Hypercalcemia of malignancy (HCM) is defined as a serum calcium level greater than 10.5 mg/dl (Gullatte et al., 2005; Kaplow & Reid, in press).

The reported incidence of HCM is 10% to 40% of patients (Crossno, 2004; Gullatte et al., 2005; National Coalition for Cancer Survivorship [NCCS], 2005; Solimando, 2001).

Etiologic factors of HCM include specific cancers, treatment modalities, and nonmalignant causes. HCM is most often associated with primary tumors of the breast, lung, head and neck, kidney, esophagus, gastrointestinal (GI) tract, and cervix; lymphomas; leukemia; multiple myeloma; and melanomas (Gullatte et al., 2005; Kaplow & Reid, in press; National Cancer Institute [NCI], 2005).

Cancer treatment modalities such as estrogen, antiestrogen agents, and all- trans retinoic acid are associated with the development of HCM (Gullatte et al., 2005).

Non–cancer-related factors associated with HCM development include immobility dehydration, excessive intake of calcium and vitamin D, decreased parathyroid hormone levels, vitamin A intoxication, hyperparathyroidism, and thiazide diuretic or lithium use (Carroll & Schade, 2003; Crossno, 2004; Gullatte et al., 2005; Kaplow, in press; NCI, 2005).

HCM most often results from bone metastasis. This causes osteoclastic bone resorption and release of calcium. Calcium is released from the bone faster than the kidneys can excrete it (Gullatte et al., 2005; Kaplow & Reid, in press). The types of HCM are osteolytic (results from direct bone destruction by a tumor or metastasis) and humoral (results from circulating factors secreted by cancer cells) (Carroll & Schade, 2003; Inzucchi, 2004; Kaplow, in press; NCI, 2005; Solimando, 2001).

Clinical manifestations of HCM vary depending on effects of calcium on the neurologic, GI, renal, and cardiovascular systems; rate of the rise of calcium levels; and patient’s stage of disease and overall condition, renal function, and degree of HCM. They are usually related to the effects of calcium on smooth, skeletal, and cardiac muscle (Gullatte et al., 2005). Neurologic symptoms include mental status changes, hallucinations, jumbled speech, depression, and fatigue. Patients may report visual changes. Diminished deep tendon reflexes may be noted (Beckles, Spiro, Colice et al., 2003; Carroll & Schade, 2003; Crossno, 2004; Inzucchi, 2004; Kaplow & Reid, in press; NCI, 2005; NCCS, 2005; Shuey & Brant, 2004; Solimando, 2001).

Several cardiovascular symptoms exist. These include potential electrocardiographic changes such as prolonged PR interval, widened QRS complex, shortened QT interval, shortened or absent ST segments, and widened QT intervals. Patients may present with atrioventricular block bradycardia, bundle-branch block, or cardiac arrest, depending on severity. Hypertension and myocardial irritability may be observed (Beckles et al., 2003; Carroll & Schade, 2003; Crossno, 2004; Inzucchi, 2004; Kaplow & Reid, in press; NCI, 2005; NCCS, 2005; Shuey & Brant, 2004).

GI manifestations may include nausea, vomiting, anorexia, abdominal pain, ileus, constipation, abdominal distention, dry mouth, increased gastric acid production, pancreatitis, or peptic ulcer disease (Beckles et al., 2003; Carroll & Schade, 2003; Crossno, 2004; Inzucchi, 2004; NCI, 2005; NCCS, 2005; Shuey & Brant, 2004; Solimando, 2001).

Renal effects are polyuria, polydipsia, nocturia, renal failure, dehydration, and nephrogenic diabetes insipidus. Calcium phosphate crystals may be present in the renal tubules (Beckles et al., 2003; Carroll & Schade, 2003; Crossno, 2004; Inzucchi, 2004; Kaplow & Reid, in press; NCI, 2005; NCCS, 2005; Shuey & Brant, 2004; Solimando, 2001).

Other symptoms that may manifest in a patient with HCM include osteoporosis, arthritis, pathologic fractures, and pruritus (Beckles et al., 2003; Carroll & Schade, 2003; Crossno, 2004; Inzucchi, 2004; Kaplow & Reid, in press; NCI, 2005; Shuey & Brant, 2004; Solimando, 2001).

Laboratory findings linked with HCM are abnormal serum creatinine, calcium, electrolytes, magnesium, phosphorus, and possibly elevated alkaline phosphatase (Crossno, 2004; Kaplow & Reid, in press; Shuey & Brant, 2004). The degree of HCM is determined by laboratory measurement of serum calcium in relation to serum albumin levels. Calcium levels should be corrected based on albumin levels, since 40% of calcium is bound to albumin (Gullatte et al., 2005; Kaplow & Reid, in press).

The primary treatment of HCM is treatment of the causal malignancy. This may require chemotherapy, radiation therapy (RT), hormonal therapy, and/or surgical resection (Gullatte et al., 2005; Kaplow & Reid, in press). Irrespective of severity, management should include treatment of any underlying non–disease-related causes.

Patients with a corrected calcium level less than 12 mg/dl may require only monitoring. Patients with moderate to severe HCM (more than 13 mg/dl) require aggressive treatment (Kaplow & Reid, in press).

The degree of monitoring required will depend on the patient’s condition and overall goals of care. Many side effects of treatment can be prevented or managed. Since serum sodium, potassium, calcium, phosphorus, and magnesium levels may decrease, levels should be monitored at least daily. Serum calcium levels will require monitoring, especially during bisphosphonate therapy. The management of symptoms and side effects is essential (NCI, 2005).

Patients treated for HCM will require close follow-up once normal calcium levels have been attained. The underlying malignancy, following its trajectory, may worsen and ongoing HCM management may be required (NCI, 2005; Shuey & Brant, 2004). Frequency of follow-up is also based on the anticipated lasting effect of the treatment modalities used (NCI, 2005).

Patients and families require education regarding what symptoms to observe and the importance of reporting symptoms early. Measures can include preventing dehydration, weight-bearing activities, managing pain, and avoiding thiazide diuretics (Gullatte et al., 2005).

Patients and families should have the sequelae of untreated HCM explained to them; these include loss of consciousness and coma, which may be acceptable outcomes for patients at end-of-life who are suffering or have uncontrollable symptoms or when treatment of the underlying malignancy is no longer feasible (NCI, 2005).

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a condition of water intoxication. It is depicted by inappropriate production and secretion of antidiuretic hormone (ADH). This causes increased tubular water reabsorption with subsequent water retention, dilutional hyponatremia, a decreased serum osmolality, and increased urine osmolality (Flounders, 2003; Kaplow & Reid, in press; Shirland, 2001). The secretion of ADH occurs despite adequate circulating fluid volume and urinary sodium excretion and (Beckles et al., 2003; Gullatte et al., 2005).

SIADH occurs in 1% to 14% of patients with malignancy. Patients with small-cell lung cancer (SCLC) have an incidence of up to 10% (Hemphill & Ismach, 2001; Kaplow, 2005; Kaplow & Reid, in press).

The causes of SIADH are (1) cancer, (2) neurologic disorders, (3) benign lung disease, and (4) drugs (Baylis, 2003; Gullatte et al., 2005). SCLC is the most common cancer associated with the development of SIADH. Other associated malignancies are non–small-cell lung cancer (NSCLC); carcinoid tumors; squamous cell carcinoma of the head and neck; breast, brain, prostate, esophagus, pancreas, colon, thymus, uterus, bladder, ovarian, or duodenal tumors; neuroblastoma; mesothelioma; Hodgkin’s and non-Hodgkin’s lymphomas; and leukemia. It can also be caused by metastasis to the central nervous system (CNS) (Flounders, 2003; Gullatte et al., 2005; Kaplow & Reid, in press).

Some chemotherapeutic agents place patients at risk to develop SIADH. These include vincristine, vinblastine, cyclophosphamide, ifosfamide, cisplatin, and melphalan. Each of these agents can cause hyponatremia and elevated ADH levels (Gucalp & Dutcher, 2001; Gullatte et al., 2005; Kaplow & Reid, in press; Tan, 2002).

Non–cancer-related etiologic factors for SIADH include medications (e.g., opioids, antidepressants, NSAIDs, thiazide diuretics, barbiturates, and anesthetic agents), CNS disorders (e.g., brain abscess or herniation, hemorrhage, head trauma), and pulmonary disorders (e.g., infection, pneumonia, lung abscess, tuberculosis). Pain, stress, and nicotine have also been identified as causative factors (Flounders, 2003; Kaplow & Reid, in press; Tan, 2002).

The symptoms depend on the degree and speed at which hyponatremia develops (Baylis, 2003). The hallmark signs of SIADH are hyponatremia, serum hypo-osmolality, and inappropriately concentrated urine for serum osmolality (Gullatte et al., 2005).

Patients present with a variety of symptoms that may be due to dilutional hyponatremia, hypocalcemia, or hypokalemia. SIADH affects the CNS, GI, renal, musculoskeletal, cardiac, and respiratory systems. CNS symptoms include mental status changes, headache, ataxia hallucinations, agitation, fatigue, malaise, tremors, hyporeflexia, myoclonus, and unexplained seizures (Gullatte et al., 2005). GI symptoms may include nausea, vomiting, diarrhea, anorexia, and abdominal cramping. If the renal system is affected, the patient may manifest thirst, weight gain without edema, and oliguria. Musculoskeletal symptoms are muscle cramps and weakness. Patients may have hypotension or normal blood pressure and heart rate as well as fluid retention. Possible respiratory symptoms include inability to maintain a patent airway and inability to mobilize secretions (Baylis, 2003; Beckles et al., 2003; Flounders, 2003; Gullatte et al., 2005; Kaplow & Reid, in press; Tan, 2002). If a serum sodium level is less than 120 mmol/L and develops acutely, the patient is at risk for the development of cerebral edema (Gullatte et al., 2005; Langfeldt & Cooley, 2003).

Diagnosis of SIADH is based on laboratory data and through the exclusion of other contributing factors of hyponatremia. The clinician should have a high index of suspicion based on the presence of risk factors in a hyponatremic patient (Gullatte et al., 2005; Janicic & Verbalis, 2003). Laboratory data consistent with a diagnosis of SIADH are a urinary sodium level of greater than 40 mEq/L, urinary osmolality greater than 1000 mOsm/kg, serum hypo-osmolality, and hyponatremia (Kaplow & Reid, in press).

Continuous monitoring of the patient is important to identify changes in clinical status. Assessment of fluid and electrolyte status and for side effects of treatment is equally essential. Collaboration among the physician, pharmacist, and nurse to manage anxiety and depression will help optimize patient outcomes, as many medications will need to be avoided (Flounders, 2003; Kaplow & Reid, in press).

Treatment of the underlying cause of SIADH may be implemented. Treatment modalities include chemotherapy, RT, and/or corticosteroids (Kaplow & Reid, in press). The foundation of management is fluid restriction to less than 800 to 1000 ml/day until serum sodium improves (Kaplow & Reid, in press; Flounders, 2003). Demeclocycline administration is recommended if fluid restriction alone is not effective (Gullatte et al., 2005; Kaplow & Reid, in press; Flounders, 2003; Tan, 2002).

Patients with acute hyponatremia and severe neurologic symptoms should receive 3% saline at a rate of 300 to 500 ml over 4 to 6 hours until a serum sodium of 125 mg/dl is attained (Crook, 2002). Serum sodium should be corrected at a rate of 0.5 to 2 mEq/h to prevent complications of therapy (Flounders, 2003; Gucalp & Dutcher, 2001; Gullatte et al., 2005; Kaplow & Reid, in press; Kozniewska, Podlecka, & Rafalowska, 2003). Loop diuretics are recommended to decrease urine concentration and promote urinary free water excretion (Gucalp & Dutcher, 2001; Gullatte et al., 2005).

The key to managing SIADH is early detection to prevent complications. Monitoring fluid status may require urine specific gravity, daily weights, serum and urine electrolytes, and strict intake and output (I/O). Patients receiving hypertonic saline require ongoing assessment for overcorrection and/or fluid overload. Neurologic assessment is essential as rapid changes in mental status may signify worsening hyponatremia and rapid changes in sodium (Gullatte et al., 2005).

SIADH resolves in less than 3 weeks when treatment of the underlying cause has been successful. Symptoms often recur if there is tumor progression (Beckles et al., 2003; Flounders, 2003; Kaplow & Reid, in press). While patients are being treated, serum chemistries may be monitored on a periodic basis (Tan, 2002).

Patients and family members should be taught signs and symptoms to observe for, actions to take, and when to seek medical attention. While the patient is receiving treatment of SIADH, comfort measures such as mouth care and administration of small amounts of ice chips may be given to combat the discomfort of thirst. Family members should also be taught to observe for changes in mental status (Flounders, 2003; Gullatte et al., 2005).

Superior vena cava syndrome (SVCS) results from obstruction of the superior vena cava (SVC). The blockage may be above or below the azygous vein from an intravascular clot, tumor in the right main upper lobe bronchus, or significant mediastinal lymphadenopathy. The obstruction impairs blood flow to the right atrium and venous drainage above the upper thorax. This results in a decreased venous return (Gullatte et al., 2005; Hemann, 2001; Kaplow & Reid, in press; Rowell & Gleeson, 2005; Wudel & Nesbitt, 2001).

An incidence of 2.4% to 21.1% of SVCS in lung cancer patients has been reported (Rowell & Gleeson, 2005).

Most cases of SVCS are due to malignancy. Of these, 80% are due to NSCLC and non-Hodgkin’s lymphoma (Beckles et al., 2003; Kaplow & Reid, in press; Thirlwell & Brock, 2003). In patients with lung cancer, SVCS is usually due to direct extension or lymph node metastasis (Beckles et al., 2003; Kvale, Simoff, & Prakash, 2003). Some cases are due to breast or testicular cancer metastasis. T-cell leukemia causes mediastinal adenopathy and enlargement of the thymus, which can compress the SVC. Rare cases of SVCS are attributed to Kaposi’s sarcoma, esophageal cancer, thymoma, mesothelioma, and Hodgkin’s disease (Kaplow & Reid, in press).

Nonmalignant causes of SVCS include tuberculosis, indwelling central venous catheters or pacemaker wires, Silastic or dialysis catheters, aneurysm of the aortic arch, or constrictive pericarditis (Gullatte et al., 2005; Kaplow & Reid, in press).

Because of the location of the SVC (it is surrounded by structures that do not compress), the SVC’s thin walls, and the low presssure of blood flow in the SVC, when regional lymph nodes or the aorta enlarge, the SVC constricts effortlessly, and thus blood flow becomes sluggish and occlusion frequently occurs (Gullatte et al., 2005).

The signs and symptoms of SVCS are related to severity and location of the obstruction. It is usually not until the obstruction is complete that clinical manifestations become obvious. This makes the diagnosis of SVCS more challenging.

Symptoms tend to be more severe when the obstruction is below the azygous vein (Rowell & Gleeson, 2005). The respiratory, cardiac, and CNS systems are affected. CNS manifestations include mental status changes, headache, dizziness (especially when leaning forward), blurred vision, and syncope. Respiratory symptoms are shortness of breath, dyspnea, hoarseness, cyanosis, cough, dysphagia, and stridor. Cardiac symptoms may include edema of the face, arm, and upper chest; dilated veins in the upper torso, shoulders, and arms; jugular venous distention; tachycardia; chest pain; and hypotension. Patients may present with erythema of the eyelids, tightness of the neck (Stokes sign), or periorbital edema (Beckles et al., 2003; Gucalp & Dutcher, 2001; Gullatte et al., 2005; Kaplow & Reid, in press).

Management of SVCS is designed for symptom management and treatment of the underlying cause. If the patient has adequate collateral circulation and symptoms are minimal, treatment may not be required (Hemann, 2001; Wudel & Nesbitt, 2001).

Patients with SVCS should be maintained with the head of the bed elevated. Oxygen therapy may be needed for dyspnea (Thirlwell & Brock, 2003). The patient should be protected from fluid overload. Upper extremity venous catheters should be avoided (Gullatte et al., 2005).

Routinely, management consists of steroids and either chemotherapy or RT. Steroids are usually given to patients receiving RT due to potential radiation-induced edema. If used, high-dose steroids should be given for a limited time period (Kaplow & Reid, in press; Rowell & Gleeson, 2005).

Patients are at risk for bleeding from thrombolytic therapy, anticoagulation, perforation, or hematoma from endovascular procedures. Interventions that are indicated for this include monitoring complete blood cell count and coagulation profiles and maintaining bleeding precautions. If possible, avoid use of a blood pressure cuff on the arm (Kaplow & Reid, in press).

Patients are also at risk for infection from antineoplastic therapy, steroids, or endovascular procedures. They should have their white blood cell count monitored and be considered for prophylactic antibiotics. There is also a potential for dehydration, electrolyte imbalance, and hypotension from diuretic therapy. Monitoring fluid and electrolyte balance, vital signs, and strict I/O are essential (Kaplow & Reid, in press).

The 30-month mortality rate of SVCS is 90%. Relief of symptoms is likely within 1 month of the onset of RT (Gullatte et al., 2005).

An 11% recurrence rate has been reported with stent insertion. A low incidence of complications is reported with stents, especially when thrombolytics are used (Kaplow & Reid, in press; Rowell & Gleeson, 2005).

Patient and family education is needed to increase knowledge of subtle signs and symptoms of SVCS. The patient and family should be taught to observe for complications related to stent placement; these include bleeding from vascular injury and thrombosis within the stent (Kvale et al., 2003). Patients and family members should be taught what to report to their physician so that early treatment can be initiated, if indicated.

Spinal cord compression (SCC) is compression of the thecal sac by a tumor. The compression may be located in the spinal cord or at the level of the cauda equina (Flounders, 2003; Kaplow & Reid, in press; Quinn & DeAngelis, 2000).

Data suggest that 0.2% to 30% of patients with cancer can develop SCC (Crossno, 2004; Kvale et al., 2003; Loblaw, Laperrier, & Mackillop, 2003; Pease, Harris, & Finlay, 2004; Purdue, 2004, Osowski, 2002). There is an incidence of 10%, 70%, and 20% in the cervical, thoracic, and lumbosacral spine, respectively (Crossno, 2004; Kaplow & Reid, in press).

SCC often results from metastatic tumors. The most frequently reported tumors are lung, breast, and prostate. Others include lymphoma, melanoma, GI cancers, seminoma, neuroblastoma, sarcoma, myeloma, and renal cell carcinoma. Patients with primary cancers of the spinal cord are also at risk (Founders & Ott, 2003; Gucalp & Dutcher, 2001; Gullatte et al., 2005; Kaplow & Reid, in press; Tan, 2002).

SCC is classified as either intramedullary (within the spinal cord), intradural (within the dura mater), extramedullary (outside the spinal cord), or extradural (outside the dura mater) (Kaplow & Reid, in press). The latter is the most common type (Founders & Ott, 2003; Tan, 2002). Tumors usually arise from the anterior vertebral body and extend into the epidural space, compressing the spinal cord and vasculature and leading to ischemic damage to motor and sensory pathways and associated gray matter (Gullatte et al., 2005). The tumor applies pressure on the spinal cord, affecting its blood supply. This can lead to infarction or vertebral collapse. When a tumor spreads to the spinal cord, it breaks up the vertebral body, causing it to collapse. The spinal cord compresses as tumor or particles of bone are pushed into the epidural space (Founders & Ott, 2003; Kaplow & Reid, in press).

Most tumors spread to the spinal cord as an embolic process. CNS cancer can also spread to the cerebrospinal fluid. This results in spread to the subarachnoid space, brain, and spinal cord (Founders & Ott, 2003). As the cancer spreads, edema of the tissues and nerves, ischemia, neural distortion, and tissue death result (Kaplow & Reid, in press; Tan, 2002).

Presentation of SCC varies, depending on location and extent of the compression, cause, blood supply involvement, and rapidity of development. Effects can be sensory, motor, and/or autonomic (Founders & Ott, 2003; Gullatte et al., 2005; Kaplow & Reid, in press).

Treatment options include surgery, steroids, RT, and chemotherapy. Goals of therapy are to provide pain relief, restore neurologic function, possibly treat the underlying malignancy, and prevent permanent disability. Management depends on the type of underlying tumor, location, and characteristics (Founders & Ott, 2003; Gullatte et al., 2005; Kaplow & Reid, in press; Osowski, 2002).

When patients with SCC are discharged from the hospital, determination should be made of the need for ambulatory care, visiting nurses, or hospice care (Flounders, 2003). Paralysis or numbness of part of the body is common in patients with SCC. Death is also a possibility if the diaphragm becomes paralyzed (Spinal Cord Trauma, 2005). If a patient has neurologic deterioration or recompresses after undergoing RT, additional RT can be considered. Patients may continue to require physical therapy. Monitoring should include assessment for side effects that can occur with high-dose steroids.

The patient and family must be educated about signs of SCC to report so that treatment can begin when indicated (Loblaw et al., 2003). If the patient is at risk for the development of SCC, the patient and family should be taught to report any new or increase in back pain. The patient and family member should be taught when to call the physician. They should also be taught about side effects of treatment to monitor (Flounders, 2003; Kvale et al., 2003; Osowski, 2002).

Patients with SCC usually have a poor prognosis. The life expectancy may be 3 months or less, but a reasonable quality of life can be attained for that time (Tan, 2002).

Hemorrhage refers to blood loss that is striking and sudden. The incidence of hemorrhage in the palliative care setting is difficult to quantify, since it depends on the cause. It has been found that 20% of patients with a recurrent cancer will sustain a catastrophic bleed. In the case of advanced head and neck cancer, hemorrhage can account for 11.6% of deaths. In one study, 5% of patients died of a carotid artery rupture (British Association of Head and Neck Oncology Nurses [BAHNON], 2005). In a study of patients with acute myeloid leukemia, 44% of patients in the final phase had episodes of bleeding noted (Stalfelt, Brodin, Pettersson et al., 2003).

Patients at risk for the development of hemorrhage are those with head and neck cancer, hematologic malignancies, or any malignancy that is adjacent to a major artery, thrombocytopenia, or coagulopathies. Patients with bladder cancer, hepatocellular carcinoma, or cirrhosis are also at risk (Letier, Krige, Lemmer et al., 2000; Shah, Mumtaz, Jafri et al., 2005; Textor, Wilhelm, Strunk et al., 2000; Uemura, Matsusako, Numaguchi et al., 2005). Any patient who has undergone surgery for head and neck cancer in areas adjacent to the carotid artery is a potential candidate (Casey, 1988; Cohen & Rad, 2004; Freeman et al., 2004). Hemorrhage is a complication of a radical neck dissection (Rodriguez, Carmeci, Dalman et al., 2001). This is especially so if the patient has received RT to the area (Cohen & Rad, 2004). RT to the neck is the most common factor leading to carotid artery rupture (Cohen & Rad, 2004; Rodriguez et al., 2001). Patients may also develop carotid artery rupture related to direct tumor invasion leading to damage to the arterial wall (BAHNON, 2005).

With head and neck cancer, hemorrhage may occur either externally from the neck, internally from within the oropharynx, or directly into the airway or tracheostomy (Cohen & Rad, 2004; Lovel, 2000).

There are several pathophysiologic reasons for a patient to develop hemorrhage. These include vessel injury, platelet dysfunction, coagulopathies (e.g., disseminated intravascular coagulation), and changes in viscosity of blood. If a tumor invades a blood vessel, significant and sudden blood loss can occur. Bone marrow failure or tumor invasion into the bone marrow can cause thrombocytopenia. If the patient develops liver failure, bleeding problems may ensue. Several medications can also lead to hemorrhage as a side effect (Heidrich & McKinnon, 2002).

Patients should be assessed for risk of bleeding based on past medical history. Factors to consider include type and location of malignancy. Patients with head and neck or GI malignancies are at the highest risk for hemorrhage. Patients who have received chemotherapy or RT are at risk due to myelosuppressive toxicities of these therapies. Surgical patients may also be at risk depending on the extent of the procedures. In addition, tumors themselves can disturb vasculature, placing the patient at risk for hemorrhage (Heidrich & McKinnon, 2002).

A complete history may assist the clinician to identify patients at risk for hemorrhage. A patient history should include determination of whether the patient has had bleeding from any site in the past, degree of bleeding, and what interventions were used. The location of tumors, history of antineoplastic therapies and dates of these therapies, any hepatic dysfunction, and the patient’s medication profile will all provide clues for the risk of hemorrhage (Heidrich & McKinnon, 2002).

Patients with minor bleeding from a wound, a flap site, a tracheostomy, or the mouth may hemorrhage. This is caused by a small rupture of the intima (BAHNON, 2005). Some patients manifest ‘pulsations’ from artery or tracheostomy or flap site, or report sternal or high epigastric pain several hours before rupture Some patients develop ‘ballooning’ of an artery prior to carotid artery rupture (BAHNON, 2005; Lovel, 2000).

Laboratory tests may provide clues as to the etiology of hemorrhage. These include platelet count, coagulation profile, and liver function tests. Determination of any herbal or over-the-counter remedies that the patient has taken may help identify the cause as well (Heidrich & McKinnon, 2002).

There are only a small number of alternatives to treat a patient in the palliative care setting who is hemorrhaging (Puetz & Bourhasin, 2002). Much of the data reported are in the form of case studies rather than clinical trials.

The patient’s coagulation profile and platelet count should be monitored. If the patient is receiving anticoagulants, these will need to be adjusted. Administration of blood products may be considered, but this can pose a challenge in the home or hospice setting. A case report describes the use of an agent, recombinant factor VIIa, that was effective in the palliative care setting (Puetz & Bourhasin, 2002).

Some patients with head and neck cancer have a particular event to achieve and wish to avoid imminent death. For these patients, additional head and neck surgery may be attempted to decrease the likelihood of a bleed. However, there are risks associated with the surgery that warrant consideration. Ligation of the involved artery to avoid carotid artery rupture carries a mortality risk of 32% to 77%, and 12% to 50% of survivors experienced permanent neurologic defects (BAHNON, 2005). Endovascular embolization of the carotid artery is considered an alternative method to avoid carotid artery rupture. This procedure has a lower (0% to 10%) mortality rate and fewer (10%) patients have neurologic damage (Luo, Chang, Teng et al., 2003). Superselective embolization with a substance, Ethibloc (Ethicon, Inc., Somerville, NJ), has been reported in the literature. This procedure was recommended for use as palliative treatment for select patients with advanced head and neck cancer (Sittel, Gossman, Jungehulsing et al., 2001).

Intraarterial embolization therapy is suggested as a treatment option for patients with urinary bladder hemorrhage from bladder cancer. Intraarterial chemoperfusion with mitoxantrone may also be effective, depending on the acuity of the bleeding (Textor, Wilhelm, Strunk et al., 2000).

Management of GI bleeding is dependent on the source. For the patient with cancer, it may require a multidisciplinary approach with a medical, surgical, and radiation oncologist (Imbesi & Kurtz, 2005). Strategies to control bleeding may include combined treatment of sclerotherapy and octreotide infusion over 48 hours for patients with acute variceal bleeding resulting from cirrhosis, or sclerotherapy alone in patients with acute variceal bleeding from hepatocellular carcinoma (Letier et al., 2000; Shah et al., 2005).

One case report describes relief of pain in a patient with hepatocellular carcinoma with hemorrhagic metastasis. This patient received percutaneous sacroplasty with combined injections of bone cement and n-butyl cyanoacrylate (Uemura et al., 2005).

In the event of hemorrhage, it is essential that a clinician remain with the patient, avoid panicking, and call for help. Towels should be applied to the bleeding site for absorption, if possible. If the patient has a tracheostomy, inflate the cuff to avoid choking. Gentle suctioning to the mouth and tracheostomy site should be applied as necessary to avoid sensation of choking, since this may add greatly to distress (BAHNON, 2005).

Patients should be spoken to gently and calmly, and attempts should be made, if possible, to keep the patient in one place. It is important to be aware of family presence and needs. It is ideal to determine in advance whether the family wishes to stay with the patient and important to be respectful of their wishes. If the family elects to stay with the patient, it is vital to ascertain that support is given (BAHNON, 2005).

The patient experiencing hemorrhage should be sedated. Administration of intravenous midazolam has the most rapid onset. If the patient does not have intravenous access, subcutaneous or intramuscular administration is possible. The dose may then be titrated until the patient is fully sedated (BAHNON, 2005).

Witnessing a hemorrhage can be very frightening for the family. Families should be referred to a counselor for support following such an episode. In addition, steps to prevent hemorrhage or minimize blood loss should be undertaken (Heidrich & McKinnon, 2002).

Although the risk for major hemorrhage is very rare, the fear is very realistic and present for the patient and family. If the patient is at risk for major hemorrhage, the patient and family must be prepared for this possibility (Feber, 2000). Management of the bleeding and treatment will depend on decisions made between the patient and family. If the patient’s life expectancy and quality of life warrants, management of hemorrhage consists of general resuscitative measures, such as volume replacement and specific measures to stop the bleeding. If the patient’s goals are palliative, management may include measures to stop bleeding without full resuscitative measures. Comfort measures only may be most appropriate for end-stage patients (Pereira & Phan, 2004).

Medication should be available in event of the emergency. For patients at home, where intravenous access is not possible, families can be taught how to administer injectable midazolam. If family members do not feel able to do this, an alternative is rectal diazepam (BAHNON, 2005).

The family should be advised to have equipment such as dark towels, gloves, and buckets readily available. The patient should be encouraged to wear dark undergarments or pads. Use of green or blue toilet disinfectant is recommended to disguise blood loss (depending on the site of bleeding) if the patient or family is frightened (North Cumbria Palliative Care, 2005).

A seizure is a symptom of irritation to the CNS resulting in excessive and abnormal neuronal discharges. An acute seizure refers to 5 minutes or more of either continuous seizures or two or more seizures between which there is incomplete return to consciousness (Regional Palliative Care Program [RPCP], 2005).

Patients at risk for the development of seizures are those with primary or metastatic cerebral tumors. Cancers that metastasize to the brain include breast, lung, melanoma, kidney, leukemia, and lymphoma. Leptomeningeal disease and AIDS have been implicated as well (Fox, 2001; RPCP, 2005; Vaicys & Fried, 2000). Patients with HIV/AIDS may develop seizures secondary to opportunistic infection (Papadakis & McPhee, 2005). Seizures reportedly occur in 25% to 30% of patients with cerebral cancer (RPCP, 2005).

Noncancer causes of seizures include metabolic alterations, infection, medications, drug withdrawal, intracranial hemorrhage, increased intracranial pressure, SIADH, encephalopathy, and hypoxia (Paice, 2001).

A seizure occurs when a large number of neurons discharge in an unusual manner. This results in paroxysmal behavioral changes. The two types of seizures described in the literature are generalized and focal. Generalized seizures involve large portions of the brain, whereas focal seizures involve specific areas of the brain (Paice, 2001).

Patients with a history of seizures or untreated myoclonus are at risk to develop seizures (RPCP, 2005). A review of the medications the patient has received may provide valuable information. Patients should also be questioned regarding use of recreational drugs (Paice, 2001).

A complete history should be taken to determine what symptoms were present upon the start of seizure activity, the type of seizure activity, and presence of an aura before the seizure started (Paice, 2001).

Laboratory tests should include assessment for hypoglycemia and electrolyte abnormalities. Renal and liver function tests should also be assessed (Papadakis & McPhee, 2005). If the patient is currently receiving anticonvulsants, obtaining serum levels may be indicated to determine if the medication is being absorbed (Paice, 2001).

Electroencephalography can be performed to help classify seizure activity and presence of a seizure disorder. MRI can be done if there are focal neurologic signs or symptoms, focal seizure, or focal electroencephalographic imbalance (Papadakis & McPhee, 2005). If the patient has a brain lesion, evaluation may be accomplished with either MRI or CT scanning (Paice, 2001).

Prophylactic measures are usually recommended in patients who have had a seizure. Phenytoin and phenobarbital are the most commonly used anticonvulsants. Valproic acid is the second most common medication used. Management of actual seizures includes administration of medications. A benzodiazepine or phenytoin may be used. If patients are unable to tolerate oral medications, phenobarbital may be administered subcutaneously. Although rare, if seizures persist, a continuous subcutaneous midazolam infusion may be used (RPCP, 2005).

While having a seizure, the patient should be protected from self-injury, turned on the side, and provided with oxygen if applicable. If hypoglycemia is the cause of the seizure, the patient should receive intravenous glucose (RPCP, 2005).

If the patient develops medication side effects before reaching therapeutic levels of the agent, it is recommended that the dosage be decreased or an alternative agent be tried. If the patient continues to have seizures and is free of side effects but has a high serum concentration of the agent, a higher dose of medication should be administered (RPCP, 2005).

If a patient is at risk for the development of seizures, the patient and family should be informed of this likelihood. They should be taught what to observe for and expect and interventions that can be implemented (RPCP, 2005). Like the sight of blood, seizures can be very frightening, but they can be managed at home by family members who can be taught to give the patient medication. Family members should also be taught that a seizure is brief and self-limited and that it is rarely the patient’s cause of death. Family should be instructed to call the physician once the seizure activity has stopped (RPCP, 2005).

Family members should be taught to remove items that might cause harm to the patient during the seizure and the placement of pillows in strategic places to prevent trauma. They can also be shown ways to protect the patient’s airway during the seizure and to refrain from giving the patient anything orally until full consciousness is restored after the seizure (Paice, 2001).

Patients may benefit from an environment low in stimulation while recovering from the seizure. They should be spoken to softly and with reassurance (Paice, 2001).