Hypercalcemia Case Study


Author/s

Shawn Maskalick, Chinwe Okoro, Logan Simcox, Ali Hasnie

Bellarmine University

Doctor of Physical Therapy Program

Class of 2016



Abstract - Hypercalcemia Characteristics

Hypercalcemia is characterized as greater than normal amounts of calcium in the blood.  Symptoms can effect the musculoskeletal, nervous, cardiovascular/pulmonary, and gastrointestinal systems (see table below). Normal serum calcium levels range between 8.2 and 10.2 mg/dL.  Mild hypercalcemia is considered when calcium levels are around 12 mg/dL and severe hypercalcium is defined as serum calcium levels at 14 mg/dL.

[1]


System Symptoms
Central Nervous System (CNS) drowsiness, lethargy, coma irritability, personality changes, confusion, headaches, depression, memory loss, difficulty concentrating, visual disturbances, balance/coordination problems, changes in deep tendon reflexes, change in muscle tone for individual with neurologic condition, positive Babinski and/or clonus reflex, changes in bowel/bladder function
Musculoskeletal muscle pain or tenderness and weakness, muscle spasms, bone pain (worse at night and on weight bearing), pathologic fracture
Cardiovascular Hypertension, Arrhythmia, Cardiac arrest
Gastrointestinal Anorexia (loss of appetite), nausea, vomiting, constipation, dehydration, thirst


[2]

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In the case described below, hypercalcemia occured secondary due to Vitamin D intoxication.

Patient Characteristics

  • 65 year old
  • White female
  • Height: 5' 8"  Weight:165
  • Retired administrative assistant
  • Runs a soup kitchen 3 days/week
  • Diagnosis:  Hypercalcemia secondary to Vitamin D intoxication & thiazide diuretic
  • Past Medical History:  Primary hypothyroidism, HTN, hyperlipidemia, & vitamin D deficiency



Examination

  • Subjective: Chief Complaint:fatigue, anorexia, nausea, abdominal pain, constipation and depression for 1 month. 
  • Objective: She appears weak and dry. Vitals: BP: 154/92  RHR:  84 bpm  Heart Sounds: audible S1,S2. Lungs were clear to ascultate bilaterally. Alert & oriented x 1 (only person).  Oxygen saturation:  95% on room air.

ROM (UE's):  WNL  

ROM (LE's):  WNL  

Gross MMT:  UE: EROT: 4/5 bilaterally, Elbow flexion: 4/5 left, 5/5 right, elbow extension: 4/5,  Shoulders, wrists, & grip strength: 5/5 bilaterally.   LE: Hip Abduction: 4/5 bilaterally, knee extension: 4/5 on the left & 5/5 on the right, hip flexion, knee flexion, plantar flexion & dorsiflexion 5/5 bilaterally.  

Reflexes:  Normal  

Sensation: Normal  

Posture: elevated/protracted shoulders, forward head position  

Gait:  limited bilateral hip extension, decreased bilateral reciprocal arm swing, shortened step length  

Static sitting:  normal

Dynamic sitting:  normal  

Bed mobility: Independent  

Sit to stand: independent  

Bed to Chair & Chair to Bed transfer: Independent  

Ambulation:  150 feet with contact guard assist    

Basic metabolic panel: hypercalcemia 13mg/dl, ionized calcium of 1.8, acute kidney injury with Cr of 2.2 & hyperphoshatemia.  Further lab data showed a low PTH & high Vit D levels.

  • Self Report/Physical Performance:  Visual Analog Scale (VAS) Best: 4/10  Current: 7/10  Worst: 9/10    6 Minute Walk Test - 375 meters 

Clinical Impression


1) Hypercalcemia & Hyperphosphotemia secondary to Vit D intoxication & thiazide diuretic
2) Acute Kidney injury secondary to Hypercalcemia
3) Dehydration secondary to Hypercalcemia

Summarization of Examination Findings

Based on the subjective and objective findings, the targeted intervention was to rehydrate with normal saline (IVF).  In a case of severe hypercalcemia, intervention would include the administration of biphosphonate or calcitonin.  The goal for restoration of function of this patient is to rehydrate the patient with normal saline in order to excrete calcium from the renal tubules.  It's important to determine the etiology of the hypercalcemia (PTH related on non-PTH related) as the management may vary. Our case is non-PTH related hypercalcemia due to Vit D intoxication.  Since the baseline vitals are stable, physical therapy intervention will begin immediately following the effect of medical intervention in order to restore hydration and the process of calcium excretion.  

Physical Therapy Intervention 

The physical therapy plan of care for this patient will be a one week program (5 days) for the acute care setting.  

Frequency:  5 days a week (Monday - Friday) 

Duration:  60 minutes

Day 1: PNF UE D1 flexion/extension 1 x 10 https://www.youtube.com/watch?v=zhQgQ2rkP1Q

            PNF UE D2 flexion/extension 1 x 10 https://www.youtube.com/watch?v=4cYrnM5IQ3Q

            PNF LE D1 flexion/extension 1 x 10 https://www.youtube.com/watch?v=A29DZxUj8e4

            PNF LE D2 flexion/extension 1 x 10 https://www.youtube.com/watch?v=lbXpl-3ZR2M

            seated LE exercises with manual resistance (hip abduction, extension, & flexion, knee extension, knee flexion, plantar flexion,                           dorsiflexion 1 x 10 for each exercise 

            Sit to stands: 3 x 5,  posture/gait training education, ambulation with tactile & verbal cues 100 feet x 2.

Day 2:  Same as above but increase ambulation distance to 150 feet

Day 3:  Same as day 1 but increase PNF exercises:  2 x 10,  LE exercises: 2 x 10, sit to stands 3 x 8, ambulation:  175 feet x 2

Day 4:  Same as day 3 but increase sit to stands 3 x 10

Day 5:  Assess for discharge:  Reevaluate MMT, 6 minute walk test,  and visual analogue scale.  Provide the patient with a HEP that includes: patient education of the exercise, pictures of the exercises, and patient demonstration and comprehension of the exercises provided.  In addition, the patient will be provided with information pertaining to the duration and frequency of each exercise as well as how to progress the program.  

            

Outcomes

The patient's vitals remained stable and rehydration through medical intervention occured within 4 to 6 hours. At day 5, calcium levels had reduced to 11mg/dL. The patient's reported VAS score for their current pain level had significantly improved from an intial 7/10 to a 4/10 at day 5.  Her reported worst pain level improved from 9/10 to 6/10, and her least level of pain improved from 4/10 to 2/10 respectively.  In addition, her aerobic endurance via the 6 Meter Walk Test also improved from 375 feet initially to 425 feet at discharge.  Ambulation distance improved from 100 feet with contact guard assist initially to 200 feet with stand by assist upon day 5.  The patient demonstrated improved posture and reciprical arm swing and step length during gait with minimal verbal cues.  Gross MMT remained unchanged.      

Discussion

Although the patient in this case presented with hypercalcemia secondary to vitamin D intoxication, it's critical to have lab work done to establish that her parathyroid levels are within normal range since she had a past medical history of hypoparathyroidism.  According to the literature, it's important to reduce or even stop any substitution of calcium and vitamin D metabolites in patients with hypoparathyroidism during periods of immobilization [3].  In addition to improving overall strenght and aerobic conditioning, current research supports physical therapy intervention for the following reasons: immobilization is a well-established but under appreciated etiology of hypercalcemia, 
immobilization-induced hypercalcemia can obviate the need to order unnecessary examinations, pre-existing renal function impairment are prone to develop immobilization hypercalcemia in a shorter time frame, and the standard treatments for immobilization hypercalcemia include the use of early rehabilitative exercises and control of the underlying illness [4].  The medical intervention suggested for this patient in order to establish rehydration and return calcium levels to normal is also supported within the research as well: onset of action for saline, calcitonin and bisphosphonate is 4 to 6 hours and 24 to 72 hours, respectively. Accordingly calcium excretion initiates at first hours of treatment and maximizes during 72 hours after starting of treatment. The duration of action of bisphosphonates is as long as 2 to 4 weeks [5].

Related Pages

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References

  1. Goodman, Catherine Cavallaro, and Snyder, Teresa E. Kelly. Differential Diagnosis for Physical Therapists: Screening for Referral. 5th ed. St. Louis, MO: Saunders/Elsevier, 2013. Print.
  2. MARY F. CARROLL, M.D., Eastern New Mexico Medical Center, Roswell, New Mexico. DAVID S. SCHADE, M.D., University of New Mexico School of Medicine and Health Sciences Center, Albuquerque, New Mexico Am Fam Physician. 2003 May 1;67(9):1959-1966.. A Practical Approach to Hypercalcemia. http://www.aafp.org/afp/2003/0501/p1959.html (accessed ).
  3. Schroth M, Dötsch J, Dörr H. Hypercalcemia and idiopathic hypoparathyroidism. Journal Of Clinical Pharmacy & Therapeutics [serial online]. December 2001;26(6):453-455. Available from: CINAHL with Full Text, Ipswich, MA. Accessed March 27, 2015.
  4. Chih-Jen C, Chung-Hsing C, Shih-Hua L. An Unrecognized Cause of Recurrent Hypercalcemia: Immobilization. Southern Medical Journal [serial online]. April 2006;99(4):371-374. Available from: Academic Search Complete, Ipswich, MA. Accessed March 27, 2015.
  5. Oghazian, M., Ataei, S., Radfar, M.. Vitamin D Intoxication with Hypercalcemia Due to Overuse of Supplement. Journal of Pharmaceutical Care, Tehran, Iran, 1, Sep. 2013. Available at: <http://jpc.tums.ac.ir/index.php/jpc/article/view/58>. Date accessed: 27 Mar. 2015.