Physical Therapy Intervention With Oncological Emergencies

INTRODUCTION

There are a group of clinical entities termed “Oncological Emergencies” that are still often appropriate for physical therapy intervention. Depending on the extent of the problem it is important to delineate strategies of when to intervene and how to treat patients. This paper will assist physical therapists by describing common problems and the role physical therapists can play in their management.

SUPERIOR VENA CAVA SYNDROME

The prevalence of Superior Vena Cava Syndrome (SVCS) is rare, occurring in approximately 5% of small cell lung cancer patients. Bronchiogenic carcinomas and lymphomas are the most common causes.

Hunter first described SVCS in 17571 in a patient with an aortic aneurysm from syphilis; however, it is now almost exclusively seen in oncology patients. Despite the fact that Small Cell Lung Cancer only occurs in about 15% to 20% of lung cancers, it is the most common cause of SVCS (65%) due to an associated prevalence of mediastinal metastasis and central lung lesions, which cause compression on the superior vena cava. The superior vena cava is particularly susceptible to compression due to the fact that it is surrounded by several rigid structures and is itself under low pressure. Superior Vena Cava Syndrome usually presents insidiously. Most patients present with dilated neck veins and facial edema, while 15% to 20% of patients have arm edema.: Depending on the problems and clinical presentation of the patient, SVCS may not require emergent care. It is considered an oncological emergency due to the potential for catastrophic events. Most treatment is palliative since the most common malignancies causing compression are not curable. Lymphoma is an exception, where curative chemotherapy brings 1-year survival rates up to 40%. Radiation therapy is the most common treatment. Stents also occasionally are used.

Physical Therapy Intervention

Physical therapy interventions indicated for individuals with SVCS include the following:

1. Patients should be positioned with the head of the bed elevated.

2. Blood pressure readings should be taken from the lower extremities.

3. Physical activity should be limited to essential ADLs with education to avoiding heavy lifting or valsalva.

4. The physical therapist and health care team members should monitor the patient for any increased difficulty with respiration to provide appropriate care, which may include positioning, energy conservation, physician notification, adaptive equipment, and oxygen.

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

Syndrome of Inappropriate Antiduretic Hormone (SIADH) is uncommon but occurs in 1% to 2% of cancer patients, most often with Small Cell Lung Cancer and occasionally caused by chemotherapy medications such as vincristine and cyclophosphamide.’

Normally, the body regulates the amount of ADH that is released, but tumor production can cause unregulated production of ADH. This unregulated production of ADH can lead to severe hyponatremia (sodium < 115mEq/L) that is characterized by lethargy, nausea, anorexia, and generalized weakness. Rapid onset of SIADH could result in coma, convulsions, or death. Moderate SIADH ( 115-125) can cause nausea, vomiting, cramps, and altered mental status. Mild hyponatremia (125-130) will cause increased thirst, cramps, and lethargy. However since tolerance to hyponatremia is variable from patient to patient, it should be evaluated on a case-by-case basis.

Physical Therapy Intervention

Physical therapy interventions for SIADH include the following:

1. Patients with mild or moderate SIADH may need physical therapy to maintain their mobility and prevent deconditioning. Therefore patients may benefit from functional training for bed mobility and transfers, as well as strengthening and range of motion exercises.

2. Fluid restrictions are vital and may be in place for 5 days or more. The physical therapist should coordinate water intake planning with nursing, as patients will be manipulative in their quest to obtain water. Patients will often be restricted to fewer than 700 mL per day/

3. The physical therapist should monitor mental status and coordinate with nursing for monitoring urinary output and weight.

TUMOR LYSIS SYNDROME

Tumor Lysis Syndrome (TLS) has prevalence as high as 40% in high- grade non-Hodgkin Lymphoma (6% of these are clinically significant).5 The TLS occurs in patients with myeloproliferative disorders such as leukemia and lymphoma, which require chemotherapy that causes lysis of a massive number of cells in a short period of time.

Because of the lysis of a large number of cells in a short period of time large amounts of potassium, phosphate, and uric acid are released resulting in acute renal failure. Tumor Lysis Syndrome also can occur with some solid tumors (ie, hepatic tumors). Symptoms usually arise from 6 to 72 hours after the initiation of chemotherapy. Oncologists are proactive in treating patients with hydration and allopurinol (which blocks uric acid production), and patients are monitored closely for urine output, daily weights, and lab values. Patients often complain of muscle weakness and cramping in skeletal muscles from TLS.

Physical Therapy Intervention

The physical therapy intervention for TLS includes the following:

1. The health care team should identify which patients are at risk for developing TLS (high-grade lymphomas/ALL).

2. The physical therapist should be aware that TLS could develop rapidly and produce severe metabolic problems. Prompt recognition of signs and symptoms is crucial. Often physical therapists are working with patients before the onset of TLS, so early recognition of classic symptoms such as muscle cramping, arrhythmias, and oliguria (decreased urine output) are essential.

3. The physical therapist should watch for CNS signs or arrhythmias (decreased BP, tachycardia, irregular HR) during activity.

SPINAL CORD COMPRESSION (SCC)

The prevalence of SCC is as high as 30% of patients with disseminated cancer that have spinal cord compression; however, only 5% experience cord dysfunction.6 The vast majority of lesions are metastatic. The most common causes are metastasis from various cancers, including lung, breast, prostate, multiple myeloma, and colon.

For many years it was thought that tumors accessed the vertebrae through the valveless venous system known as Batson’s plexus. Batson’s plexus drains both the vertebrae and skull and anastamoses with veins draining the breasts and thoracic, abdominal, and pelvic organs. More recently, experimental models have emphasized the role of arterial seeding of the vertebrae with tumors.7 Sixty percent of spinal metastasis is in the thoracic spine, and another 30% is in the lumbosacral region. This percentage is actually proportional to the volume of bone in those areas. Back pain will precipitate any cord compression. Medical management will involve steroids, XRT. chemotherapy, or surgery. In some patients where surgical stabilization is not indicated or feasible a thoracolumbosacral orthosis will be prescribed. The Frankel classification has been in place for many years and helps to classify functional ability.8

FRANKEL CLASSIFICATION

Prognosis

By definition, spinal cord compression is associated with poor control of the primary tumor. Pretreatment ambulatory status is the most important predictor of ambulation posttreatment and also of improved survival.” Slow development of symptoms also predicts a better outcome. Sorensen et al1″ improved function in patients (12 of 13) who received dexamethasone vs. those who did not (4 of 8). Patients who are evaluated for surgery are not always surgical candidates, despite bone instability; those patients should be placed in a TLSO that both prevents flexion and rotation which are movements that put the greatest stress on vertebral bodies.

Physical Therapy Intervention

The physical therapy interventions associated with spinal cord compression include the following:

1. The physical therapist should perform serial muscle testing to detect improvement or decline in motor function. Steroids can occasionally create dramatic results.

2. Medical treatment is based on a variety of indicators such as prognosis, type, and location of cancer as well as bone stability.

3. Check to assure that the patients’ spine is stable prior to out of bed activities.

4. Monitor pain and whether or not the pain is worsened by activity.

5. Rehabilitation goals will be dependent on level of lesion, whether the lesion is incomplete or complete, and the overall patient prognosis.

DISSEMINATE INTRAVASCULAR COAGULATION

The prevalence of disseminate intravascular coagulation (DIC) is as high as 13% in acute leukemia patients.” The DIC is seen most often in acute leukemia, colon, and pancreas cancers. Acute bleeding or thrombosis leading to hypopertusion, end organ damage, and infarction characterizes acute DIC. Patients may develop fever, tachycardia, tachypnea, and hypotension. It is most commonly seen in patients with acute promyelocytic leukemia. It is thought that the leukemic blasts release plasminogen activators precipitating the coagulopathy.’: Hemoglobin and platelet counts are decreased. Patients may also have hematuria and hematochezia.

Physical Therapy Intervention

Physical therapy interventions for individuals with DIC include the following:

1. Clinical manifestations can vary greatly; patients may suffer mild problems such as petechia and bruising or more significant manifest\ations such as organ dysfunction or strokes.

2. Monitor platelet counts daily prior to intervention.

3. Emphasize safety.

HYPERCALCEMIA

The prevalence of hypercalcemia is very common; as many as 10% to 20% of cancer patients develop hypercalcemia.

Normal serum calcium is usually 8.7-10.4, with mild hypercalcemia defined as 12 and severe hypercalcemia as 14 or greater. Symptoms of hypercalcemia include nausea, vomiting, altered mental status, polyuria, weakness or vague muscle/joint pain, and headaches. Hypercalcemia related to malignancy is usually related to bone metastasis, mainly due to osteolytic activity. Malignant tissues also can release a gene that produces a parathyroid hormone-related protein, which increases bone reabsorption.” Solid tumors such as lung or breast cancer or certain hematological malignancies such as multiple myeloma are the most common patients who develop hypercalcemia.

Physical Therapy Intervention

The most common physical therapy interventions for individuals with hypercalcemia include:

1. Patients with severe hypercalcemia (above 14) are usually too unresponsive and altered mentally to mobilize. When patients are able, they should be assisted out of bed, with the preference being weight-bearing exercises such as ambulation, which helps stimulate bone metabolism.

2. The physical therapist must be aware of the integrity of any bone where metastasis can increase the risk of pathological fractures.

3. Patients can use footboards in bed to help stimulate bone to retain calcium.

SEVERE THROMBOCYTOPENIA

The prevalence of thrombocytopenia is very common. This may be due to impaired production such as aplastic anemia, platelet destruction such as ITP or DIC, or sequestration such as spleenomegaly.

Physical therapists commonly treat patients with thrombocytopenia. Severe thrombocytopenia (< 10,000) puts an individual at significantly increased risk for spontaneous bleeding. Intracranial hemorrhage is the most feared complication. Platelet counts can vary from day to day; patients who are at risk (such as those with severe pancytopenia) must be monitored closely.

Physical Therapy Intervention

The most common physical therapy interventions for patients with thrombocytopenia include:

1. Identify patients at risk. Any pancytopenic patient must be identified and counts monitored daily prior to PT intervention.

2. Platelet destruction or sequestration will cause faster drops in platelet counts than platelet production problems.

3. Safety/falls prevention is paramount in patients with severe thrombocytopenia (< 10,000).

Guidelines for Exercise

4. Maintain locomotion skills in patients with prolonged hospitalization or pancytopenia.

SUMMARY

Oncology patients present challenges to the physical therapist. Understanding treatment regimens and their potential side effects are essential to provide competent, safe, and appropriate physical therapy treatment. Early recognition of potential emergencies is a crucial component to state of the art physical therapy interventions to this most deserving population.

REFERENCES

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2. Kvale PA, Simoff M, Prakash UB: American College of Chest Physicians. Lung Cancer. Palliative Care. Chest. 2003;123(1 Suppl):2845-311S.

3. Plotkin SR. Neurologic complications of cancer therapy. Neuml Clin. 2003;21(1):279-318.

4. Carlson HE. Metabolic Complications. In: Casciato DA, Lowitz BB, ed. Manual of Clinical Oncology. 4th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2000:526-543.

5. Davidson MB. Pathophysiology, clinical consequences and treatment of tumor lysis syndrome. Am J Med. 2004;! 16(8): 546-554.

6. Bach F, Larsen BH, Rohde K, et al. Metastatic spinal cord compression. Occurrence, symptoms, clinical presentations and prognosis in 398 patients with spinal cord compression. Acta Neurochir (Wien). 1990; 107:37-43.

7. Arguello F, Baggs RB, Duerst RE, et al. Pathogenesis of vertebral metastasis and epidural spinal cord compression. Cancer. 1990;65:98-106.

8. Frankel HL, Hancock DO, Hyslop G, et al. The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia. I. Paraplegia. 1969;7:179-192.

9. Rades D, Heidenreich F, Karstens JH. Final results of a prospective study of the prognostic value of the time to develop motor deficits before irradiation in metastatic spinal cord compression, lnt J Radiat Oncol Biol Phys. 2002;53: 975-979.

10. Sorensen PS, Helweg-Larsen S, Mouridsen H, Hansen HH. Effect of high-dose dexamethasone in carcinomatous metastatic spinal cord compression treated with radiotherapy: a randomized trial. Eur J Cancer. 1994;30A:22-27.

11. Nur S, Anwar M, Saleem M, Ahmad PA. Disseminated intravascular coagulation in acute leukemias at first diagnosis. Eur J Haematol. 1995;55(2):78-82.

12. Bick RL. Disseminated intravascular coagulation. Objective criteria for diagnosis and management. Med Clin North Am. 1994;78(3): 511-543.

13. Deftos LJ. Hypercalcemia in malignant and inflammatory diseases. Endocrinol Metab Clin North Am. 2002;31 ( 1 ): 141 158.

Bill Tatu, MPT

Virginia Commonwealth University Medical Center, Richmond, VA

Copyright Rehabilitation in Oncology 2005