scholarly journals Iatrogenic Hypocalcemia With Treatment of Milk-Alkali Syndrome

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A202-A202
Author(s):  
Sharan D Parikh ◽  
Geetha K Bhat

Abstract Hypercalcemia is common disorder with the most likely etiology being primary hyperparathyroidism in the outpatient setting and malignancy in the hospitalized. With emergence of proton pump inhibitors and histamine blockers, milk-alkali syndrome has become a rarity. We report a unique case of hypercalcemia secondary to milk-alkali syndrome overtreated with bisphosphate therapy resulting in hypocalcemia. A 77-year-old woman with a past medical history of hypertension, gastroesophageal reflux disease presented with slurring of speech for 2 days with nausea and vomiting. Labs showed a calcium of 15.4 mg/dL, with an albumin of 4.0 g/dL. Other pertinent labs showed an ionized calcium of greater than 7.3 mg/dL, pH of 7.49, PTH of 15 pg/mL, PTHrP of 9 pg/mL, vitamin D 25-OH of 16 ng/mL, TSH of 2.16 IU/mL and acute kidney injury. Patient was started on intravenous fluids and given both calcitonin and pamidronate on presentation by the admitting team. When seen in consultation, history revealed that patient was consuming more than eight calcium carbonate antacid tablets daily and was also on hydrochlorothiazide. The calcium level decreased to 8.7 mg/dL within 48 hours. There was a concern for potential hypocalcemia due to pamidronate. Patient was advised to restart calcium carbonate 500 mg twice daily upon discharge with close follow up. However, supplementation was not started and repeat calcium was 6.7 mg/dL twelve days later. The calcium normalized within a week after starting temporary calcium supplementation. A now rare cause of hypercalcemia, milk-alkali syndrome is often overlooked in the differential diagnosis resulting in overtreatment and potentially dangerous hypocalcemia. Emergent management of intravenous hydration and bisphosphonate therapy is often immediately given by clinicians. Bisphosphonate therapy is not immediately effective and demonstrates calcium lowering effects by the second to fourth day. However, patients with milk-alkali syndrome generally improve with intravenous hydration and cessation of the causative agent. This case demonstrates the importance of obtaining a proper history with a complete list of medications and over the counter supplementations prior to treatment.

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A953-A953
Author(s):  
Rishi Raj ◽  
Ayesha Ghayur ◽  
Qurrat Elahi ◽  
Chinmaya Patel

Abstract Background: Noncompliance to levothyroxine (LT4) is common however only rarely it leads to severe side effects. We report a case of rhabdomyolysis leading to acute kidney injury (AKI) requiring hemodialysis (HD) due to noncompliance to LT4 therapy for one month. Clinical Case: A 68-year-old Caucasian male presented with a 2-week history of worsening fatigue and generalized weakness, accompanied by pain in bilateral lower extremities. Medical history included coronary artery disease, heart failure with reduced ejection fraction, hypertension, dyslipidemia, hypothyroidism, type 2 diabetes mellitus, CKD. Home medications included LT4 200 mcg daily, metoprolol 25 mg daily, doxazosin 2 mg daily, amlodipine 5 mg daily, fluocinonide 40 mg daily, fosinopril 40 mg twice daily, metformin 500 mg twice daily and rosuvastatin 40 mg daily. Further history revealed the patient to be not taking LT4 as “he ran out of it for a month” and only resumed taking it 3 to 4 days before coming to the hospital. On examination, he had proximal muscle weakness with power 3/5 in bilateral lower extremities and mild tenderness on thigh muscles. Labs revealed creatinine 13.1 mg/dL (0.60-1.10 mg/dL), BUN 101 mg/dL (0-30 ng/dL), eGFR 4.0 ml/min/1.73m2, CK 69,500 U/L (22-198 U/L), TSH 55.8 uIU/ml (0.45-4.5 uIU/ml), and FT4 0.61 ug/dL (0.8-1.8 ug/dL). ABG showed metabolic acidosis. Routine labs three months prior revealed normal thyroid function tests (TSH 1.6 uIU/ml and FT4 1.3 ug/dL) on LT4 200 mcg and baseline CKD stage 3b (EGFR 51 ml/min/1.73m2 with baseline creatinine 1.4 mg/dL). The patient was diagnosed with severe rhabdomyolysis secondary to noncompliance with LT4 therapy in presence of concurrent statin use, leading to AKI. Rosuvastatin was stopped and he was treated with aggressive intravenous hydration, sodium bicarbonate, and LT4 200 mcg daily. Despite two days of aggressive treatment, CK remains elevated and hence HD was initiated. The patient underwent three sessions of HD during the course of his hospitalization. Due to lack of renal recovery, outpatient HD was arranged. At 4 weeks of outpatient follow-up, the patient was oliguric and HD dependent. At 8 weeks outpatient follow up, CK, TSH, and FT4 was normal on LT4 200 mcg daily and became dialysis independent. Conclusion: Noncompliance to LT4 therapy along with concomitant use of statin can result in severe rhabdomyolysis induced AKI in patients with CKD.


2019 ◽  
Vol 48 (4) ◽  
pp. 030006051988810 ◽  
Author(s):  
Shang-Feng Tsai ◽  
Jun-Li Tsai ◽  
Cheng-Hsu Chen

Rhabdomyolysis is diagnosed based on the levels of blood biomarkers such as creatine kinase (CK), but the use of CK levels to predict long-term renal function remains controversial. This current report presents a case with a very high CK level with the presentation of acute kidney injury (AKI) who regained full renal function. A 29-year-old man, in a manic mood and presenting with dyspnoea, was admitted to hospital following an episode of ketamine use along with a history of drug abuse. The laboratory analyses identified rhabdomyolysis (CK, 35 266 U/l) and AKI (serum creatinine, 3.96 mg/dl). Despite treatment with intravenous normal saline (4000 ml/day), his CK level reached at least 300 000 U/l. He underwent 13 sessions of haemodialysis and his renal function fully recovered. The final measurements were serum creatinine 1.0 mg/dl and CK 212 U/l. These findings support the view that the predictive power of CK level on AKI is limited, especially regarding long-term renal function. Close follow-up examinations of renal function after haemodialysis are mandatory for patients with rhabdomyolysis.


2021 ◽  
pp. 772-778
Author(s):  
Matthew Agnew ◽  
Anita Kottapalli ◽  
Ven Kottapalli

A 38-year-old woman with a history of Crohn’s disease, multiple bowel resections, and ileostomy placement presented to the hospital with symptoms of increased ileostomy output for 1 week. She reported that she was emptying her bag fifteen times a day as opposed to her normal 3–4 times a day. Upon workup, she was found to have an acute kidney injury (AKI), and stool studies were positive for <i>Cryptosporidium</i>. She was treated with nitazoxanide 500 mg p.o. BID for 3 days along with continued rehydration. The patient was discharged after creatinine (Cr) and electrolytes returned to baseline. She continued to have elevated ileostomy output, and 1 week later, she was readmitted for another AKI and worsening of symptoms. At this hospitalization, stool studies were negative for <i>Cryptosporidium</i>, and the gastroenterologist consult recommended evaluation for active Crohn’s and Lomotil for possible short bowel syndrome. Eventually, her laboratory results improved, and she was discharged again before the full workup was completed. The patient’s ileostomy output continued to remain high following the second hospital discharge, and she eventually returned with another AKI, her third visit in a month. The workup for active Crohn’s was completed, with fecal calprotectin, serum cortisol, and small bowel follow-through all returning to normal. At this time, postinfectious inflammatory syndrome was suspected, and she was started on 60 mg of prednisone for 2 weeks. Steroid therapy elicited a significant response with normalization of her ileostomy output and return of laboratory results to baseline. The patient was discharged without return of symptoms at follow-up.


2020 ◽  
Vol 4 (2) ◽  
pp. 234-240
Author(s):  
Artur Schander ◽  
Andrew Glickman ◽  
Nancy Weber ◽  
Brian Rodgers ◽  
Michael Carney

Introduction: Emergency physicians are trained to treat a variety of ailments in the emergency department (ED), some of which are emergent, while others are not. A common complaint seen in the ED is a sore throat. While most sore throats are easily diagnosed and treated, less common causes are often not considered in the differential diagnoses. Therefore, the purpose of this case study was to present an atypical case of sore throat and discuss differential diagnoses. Case Presentation: The patient was a 45-year-old female who presented to the ED with a three-day history of sore throat that was exacerbated by eating and drinking. The patient was not on any prescription medications, but tried over-the-counter medications for the sore throat without any improvement in symptoms. Review of systems was positive for sore throat, fevers, and chills. Physical examination of her oropharynx revealed mildly dry mucous membranes with confluent plaques and white patchy ulcerative appearance involving the tongue, tonsils, hard palate, and soft palate. Rapid streptococcal antigen, mononucleosis spot test, and KOH test were performed and found to be negative. Discussion: After initial testing was negative, a follow-up complete blood count with differential and complete metabolic profile were ordered. The patient was found to have decreased lymphocytes and platelets. Based upon those results, a diagnosis was made in the ED, the patient was started on medication, and further laboratory workup was ordered to confirm the diagnosis. ED providers should consider non-infectious as well as infectious causes for a sore throat, as this might lead to a diagnosis of an underlying condition.


2021 ◽  
Vol 36 (4) ◽  
pp. 187-190
Author(s):  
Alecia B. Zika ◽  
Christine M. Ruby

Older people are particularly susceptible to acute kidney injury (AKI) for a variety of reasons. Because of this, medication changes during admission and transitions of care follow-up are often necessary to ensure the safety of these patients. The American Geriatrics Society's Beers Criteria provide guidance for select medications that are potentially inappropriate in the older adult population. However, other medications, particularly those for cardiovascular disease and diabetes that are not included in the kidney function-specific section of the Beers Criteria (Table 6), can sometimes be overlooked. This manuscript will provide insight to both pharmacists and student pharmacists on the importance of being vigilant for medications that may need dosage adjustment during episodes of AKI. As interns in the outpatient setting, pharmacy students can provide education to patients and their families in order to ensure these medications are being taken correctly and are properly restarted if their discontinuation was intended for only a short time.


2021 ◽  
Vol 14 (6) ◽  
pp. e241203
Author(s):  
Harry David True ◽  
Rupert George Ricks ◽  
Joel Anthony Smith

We present a case of non-surgically managed bilateral osteonecrosis of the external auditory canal with a history of long-term medical therapy for osteoporosis. A 79-year-old woman with severe osteoporosis and destructive osteoarthritis received >10 years of once weekly bisphosphonate therapy before switching to denosumab. Four months later, the patient presented with bilateral loss of hearing and right-sided otalgia. Necrotising otitis externa, cholesteatoma and malignancy were considered but with histology, microbiological and CT assessment, bilateral osteonecrosis of the external auditory canal was diagnosed. Surgical debridement with canalplasty was avoided due to our patient’s comorbidities. Treatment continued for 5 months with regular aural toilet, Terra-Cortril ointment and bismuth-iodine-paraffin paste packing. At 1-year follow-up, bilateral external auditory canals were completely re-epithelialised with no pain or affected hearing. We report the first case of bilateral osteonecrosis of the external auditory canal associated with denosumab and bisphosphonates with successful conservative management.


2018 ◽  
Vol 5 (2) ◽  
pp. 31
Author(s):  
Yadav Pandey ◽  
Krishna Prasad Joshi ◽  
Priya Priyambada ◽  
Anmol Chaudhary

Introduction: Hypercalcemia is relatively common in clinical practice. Primary hyperparathyroidism and malignancy accounts for more than 90 percent of all cases of hypercalcemia. Milk alkali syndrome which is hypercalcemia classically caused by ingestion of large amount of calcium and absorbable alkali which was once virtually disappeared as a cause of hypercalcemia has emerged as a third leading cause of hypercalcemia. We present a case of hypercalcemia secondary to ingestion of calcium carbonate tablets resulting in milk alkali syndrome.Case presentation: Patient is a 45-year-old female with history of gastroesophageal reflux disease came to the emergency department with complaints of dizziness, constipation, fatigue and confusion for 3 weeks. She was hypotensive to 83/53 mmHg at arrival. Significant laboratory results were - Potassium of 2.2 mmol/L (3.5-5.1 mmol/L), chloride 73 mmol/L (98-107 mmol/L), Bicarbonate 50 mmol/L (22-29 mmol/L), Blood urea 22 mg/dl (9.8-20.1 mg/dl), Cr 1.4 mg/dl (0.5-1.0 mg/dl), total calcium of 16.6 mg/dl (9-11 mg/dl), ionized calcium 2.02 mmol/L (1.15-1.33 mmol/L), PTH was low to 8.9 pg/ml (10-65 pg/ml). Arterial blood gas showed metabolic alkalosis. Extensive evaluation to find the cause of hypercalcemia was negative. Detailed history after initial stabilization, revealed that she had been taking 10 tablets of calcium carbonate tablets per day and 1 glass of milk daily for reflux symptoms for the last eight weeks. Based on the history and after ruling out all the other serious causes, diagnosis of milk alkali syndrome was made and patient was discharged with proton pump inhibitor with advice to avoid calcium carbonate. Her hypercalcemia responded well to fluid resuscitation.Conclusions: Milk alkali syndrome once a rare cause of hypercalcemia has emerged as a third leading cause of hypercalcemia in completely different scenario. It is important to evaluate the patient with proper history including the use of over the counter calcium supplements to determine the etiology of hypercalcemia. Our case highlights the importance of proper history taking in the evaluation of hypercalcemia and that not all the cause of severe hypercalcemia is secondary to malignancy. 


Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0003312021
Author(s):  
Nicole V. Tolan ◽  
Salman Ahmed ◽  
Tolumofe Terebo ◽  
Zain M. Virk ◽  
Athena K. Petrides ◽  
...  

Background: Acute kidney injury (AKI) is an abrupt decrease in kidney function associated with significant morbidity and mortality. Electronic notifications of AKI have been utilized in hospitalized patients, but their efficacy in the outpatient setting is unclear. Methods: We evaluated the impact of two outpatient interventions: an automated comment on increasing creatinine results (intervention I; 6 months; n=159) along with an email to the provider (intervention II; 3 months; n=105) compared to a control (baseline; 6 months; n=176). A comment was generated if a patient's creatinine increased by >0.5 mg/dL (previous creatinine ≤2.0 mg/dL) or by 50% (previous creatinine >2.0 mg/dL) within 180 days. Process measures included documentation of AKI and clinical actions. Clinical outcomes were defined as recovery from AKI within 7 days, prolonged AKI from 8 to 89 days, progression to CKD within 120 days. Results: Providers were more likely to document AKI in interventions I (p=0.004; OR=2.80) and II (p=0.01; OR=2.66). Providers were also more likely to discontinue nephrotoxins in intervention II (p<0.001; OR= 4.88). The median time to follow-up creatinine trended shorter among patients with AKI documented (21 vs. 42 days; p=0.11). There were no significant differences in clinical outcomes. Conclusions: An automated comment was associated with improved documented recognition of AKI and the additive intervention of an email alert was associated with increased discontinuation of nephrotoxins, but neither improved clinical outcomes. Translation of these findings into improved outcomes may require corresponding standardization of clinical practice protocols for managing AKI.


2021 ◽  
Vol 11 (9) ◽  
Author(s):  
Muthu Sathish ◽  
Chellamuthu Girinivasan ◽  
Chandrasekaran Srinivasacholan ◽  
Palani Gowtham

Introduction: Melorheostosis is a rare sclerosing bone disease characterized by linear hyperostotic bone dysplasia with its radiological appearance as melting candle wax dripping by its side. It usually affects long bones, especially the lower limb. The exact cause of the disease has not been clearly explained though many theories are available. It is insidious in onset and symptoms being pain, deformity, and joint stiffness. Although there is no definitive treatment, the administration of bisphosphonates dramatically reduces pain and improves the patient clinically. Case Report: We described a case of a 28-year-old female who presented with a history of pain and swelling in her left leg for the past 2 years. The onset of complaints was insidious. On physical examination, there was tender swelling over the shaft of the tibia with irregular borders. Knee and ankle range of movements were normal. Radiographs showed hyperostosis of the proximal two-thirds of the tibia of the left leg with a flowing candle wax appearance. The patient was treated with a single dose of intravenous zolendronic acid and physical therapy. The patient had dramatic alleviation of pain without the need for any further treatment till 1 year follow-up. Conclusion: Although there is no specific treatment available for this disease, the intravenous infusion of zolendronic acid has dramatically improved the patient clinically. Keywords: Melorheostosis, flowing candle wax, bisphosphonates, zolendronic acid.


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