kg over 8 months, with
decreased food intake and increasing exercise.

More recently, she had been complaining of postural symptoms on standing, which had
precipitated the fall.

She denied any other recent illnesses. Her other past medical history was
significant for being a smoker (smoking 6 cigarettes a day for 4 years), two
ovarian cysts, amenorrhea, anxiety and chronic low back pain from a motor vehicle
accident. No significant family history. Allergy to fish.

The patient has a history of anorexia with an admission to the Hollywood Clinic in
2014. At the time, she had one year of weight loss, with the development of
anorexic symptoms after a motor vehicle accident in 2013. She had been heavily
abusing alcohol, drinking half to one bottle of vodka a day, as well as ibuprofen,
codeine and laxatives. She was admitted to the eating disorders program and
commenced on calcium, phosphate and vitamin supplements as well NG feeds of Ensure
Plus as part of stage 1 of the program. Blood tests conducted at the time showed
elevated calcium (corrected) of 3.06 mmol/L (2.20-2.55), calcium (ionized) 1.67
mmol/L (1.12 – 1.30), elevated phosphate 2.1 (0.8-1.5). Her basic electrolyte
panel showed a sodium of 132 with a creatinine of 153 (creatinine two months
earlier was 51 umol/L). Physical examination was unremarkable.

What would you do next?

Her PTH level was undetectable (< 0.3 pmol/L), and her ACE was elevated at 77 U/L
(< 51). 25-OH Vit D was borderline 66 nmol/L (> 74, to rule out vitamin D
overdose). TFT were normal, TSH 0.67 (0.40-4), FT4 8.

She was given rapid IV hydration. Her ibuprofen and calcium supplementation was
ceased. Fasting metabolic bone study was conducted which showed a normal urine
calcium:cr ratio, and normal bone turnover markers, in addition to the normalizing
calcium and phosphate.

Any further investigations?

CT chest and abdomen done during that admission conducted showed pancreatic
calcifications. No evidence of granulomatous disease or skeletal lytic lesions. PTH
related peptide was undetectable (< 2.0). CA 19,9 was 19 (< 37).

It was found that she was abusing laxatives surreptitiously and began sabotaging
her treatment. She was discharged from the EDP, with follow-up arranged to her
medical specialist, which she did not attend.

The patient re-presented to hospital earlier this year. At JHC ED, she was mildly
hypotensive, assessed as clinically dry, and was given IV hydration. She spent two
weeks in Joondalup under the mental health team being trialed on oral diet with
oral ensure and multivitamins, before being transferred to the Hollywood Clinic,
re-admitted under the EDP. On examination at Hollywood, she was a thin cachectic
woman with a BP of 110/70, HR 80 bpm, afebrile. Her JVP was not elevated. She had
normal skin turgor, and her oral mucosa was well hydrated. Her cardiac, respiratory
was unremarkable. On abdominal exam, she had minimal tenderness in bilateral flanks
but no renal angle tenderness.

She had been recommenced on CaCO3 (1.2 g daily), Multivitamins (2 tablets daily,
each containing 200 mg calcium carbonate, 20 mg phosphorus), quetiapine 600 mg,
mirtazapine 30 mg, temazepam 10 mg, lorazepam 1 mg pre-meals, movicol 1 sachet BD,
disulfuram 200 mg mane. She was recommenced on stage 1 of the EDP and given three
daily Ensure Plus supplements via NG.

ECG conducted showed a QTc of 460 msec, and was in sinus rhythm.

Her blood tests on admission was a similar profile to her admission in 2014. Her
calcium (corrected) was elevated 2.93, she had acute kidney injury creatinine of
145, elevated phosphate 1.6. TFTs showed an elevated TSH with low FT4. She had a
detectable PTH 0.5 pmol/L (1.5-8.0).

Her calcium and multivitamins were discontinued. She was given IV 0.9% saline, and
by day 3 her calcium had started to improve although her renal function worsened.
Repeat rapid IV hydration resulted in her calcium normalizing and by Day 4 of
admission her creatinine was 77 and calcium 2.24.

Vitamin A levels were performed which were mildly elevated 3.2 (1.6 – 2.3) although
unlikely to be causing any toxicity. Repeat metabolic bone study conducted showed
normal ionized calcium and PTH levels. Vitamin D levels were normal.

However, despite being on the EDP, the patient’s weight remained persistently low
resulting in uptitration of her supplements, with 4 feeds of Ensure Plus with three
feeds of resource 2.0 fibre a day.

To summarize the salient features of this case, we have an anorexic woman with
repeat episodes of hypercalcemia, hyperphosphatemia, and acute kidney injury
rapidly corrected with iv hydration, cessation of calcium supplementation, and
laxative abuse. She had normal PTH, non-toxic vitamin levels, mildly elevated ACE
with no signs of granulomatous disease on CT. No signs of increased bone turnover.

If we look at the content of Ensure and Resource drinks, we can see they actually
contain quite a lot of calcium and phosphorus. When her weight was dropping, her
supplementation would be increased to 3 ensures and 2 resource drinks a day.

At these times she was actually prescribed regular movicol and she was
surreptitiously abusing laxatives – the nurses were raiding her room and finding
laxatives.

So this history leads us to the primary diagnosis of milk-alkali syndrome as the

cause

Milk alkali syndrome case presentation

This is a case of a 28-year-old female with a history of restrictive anorexia

nervosa.

She initially presented to JHC Emergency Department this year following a fall with
two facial lacerations. Her blood calcium (corrected level) was found to be 2.64
mmol/L (2.20-2.55).

The patient’s family and partner reported weight loss of 11 kg over 8 months, with
decreased food intake and increasing exercise.

More recently, she had been complaining of postural symptoms on standing, which had
precipitated the fall.

She denied any other recent illnesses. Her other past medical history was
significant for being a smoker (smoking 6 cigarettes a day for 4 years), two
ovarian cysts, amenorrhea, anxiety and chronic low back pain from a motor vehicle
accident. No significant family history. Allergy to fish.

The patient has a history of anorexia with an admission to the Hollywood Clinic in
2014. At the time, she had one year of weight loss, with the development of
anorexic symptoms after a motor vehicle accident in 2013. She had been heavily
abusing alcohol, drinking half to one bottle of vodka a day, as well as ibuprofen,
codeine and laxatives. She was admitted to the eating disorders program and
commenced on calcium, phosphate and vitamin supplements as well NG feeds of Ensure
Plus as part of stage 1 of the program. Blood tests conducted at the time showed
elevated calcium (corrected) of 3.06 mmol/L (2.20-2.55), calcium (ionized) 1.67
mmol/L (1.12 – 1.30), elevated phosphate 2.1 (0.8-1.5). Her basic electrolyte
panel showed a sodium of 132 with a creatinine of 153 (creatinine two months
earlier was 51 umol/L). Physical examination was unremarkable.

What would you do next?

Her PTH level was undetectable (< 0.3 pmol/L), and her ACE was elevated at 77 U/L
(< 51). 25-OH Vit D was borderline 66 nmol/L (> 74, to rule out vitamin D
overdose). TFT were normal, TSH 0.67 (0.40-4), FT4 8.

She was given rapid IV hydration. Her ibuprofen and calcium supplementation was
ceased. Fasting metabolic bone study was conducted which showed a normal urine
calcium:cr ratio, and normal bone turnover markers, in addition to the normalizing
calcium and phosphate.

Any further investigations?

CT chest and abdomen done during that admission conducted showed pancreatic
calcifications. No evidence of granulomatous disease or skeletal lytic lesions. PTH
related peptide was undetectable (< 2.0). CA 19,9 was 19 (< 37).

It was found that she was abusing laxatives surreptitiously and began sabotaging
her treatment. She was discharged from the EDP, with follow-up arranged to her
medical specialist, which she did not attend.

The patient re-presented to hospital earlier this year. At JHC ED, she was mildly
hypotensive, assessed as clinically dry, and was given IV hydration. She spent two
weeks in Joondalup under the mental health team being trialed on oral diet with
oral ensure and multivitamins, before being transferred to the Hollywood Clinic,
re-admitted under the EDP. On examination at Hollywood, she was a thin cachectic
woman with a BP of 110/70, HR 80 bpm, afebrile. Her JVP was not elevated. She had
normal skin turgor, and her oral mucosa was well hydrated. Her cardiac, respiratory
was unremarkable. On abdominal exam, she had minimal tenderness in bilateral flanks
but no renal angle tenderness.

She had been recommenced on CaCO3 (1.2 g daily), Multivitamins (2 tablets daily,
each containing 200 mg calcium carbonate, 20 mg phosphorus), quetiapine 600 mg,
mirtazapine 30 mg, temazepam 10 mg, lorazepam 1 mg pre-meals, movicol 1 sachet BD,
disulfuram 200 mg mane. She was recommenced on stage 1 of the EDP and given three
daily Ensure Plus supplements via NG.

ECG conducted showed a QTc of 460 msec, and was in sinus rhythm.

Her blood tests on admission was a similar profile to her admission in 2014. Her
calcium (corrected) was elevated 2.93, she had acute kidney injury creatinine of
145, elevated phosphate 1.6. TFTs showed an elevated TSH with low FT4. She had a
detectable PTH 0.5 pmol/L (1.5-8.0).

Her calcium and multivitamins were discontinued. She was given IV 0.9% saline, and
by day 3 her calcium had started to improve although her renal function worsened.
Repeat rapid IV hydration resulted in her calcium normalizing and by Day 4 of
admission her creatinine was 77 and calcium 2.24.

Vitamin A levels were performed which were mildly elevated 3.2 (1.6 – 2.3) although
unlikely to be causing any toxicity. Repeat metabolic bone study conducted showed
normal ionized calcium and PTH levels. Vitamin D levels were normal.

However, despite being on the EDP, the patient’s weight remained persistently low
resulting in uptitration of her supplements, with 4 feeds of Ensure Plus with three
feeds of resource 2.0 fibre a day.

To summarize the salient features of this case, we have an anorexic woman with
repeat episodes of hypercalcemia, hyperphosphatemia, and acute kidney injury
rapidly corrected with iv hydration, cessation of calcium supplementation, and
laxative abuse. She had normal PTH, non-toxic vitamin levels, mildly elevated ACE
with no signs of granulomatous disease on CT. No signs of increased bone turnover.

If we look at the content of Ensure and Resource drinks, we can see they actually
contain quite a lot of calcium and phosphorus. When her weight was dropping, her
supplementation would be increased to 3 ensures and 2 resource drinks a day.

At these times she was actually prescribed regular movicol and she was
surreptitiously abusing laxatives – the nurses were raiding her room and finding
laxatives.

So this history leads us to the primary diagnosis of milk-alkali syndrome as the

cause

Milk alkali syndrome case presentation

This is a case of a 28-year-old female with a history of restrictive anorexia

nervosa.

She initially presented to JHC Emergency Department this year following a fall with
two facial lacerations. Her blood calcium (corrected level) was found to be 2.64
mmol/L (2.20-2.55).

The patient’s family and partner reported weight loss of 11 kg over 8 months, with
decreased food intake and increasing exercise.

More recently, she had been complaining of postural symptoms on standing, which had
precipitated the fall.
She denied any other recent illnesses. Her other past medical history was
significant for being a smoker (smoking 6 cigarettes a day for 4 years), two
ovarian cysts, amenorrhea, anxiety and chronic low back pain from a motor vehicle
accident. No significant family history. Allergy to fish.

The patient has a history of anorexia with an admission to the Hollywood Clinic in
2014. At the time, she had one year of weight loss, with the development of
anorexic symptoms after a motor vehicle accident in 2013. She had been heavily
abusing alcohol, drinking half to one bottle of vodka a day, as well as ibuprofen,
codeine and laxatives. She was admitted to the eating disorders program and
commenced on calcium, phosphate and vitamin supplements as well NG feeds of Ensure
Plus as part of stage 1 of the program. Blood tests conducted at the time showed
elevated calcium (corrected) of 3.06 mmol/L (2.20-2.55), calcium (ionized) 1.67
mmol/L (1.12 – 1.30), elevated phosphate 2.1 (0.8-1.5). Her basic electrolyte
panel showed a sodium of 132 with a creatinine of 153 (creatinine two months
earlier was 51 umol/L). Physical examination was unremarkable.

What would you do next?

Her PTH level was undetectable (< 0.3 pmol/L), and her ACE was elevated at 77 U/L
(< 51). 25-OH Vit D was borderline 66 nmol/L (> 74, to rule out vitamin D
overdose). TFT were normal, TSH 0.67 (0.40-4), FT4 8.

She was given rapid IV hydration. Her ibuprofen and calcium supplementation was
ceased. Fasting metabolic bone study was conducted which showed a normal urine
calcium:cr ratio, and normal bone turnover markers, in addition to the normalizing
calcium and phosphate.

Any further investigations?

CT chest and abdomen done during that admission conducted showed pancreatic
calcifications. No evidence of granulomatous disease or skeletal lytic lesions. PTH
related peptide was undetectable (< 2.0). CA 19,9 was 19 (< 37).

It was found that she was abusing laxatives surreptitiously and began sabotaging
her treatment. She was discharged from the EDP, with follow-up arranged to her
medical specialist, which she did not attend.

The patient re-presented to hospital earlier this year. At JHC ED, she was mildly
hypotensive, assessed as clinically dry, and was given IV hydration. She spent two
weeks in Joondalup under the mental health team being trialed on oral diet with
oral ensure and multivitamins, before being transferred to the Hollywood Clinic,
re-admitted under the EDP. On examination at Hollywood, she was a thin cachectic
woman with a BP of 110/70, HR 80 bpm, afebrile. Her JVP was not elevated. She had
normal skin turgor, and her oral mucosa was well hydrated. Her cardiac, respiratory
was unremarkable. On abdominal exam, she had minimal tenderness in bilateral flanks
but no renal angle tenderness.

She had been recommenced on CaCO3 (1.2 g daily), Multivitamins (2 tablets daily,
each containing 200 mg calcium carbonate, 20 mg phosphorus), quetiapine 600 mg,
mirtazapine 30 mg, temazepam 10 mg, lorazepam 1 mg pre-meals, movicol 1 sachet BD,
disulfuram 200 mg mane. She was recommenced on stage 1 of the EDP and given three
daily Ensure Plus supplements via NG.

ECG conducted showed a QTc of 460 msec, and was in sinus rhythm.

Her blood tests on admission was a similar profile to her admission in 2014. Her
calcium (corrected) was elevated 2.93, she had acute kidney injury creatinine of
145, elevated phosphate 1.6. TFTs showed an elevated TSH with low FT4. She had a
detectable PTH 0.5 pmol/L (1.5-8.0).

Her calcium and multivitamins were discontinued. She was given IV 0.9% saline, and
by day 3 her calcium had started to improve although her renal function worsened.
Repeat rapid IV hydration resulted in her calcium normalizing and by Day 4 of
admission her creatinine was 77 and calcium 2.24.

Vitamin A levels were performed which were mildly elevated 3.2 (1.6 – 2.3) although
unlikely to be causing any toxicity. Repeat metabolic bone study conducted showed
normal ionized calcium and PTH levels. Vitamin D levels were normal.

However, despite being on the EDP, the patient’s weight remained persistently low
resulting in uptitration of her supplements, with 4 feeds of Ensure Plus with three
feeds of resource 2.0 fibre a day.

To summarize the salient features of this case, we have an anorexic woman with
repeat episodes of hypercalcemia, hyperphosphatemia, and acute kidney injury
rapidly corrected with iv hydration, cessation of calcium supplementation, and
laxative abuse. She had normal PTH, non-toxic vitamin levels, mildly elevated ACE
with no signs of granulomatous disease on CT. No signs of increased bone turnover.

If we look at the content of Ensure and Resource drinks, we can see they actually
contain quite a lot of calcium and phosphorus. When her weight was dropping, her
supplementation would be increased to 3 ensures and 2 resource drinks a day.

At these times she was actually prescribed regular movicol and she was
surreptitiously abusing laxatives – the nurses were raiding her room and finding
laxatives.

So this history leads us to the primary diagnosis of milk-alkali syndrome as the

cause