oncological definition causes and symptoms management

1. Oncological
emergencies
Presentedby,
M.Josephin.,
tutor

2. Types
MetabolicOncologicEmergencies
• Tumor Lysis Syndrome (TLS)
• Sepsis & Septic Shock
• Disseminated Intravascular
Coagulation (DIC)
• Hypercalcemia
• Syndrome of Inappropriate
Antidiuretic Hormone Secretion
(SIADH)
StructuralOncologicEmergencies
• Spinal Cord Compression
• Superior Vena Cava Syndrome
• Cardiac Tamponade

3. tumor Lysis syndrome(tls)
• Metabolic imbalance Caused by
breakdown of malignant cells
• Large number of rapidly proliferating cells
killed
• Cell Lysis, rupture of tumor cell
membranes
• Intracellular components released into
blood stream

4. tumor Lysis syndrome(tls)
Intracellular components
 Potassium
 Phosphorous
 Nucleic acids (DNA, RNA)
 Cell killed (lysed), cell membrane ruptures
 Nucleic acids released into blood stream
 Potassium & Phosphorous released into blood stream
Results in:
 Hyperuricemia
 Hyperkalaemia
 Hypophosphatemia
 Hypocalcaemia

5. Most common in: Patients with large Tumor burden that is highly responsive to
antineoplastic therapy (resulting in rapid cell kill)
Tumor-related
High-grade lymphomas
Risk for Hematologic malignancies (acute or chronic leukemia's with increase WBC)
Risk for Tumours with high growth fractions (anticipated to be responsive to treatment)
Patient-related
Large Tumor burden/bulky tumours
Elevated LDH
Pre-existing renal dysfunction
Treatment-related
Chemotherapy & biologic agents
Radiation therapy
Risk factors

6.  Onset: Usually within 12-72 hrs. after initiation of
antineoplastic therapy
 Duration: May persist for 5-7 days post-therapy
 Incidence: Exact incidence unknown, Occurs
mostly in patients with
• Hematologic malignancies with large proliferative
growth fractions
• Large bulky disease (acute leukaemia's, high-grade
lymphomas

7. Clinical manifestations
 Often asymptomatic initially
 Detected initial via abnormalities in blood chemistries
 Signs & symptoms patients exhibit depend on extent of
metabolic abnormalities
◦ Hyperkalaemia
◦ Hyperuricemia
◦ Hypophosphatemia
◦ Hypocalcaemia

8. management
Prevention Strategies
 Recognition of at-risk patients
 Prevention of hyperuricemia
 Frequent monitoring of electrolytes
Intervention Strategies
 Hydration
 IV Normal saline or 5% dextrose, begin 24 – 48 hours prior to therapy and
ensure urine output >150 – 200 ml/hr
 Control of hyperuricemia
 Aggressive correction of electrolytes
 Management of acute renal failure

9. management
 Monitor serial lab values
 Serum potassium, phosphorous, calcium, uric acid
Renal function studies – BUN & creatinine
 Frequency of monitoring
 ◦ Prior to initiation of therapy Every 8 – 12 hours
during the first 48 – 72 hours of treatment

10. Nursing intervention
Recognize patients at risk
• Leukemia, lymphoma, small-cell lung cancer
• Large tumors with large growth fractions or elevated LDH
• Recent chemo or radiation therapy
• High LDH, concurrent renal disease
 Careful assessment of fluid balance
 Patient teaching – strategies to reduce incidence or severity of
symptoms
 Maintain adequate oral fluid intake
 Take Allopurinol as ordered Signs & symptoms to report to health
care team

11. Sepsis and septic shock
Septicaemia: Invasion of blood by microorganisms Sepsis:
Systemic response to infection (vasodilation, displacement of
intravascular volume)
Septic Shock: Vascular collapse caused by vasodilation, leakage
intravascular volume into interstitial space
Continuum Septic Shock:

12. Risk factor
Neutropenia
◦ Single most important risk factor ◦ Increased duration and severity of
neutropenia increases risk
Treatment-related risk factors
◦ Chemotherapy
◦ Biotherapy
◦ Radiation
◦ therapy
◦ Infiltration of bone marrow by solid tumor
Patient-related
◦ Disruption in mucosal barriers
◦ Splenectomy and functional asplenia
◦ Corticosteroids or other immunosuppressant's

13. pathophysiology
Micro-organisms in blood stream release chemical mediators &
hormones
◦ Endotoxins – released by gram negative bacteria
◦ Exotoxins – released by gram positive bacteria
Profound systemic vasodilation
◦ Hypotension
◦ Tachycardia
Increased vascular permeability
◦ Fluid leaks from vascular space to interstitial space
◦ Decreases circulating blood volume
◦ Hypoxic tissues
◦ Metabolic acidosis

14. Causes of sepsis
 Escherichia coli
 Klebsiella pneumoniae
 Pseudomonas aeruginosa
 Gram-positive bacteria (increased incidence due to
use of vascular access devices)
 Streptococcus pneumoniae
 Staphylococcus aurous
 Corynebacterium
 Invasive fungal infections, viruses

15. Diagnostic evaluation
• CBC with differential
• Complete metabolic panel
• Serum lactate
• Blood cultures X 2
• Cultures of body fluids
• Urine, stool, throat, wounds, sputum
• Chest X-Ray

16. Treatment of sepsis
• Immediate initiation IV antibiotics (within 3
hours)
• Fluid resuscitation
• Goals:
◦ MAP: > 65 mmHg
◦ CVP: 8-12 mmHg
◦ Urine output: > 0.5 mg/kg/hr
• Oxygen therapy
• Antipyretics

17. Nursing management
• Frequent vital signs & assessments
◦ LOC, skin colour & temp, lungs
• Ensure antibiotics administered within 3 hours
• Maintain oxygenation
◦ Oxygen therapy & ventilator support
• Administer IV fluids,
◦ Expand intravascular volume (fluid resuscitation)
• Monitor I & O
• Antipyretics
• Assess for fluid overload

18. Disseminatedintravascular coagulation
• Disseminated intravascular coagulation (DIC) involves an
abnormal activation of the clot formation and fibrin
mechanisms in the blood, resulting in the consumption of
coagulation factors and platelets. Patients with DIC are at high
risk for thrombus formation, infarctions, and bleeding.
• Syndrome of:
◦ Thrombus formation (clotting)
◦ Simultaneous Hemorrhage
• Caused by over stimulation of normal coagulation processes

19. causes
• Acute Promyelocytic Leukemia (APL)
• Solid Tumours (adenocarcinomas)
• Chemotherapy
• Infection/sepsis
• Hemolytic transfusion reaction

20. Types of dic
Acute DIC
• Medical emergency
Chronic DIC
• Produces coagulation abnormalities, with or without clinical
manifestations, that can be medically managed
• Most cases of chronic DIC due to underlying malignancy

21. Diagnosis

22. Clinical manifestation
Decreased tissue/organ perfusion
◦ Brain, CV, Lungs, Kidney, GI Tract, Skin
Decreased platelet count
◦ Petechiae, ecchymosis
Haemorrhage
◦ Tachycardia, hypotension
◦ Tachypnea
◦ Overt bleeding
◦ Occult bleeding

23. Treatment
Early recognition & treatment of underlying disorder
◦ Chemotherapy for malignancy
◦ Antibiotics for infection
Correct hypoxia
◦ Oxygen to maintain saturation >95%
Correct hypovolemia, hypotension and acidosis
◦ Normal Saline
◦ Blood transfusion if needed

24. Treatment
Stop the micro clotting to maintain perfusion & protect vital function
◦ IV Heparin
◦ Anti thrombin III (inhibits action of thrombin)
Stop the bleeding
◦ Pressure to active sites of bleeding
◦ Blood products (FFP, cryoprecipitate, platelets,
◦ red blood cells)
◦ Antifibrinolytic agents (EACA)

25. Nursing intervention
Prevent severity of symptoms
◦ Direct pressure sites of bleeding, pressure dressings, sand bags
Monitor for progression DIC
◦ Worsening vital signs, hypotension, anuria and LOC
Monitor response to therapy
◦ Sites & amounts of bleeding
◦ Changes in lab values
◦ Assess tissue perfusion parameters – colour, temperature, peripheral pulses
Patient Teaching
◦ Avoid ASA or NSAID’s (effects on platelet aggregation)
◦Signs and symptoms of DIC (bleeding and/or clotting)

26. Hypercalcemia of malignancy
• It is a metabolic disorder, most commonly develops as a
consequence of pathologic destruction of bone, mediated by
factors released by malignant cells
• One of the most common, life-threatening complications of
malignancy

27. Normal regulation of calcium
• Parathyroid gland
◦ Production of parathyroid hormone (PTH)
◦ PTH is major hormone regulating extracellular Ca++
• PTH increases Ca++ by 3 mechanisms:
◦ Direct action on bone
Stimulates activity of osteoclasts → breaks down bone (bone
resorption)
◦ Direct action on kidneys
Increases renal excretion of phosphate stimulates reabsorption
of Ca++
◦ Indirect action in gut
Enhances absorption of ingested Ca++ by stimulating kidney
conversion of vitamin D to biologically active form

28. Distribution of calcium
• Bone stores: 99% of body’s calcium
• Serum calcium: 1% circulates in serum,
divided into fractions:
◦ 50% is free ionized calcium
◦ 40% is bound to protein

29. etiology
• Tumor-induced bone breakdown releasing Ca++
into bloodstream
• Tumor secretion of a parathyroid hormone-related
protein
• Squamous cell tumors: Lung, breast, prostate, head
& neck, esophagus, kidney
• chronic myeloid leukemia (blast phase), adult T-
cell leukemia – lymphoma

30. Signs & symptoms
• Lethargy, confusion
• Cardiac dysrhythmias
• Constipation
• Muscle hypertonia

31. Nursing intervention
• Careful monitoring of patients taking
• Digitalis preparations (action potentiated in
Hypercalcemia states)
• Measures to decrease calcium removal from bone
• Fluid balance & renal function
• GI motility , Cardiac Status and Mental status

32. Syndrome of inappropriate antidiuretic hormone
• Syndrome of inappropriate antidiuretic hormone
(SIADH) is a Paraneoplastic endocrine disorder
associated with several malignancies

33. causes
• Pain
• Stress
• Nausea
• Surgery
• Pulmonary disease
• Central nervous system disorders
• Physical and emotional stress

34. treatments
• Restrict fluids: (500–1000 mL/day)
• Perform neurologic assessment
• Institute effective anticancer treatment
• Monitor sodium levels
• Demeclocycline (600–1200 mg/day)
• Monitor renal function with demeclocycline therapy
• Assess other causes
• Institute seizure precaution

35. Structural oncologic emergencies
• Spinal Cord Compression
• Superior Vena Cava Syndrome (SVCS)
• Cardiac Tamponade

36. Spinal cord compression
• Spinal cord compression occurs when a malignant growth
compress the spinal cord. Patients at risk include those with
cancers that spread to the bone and spinal cord, such as lung,
breast, and prostate cancer.
Symptoms
• Pain
• Motor dysfunction

37. Spinal cord compression
• Compression of spinal cord
Direct Tumor pressure on cord
Tumor invasion of the vertebral column causing collapse & pressure on
cord
• Compression causes:
◦ Edema
◦ Inflammation
◦ Mechanical compression
• Leads to:
◦ Direct neural injury to cord
◦ Vascular Damage

38. Symptoms

39. Diagnostic evaluation
• MRI
• Spinal x-rays
• CT scan
• Bone scan and/or PET scan
• Histology of primary Tumor

40. treatment
• IMMEDIATE & AGGRESSIVE
• Corticosteroids – usually initial treatment
• High-dose steroids to decrease spinal cord edema & inflammation
• High-dose Dexamethasone (16 mg loading, short course of 16 mg daily)
followed by tapering doses over several days

41. Superior vena cava
• Superior vena cava syndrome (SVCS) occurs in patients with lung
cancer or cancers of the mediastinum when the tumor or enlarged
lymph nodes block circulation in the vena cava.
• This results in edema of the head, neck, and arms.
• Obstruction of blood flow through the superior vena cava (SVC)
• Obstruction leads to venous return from head, neck, upper arms,
upper thorax impaired
• Venous pressure increases

42. Causes
• Lung Cancer
• Non-Hodgkin Lymphoma
• Solid tumours lymph node metastasis (e.g. breast cancer)
• Post-radiation fibrosis
• Non-Malignant Causes
• Related to indwelling central venous catheter
• Mediastina fibrosis Related to infection
• Benign mass

43. symptoms
• Dyspnoea
• Facial and neck swelling
• Sensation of fullness in head
• Cough
• Arm Swelling
• Chest pain
• Venous distention of neck & chest wall
• Cyanosis of face & upper torso
• Decreased or absent

44. Diagnostic evaluation
• Based on characteristic signs & symptom of central
venous obstruction
• Imaging studies
• Chest x-ray
• Computed tomography scan (contrast enhanced)
• MRI
• Histologic diagnosis

45. treatment
• Radiation Therapy
• Chemotherapy
• Primarily treatment for chemo-sensitive malignancies
• Small cell lung cancer
• Non-Hodgkin lymphoma
• Surgical intervention
• Thrombolytic therapy
• SVC caused by intraluminal thrombus

46. Pericardial effusion
• Pericardial effusion is caused by direct invasion
of the cancer into pericardium. The pericardial sac
fills with fluid and may lead to life-threatening
compression of the heart (called Tamponade).
Signs and symptoms
◦ Chest Pain
◦ Dyspnea
◦ Low Blood Pressure
◦ Distant Heart Sound

47. etiology
• Patients with cancer may develop a pericardial
effusion due to a variety of reasons.
• Secondary to metastatic disease of the pericardium
• Breast and lung cancers, leukemia, and lymphoma.
• Metastatic disease to the heart
• Primary heart malignancies

48. pathophysiology

49. symptoms
• Dysphagia, cough, heaviness
• hoarseness, hiccups
• Dullness to percussion,
• weak heart sounds, chest
• fullness/discomfort Nausea
• vomiting, diarrhoea
• hepatomegaly
• abdominal distention

50. Treatment
• Fluid and water restriction.
• Stop the buildup of excess fluid in the body.
• Vasopressin antagonists.
• These medications block the action of the vasopressin.
Surgery.
• Severe and/or chronic SIADH may require surgical
intervention wherein the surgeon removes the tumor that
produces ADH.