GROUP 5 PALLIATIVE-ONCOLOGICAL EMERGENCIES.pdf

A TERM PAPER ON ONCOLOGICAL EMERGENCIES AND MANAGEMENT SUBMITTED BY GROUP 5 MEMBERS AMMEH EDEBO-OJO OLUWATUMININU 205087 ADEBOYE ADEIFE ANTHONIA 205082 BALOGUN SEKINAH OLAMIDE 205091 OLAWUNI FEHINTOLA AANUOLUWA 205096 OMOLOSO IBRAHIM OLAMIDE 206848 IN PARTIAL FULFILMENT OF THE AWARD OF BACHELOR OF N...

A TERM PAPER ON ONCOLOGICAL EMERGENCIES AND MANAGEMENT SUBMITTED BY GROUP 5 MEMBERS AMMEH EDEBO-OJO OLUWATUMININU 205087 ADEBOYE ADEIFE ANTHONIA 205082 BALOGUN SEKINAH OLAMIDE 205091 OLAWUNI FEHINTOLA AANUOLUWA 205096 OMOLOSO IBRAHIM OLAMIDE 206848 IN PARTIAL FULFILMENT OF THE AWARD OF BACHELOR OF NURSING SCIENCE, DEPARTMENT OF NURSING, UNIVERSITY OF IBADAN COURSE CODE: NSG 528 COURSE TITLE: COMMUNITY HEALTH NURSING LECTURER-IN-CHARGE: DR. IFEOLUWA KOLAWOLE 16TH FEBRUARY, 2024 TABLE OF CONTENT Title page Table of content Introduction Metabolic Oncological Emergencies Hypercalcemia Hyponatremia SIADH Neurologic Oncological Emergencies Malignant spinal cord compression Brain metastasis causing ICP Cardiovascular Oncological Emergencies Malignant pericardial effusion Cardiac tamponade Superior vena-cava syndrome Pulmonary Oncological Emergencies Pulmonary embolism Massive hemoptysis Diffuse alveolar haemorrhage Haematologic Oncological Emergencies DIC Hepatic veno-occlusive disease Infectious Oncological Emergencies Neutropenic fever Surgical Oncological Emergencies Obstruction Infection Perforation Bleeding Others Pathological fractures Conclusion Reference 1 2 2 2 5 8 11 11 14 18 18 20 22 26 26 29 31 34 34 36 38 38 41 41 46 47 49 52 52 53 54 1 ONCOLOGICAL EMERGENCIES INTRODUCTION The patients with cancer may develop an emergent clinical situation due to the cancer or as a complication of therapy. These emergent clinical situations can affect any of the body systems, including; metabolic, neurologic, cardiovascular, pulmonary or haematologic systems. The emergencies can also be Infectious or surgical complications. A. METABOLIC ONCOLOGICAL EMERGENCIES HYPERCALCEMIA This is a high in calcium level in the blood serum. The normal range is 2.1-2.6mmol/L (8.810.7mg/dL, 4.3-5.2 mEq/L) with levels greater than 2.6mmol/L defined as hypercalcemia. Those with a mild increase that has developed slowly typically have no symptoms. Pathophysiology: Hypercalcemia will be experienced by up to one-third of cancer patients at some point in their disease course. Among patients hospitalized for hypercalcemia, malignancy is the most common cause, although primary hyperparathyroidism is much more prevalent in the general population. Breast, lung, and renal cell carcinomas; multiple myeloma; and adult T-cell leukemia/lymphoma are the prevailing causes of hypercalcemia. Bone metastases may also cause a local paracrine effect by producing several factors that stimulate osteoclasts, leading to bone resorption with resultant hypercalcemia and bone destruction. This is most commonly seen in metastatic breast cancer and multiple myeloma. Prostate cancer, despite the frequency with which it metastasizes to bone, only rarely causes hypercalcemia. Signs and symptoms The symptoms of hypercalcemia are nonspecific, and delayed recognition of this metabolic derangement can worsen morbidity and mortality. The mnemonic “bones, stones, moans, and groans” is used to emphasize skeletal pain, nephrolithiasis, abdominal discomfort, and altered mentation as presenting symptoms. Bone pain is usually related to discrete metastasis rather than diffuse liberation of calcium. Even in the setting of profound hypercalciuria, not all patients will form kidney stones, which may be due to differences in the urine mineral concentration needed to precipitate calculi. Abdominal pain can arise from dysregulated intestinal motility, pancreatitis, or 2 severe constipation. Changes in sensorium can occur along a spectrum from lethargy to coma. In addition, hypercalcemia shortens the QT interval and can produce cardiac arrhythmias. Other signs and symptoms include fatigue, lethargy, constipation, stupor and coma. Fig.1. Signs and symptoms of hypercalcemia Diagnosis Ionized calcium is the most reliable laboratory test with which to detect hypercalcemia and is considered to be elevated when above 1.29 mmol/L.11 If measuring total calcium, it is important to correct for hypoalbuminemia, using the following formula: corrected calcium in mg/dL = measured total calcium in mg/dL + 0.8(4 − measured albumin in g/dL).12 There is no absolute level of calcium at which patients will become symptomatic, and the rate of increase is likely more significant than the magnitude of elevation; relatively high levels may be well tolerated if the rate of increase has been gradual. Measuring parathyroid hormone-related peptide (PTHrP) has not been proven to affect outcome and should not guide initial management. Serum chloride is a more readily available test, and hypochloremia less than 100 mEq/L supports a diagnosis of humoral hypercalcemia. PTH levels can be checked to investigate the possibility of primary hyperparathyroidism; however, PTH levels 3 are often low in patients with humoral hypercalcemia due to suppression of endogenous PTH release by PTHrP-mediated negative feedback. Medical management In patients with advanced malignancies in whom efforts to lower calcium do not demonstrably prolong life, there can be a palliative benefit to improving the symptoms of hypercalcemia. Urgent intervention is needed to normalize symptomatic hypercalcemia. Table 1. Pharmacological management of hypercalcemia Hydration is the cornerstone of initial management because almost all patients with clinically meaningful hypercalcemia have intravascular volume depletion. Correction of volume depletion will help to restore a brisk urine output. If the patient has intact left ventricular systolic function, normal saline can be safely infused at rates up to 500 mls/hour until hypovolemia has resolved. At that time, loop diuretics, such as 40 mg of furosemide intravenously (IV) every 12 to 24 hours, can be initiated to promote calciuresis. Thiazide diuretics should be avoided as they increase calcium reclamation from the urine. 4 Hemodialysis may be a faster and less hazardous method of correcting hypercalcemia in patients with diminished kidney function. Dialysis also allows calcium attenuation in the setting of congestive heart failure or other conditions that preclude the administration of high volumes of intravenous fluids. Glucocorticoids, such as 60 mg of prednisone orally daily or 100 mg of hydrocortisone iintravenously every 6 hours, can be helpful in mediating the release of cytokines and prostaglandins that stimulate osteoclasts. Nursing management Assess the level of consciousness and neuromuscular status, including muscle tone, strength, and movement. Auscultate bowel sounds Monitor cardiac rate and rhythm. Be aware that cardiac arrest can occur in a hypercalcemic crisis. Monitor intake and output; calculate fluid balance. Strain urine if flank pain occurs. Encourage fluid intake of 3 to 4 liters per day, including sodium-containing fluids (within cardiac tolerance) Encourage frequent repositioning and range-of-motion (ROM) and/or muscle-setting exercises with caution. Promote ambulation as tolerated. Monitor laboratory studies such as calcium, magnesium, and phosphate. Administer prescribed medications as scheduled HYPONATREMIA The assessment of hyponatremia in cancer patients, as in all patients, requires a critical determination of volume status. Fluid in the body is divided among compartments: the circulatory volume (plasma), the interstitial space outside the vasculature, and the cells. Osmotic gradients drive fluid between compartments, with movement toward higher concentrations. The sodium concentration is the largest contributor to plasma osmolarity and reflects how much water is present in the blood relative to the cells, in which the majority of the body's water is stored. Laboratory measurement of the sodium concentration thus reveals the distribution of water among 5 the body's fluid compartments, and hyponatremia means that intravascular water is present in excess relative to sodium, either through water retention and/or sodium loss. Presentation The amount of sodium in the body, not the plasma sodium concentration, determines the volume of fluid outside the cells, and this volume can be readily measured by physical examination. If the total body sodium is high, then the extracellular fluid volume is large and the patient will appear edematous. If the total body sodium is low, then the extracellular space (including the circulatory volume) will contract and the patient will progressively develop tachycardia and hypotension. A low plasma sodium concentration can thereby be associated with clinical hypervolemia, hypovolemia, or euvolemia, depending upon total sodium content. The physician must correctly evaluate the hyponatremic patient's volume to understand both their sodium and water balance and then select the appropriate treatment. Euvolemic hyponatremic patients with cancer have normal extracellular fluid volume, reflecting appropriate total sodium content, but excessive water in the intravascular space, most commonly mediated through the syndrome of inappropriate antidiuretic hormone (SIADH). Antidiuretic hormone promotes free water uptake in the distal tubules by binding to the vasopressin 2 (V2) receptor. Compounding the problem is continued free water intake because the thirst mechanism is not sufficiently inhibited. SIADH should be suspected based upon the location of primary and metastatic tumors because SIADH is more commonly encountered in diseases originating in or involving the lungs, pleura, thymus, and brain.10% to 45% of patients with small cell lung cancer will show evidence of SIADH. Iatrogenic causes of hyponatremia include cisplatin, cyclophosphamide, ifosfamide, the vinca alkaloids, and imatinib. Each of these drugs can cause SIADH, but all can also produce hyponatremia through a variety of other mechanisms (e.g, platinum-induced salt-wasting nephropathy), and therefore careful evaluation is required to determine the underlying etiology of hyponatremia in patients receiving these medications. Drugs with high emetogenic potential can stimulate ADH release through nausea, an appropriate physiologic response that may be confused with SIADH. Diagnosis: Hyponatremia can be classified as mild (131-135 mmol/L), moderate (126-130 mmol/L), or severe (