Onco Emergency 2020.pptx

Oncologic Emergency
By Ame M.(BSc, MSc in EMCCN)

INTRODUCTION AND GENERAL OVERVIEW OF
CANCER
• Cancer is a disease process in which healthy cells stop
functioning and maturing properly.
• Most often triggered and started because of DNA mutation,
the end result is the same.
• There is an accelerated process of inappropriate uncontrolled
cell growth – a chaotic process that is abnormal.
• Cancerous cells represent the summation of the body’s
response to a continuous attack on its balancing and regulatory
mechanisms by over 30 known factors and countless more.

CANCER
• “The tumor is not part of the human organism, but represents
a rebellion of the cells against the human organism.
• Consequently, cancer should be considered a disease of the
whole organism, not a disease of cells.”
• On a simplistic level, cancer can be viewed as the result of a
gradual systemic poisoning and weakening of the body’s
immune system by a multiplicity of stress factors collectively
known as carcinogens.

CANCER
• These carcinogens, used in a broad sense here for the sake of easy
understanding, include(just to name a few):
– chemicals,
– electromagnetic energy,
– a faulty diet,
– free radicals,
– genetic disposition,
– toxic metal buildup,
– radiation,
– parasites,
– viruses, and
– emotional stress.
• It is the summation of all these carcinogens and immune-suppressing
agents acting collectively on our biochemical and psychological makeup
that facilitates cancer cell development.

INTRODUCTION AND GENERAL OVERVIEW
OF CANCER
Basic Cancer biology
Cancer is a result of gene mutation, either in:
Oncogenes (genes that are typically involved in some component
of the cell cycle, now altered)
Tumor suppressor genes (genes that usually regulate cell cycle
and apoptosis that may become mutates, removing the “brakes”
from the cell cycle
Sometimes an accumulation of somatic mutations must occur
before the cancer develops.

What Is Cancer?
• Cancer
– a large group of diseases ch’zed by the uncontrolled growth and
spread of abnormal cells.
• Neoplasm
– new growth of tissue that serves no physiological function
• Tumor
– clumping of neoplasmic cells
• Metastasis
– malignant tumors that are not enclosed in a protective capsule &
have the ability to spread to other organs

Characteristics of Cancer Cells
After the billions spent on research, we now know the
following characteristics of cancer cells.
These characteristics are of fundamental importance.
All cancer treatments, conventional or otherwise, focus on
manipulating the cell and its environment.
Knowing the characteristics is therefore a key to winning the
cancer war.
These characteristics are:

Cancer cells
have greatly prolonged life spans compared to normal cells.
fail to develop the specialized functions of their normal counterparts.
Masses of cancer cells may become like parasites,
developing their own network of blood vessels and siphoning off key
nutrients from the body.
Cancer cells
prefer sugar as source of energy as compared to normal cells which favor
oxygen.
are more sensitive to heat and less able to tolerate high temperature
compared to normal cells.
form a tumor, or a swelling caused by the abnormal growth if left
unchecked.

The tumor can invade adjacent normal tissue or spread
through lymph vessels or the blood vessels to other normal
tissues.
Cancer cells
are usually benign and are carried by many people within their body.
Such benign tumors are encapsulated by fiber and insulated
from the body and from their toxins.
Cancers that metastasize quickly are less mature and more
aggressive.
They are more malignant.

aggressive cancer has a doubling time of 60 days or less;
moderate cancer doubles in 61-150 days, and
indolent cancer doubles in 151-300 days, and
very indolent cancer takes 300 days or more.
The average size of a breast cancer when first detected by
mammography is about 600 million cells, or about 0.25 inches
across; the average size detectable by manual palpation is about 45
billion cells and about 1.25 inches in diameter.
Cancer cells that metastasize exhibit little to no cell-to-cell
adhesion as compared to normal cells that tend to adhere to each
other to form well-defined tissues (except blood cells).

Scope/fact about Cancer
• Among the leading causes of morbidity and mortality worldwide,
• with approximately 14 million new cases
• 8.2 million cancer related deaths in 2012,
• more than 60% of world’s total new annual cases occur in Africa,
Asia and Central and South America
• These regions account for 70% of the world’s cancer deaths.
• The five most common sites of cancer diagnosed in 2012 were:
– lung, prostate, colorectal, stomach, and liver cancer (among men)
– breast, colorectal, lung, cervix, and stomach cancer (among Women)

Cancer in Ethiopia
• a total of 5701 cancer cases registered from September 2011 to August
2014.
• Among those 3820 (67%) were females and 1881 (33%) were males.
• The most common type of cancers among:
– females were cancers of the;
• Breast(33%),
• Cervix uteri (17%) and
• Ovary (6%),
• while among males cancers of;
– Colorectal (19%),
– Leukemia (18%) and
– Prostate (11%

Etiology
• is unknown and anything that has the potential to cause cellular DNA
mutation has the capacity to cause malignancy.
• varies across the specific types of cancer
• is multifactorial, with genetic, environmental, medical, and lifestyle
factors interacting to produce a given malignancy.
• Most cancer caused by genetic mutations often, by a series of
mutations.

Risks For Cancer
• Smoking
• Obesity
• Biological Factors
– Genetics
• Reproduction
• Hormones
• Social & Psychological Factors
– Stress,
– Sleep disturbances,
– Diet
• Occupational & Env’tal Factors
• Chemicals In Foods
• Viral Factors
• Medical Factors

Major proven cancer risk factors of today are:
Sunlight - Solar radiation
Chronic Exposure to Electromagnetic Fields (EMFs)
Among adults, there is a strong association between EMFs and brain cancer, and,
to a less extent, breast cancer.
Melatonin production is reduced in those afflicted with breast cancer, and
excessive exposure to weak EMF can disturb the brain’s production of melatonin.
Ionizing Radiation
Ionizing radiation, such as X-rays, consists of high-energy rays that can disrupt
the electron from matter, causing genetic mutations that can lead to cancer.
Radiologists have historically a higher incidence of cancer, as have other workers
exposed to low-dose radiation.
X-rays (or gamma rays) also emanate from fluorescent lights, computer monitors,
and television screens.
Medical X-rays may be responsible for many breast cancers,

Pesticide/Herbicide Residues
Industrial Toxins
Highly toxic chemicals and heavy metals used in industries often find their
way into our body.
Such compounds include lead (from cigarette smoke, ceramic glazes on
cooking utensils, canned food), mercury (from dental fillings, fish)
aluminium (from antacids, over-the-counter drugs and douches), nickel and
cadmium (from cigarettes, instant coffee and teas, nickelcadmium
batteries).
They have a tendency to accumulate in the fat cells, affecting the central
nervous system, brain, and glands.
Polluted, Chlorinated and Fluoridated Water
Tobacco
Hormone Therapies

Wrong Diet and Nutrition
Emotional Stress
Intestinal Toxicity and Digestive Impairment
Viruses
Blocked Detoxification Pathway
Cellular Oxygen Deficiency
Cellular Terrain
Genetic Factors

Risks For Cancer …..
• Smoking
– 30% of all cancer deaths,
– 87% of lung cancer deaths.
• Obesity
– 50% higher risk for breast
cancer in postmenopausal
women,
– 40% higher risk in colon
cancer for men.
• Biological Factors
– Some cancers appear to run in families:
• breast, stomach, colon, prostate, uterus, ovaries
and lung cancer.
– Hodgkin’s disease and certain leukemia's
show similar patterns.
– A rare form of eye cancer appears to be
transmitted genetically from mother to child.
– Inherited defect transmitted to the child in
DNA
– Remember you can’t inherit cancer its just
that you maybe more susceptible to getting it.

Risks For Cancer …...
• Reproductive & Hormonal Risks for Ca
• increase a woman’s chances of breast Ca.
• Pregnancy & oral contraceptives
• The following have been shown to
reduce risk of breast ca.
– Late menarche,
– early menopause,
– early first childbirth,
– having many children
• Social & Psychological Factors
– Stress has been implicated in
increased susceptibility to
several types of cancers.
– Sleep disturbances, diet, or a
combination of factors may
weaken the body’s immune
system.

• Occupational and
Environmental Factors
– Asbestos
– Nickel
– Chromate
– Benzene
– Arsenic
– Radioactive substances
– Cool tars
– Herbicides/pesticides
• Chemicals in Foods
– Sodium Nitrate
• when ingested forms a potential
carcinogen, nitrosamine
• is still used b/c it is effective in
preventing botulism
– Pesticide and herbicide residues

• Viral Factors
– Herpes - related viruses may
be involved in the dev’t of
leukemia, Hodgkin’s disease,
cervical Ca, and Burkitt’s
lymphoma.
– Human papillomavirus (HPV),
virus that causes genital warts,
has been linked to cervical Ca.
– Helicobacter pylori causes
ulcers which are a major factor
in the dev’t of stomach Ca.
• Medical Factors
– Some medical Tx actually increase a
person’s risk for Ca.
– Diethylstilbestrol (DES)
• used 1940 to 1960 to control
bleeding during pregnancy, the
daughters of mothers that used
DES were found to have an
increased risk for Ca of the
reproductive organs.
– Estrogen supplementation
– Chemotherapy used to treat one form
of Ca may increase risk for another
type of Ca.

• We now know that 80 to 90% of all cancers are related to three
major groups of risk factors:
1. Nutrition –
– a high-fat, high-cholesterol, low-fiber, high-sugar diet.
2. Lifestyle –
– alcohol, smoking, stress, sedentary lifestyle.
3. Environment –
– industrial toxics, electromagnetic radiation, chemical carcinogens, air
and water pollution, among others.

Tumors: Types and Causes
Carcinoma
• originates from epithelial tissue
• is the most common type of cancer.
• also called solid tumors
• common sites for carcinomas:
- Skin, Lungs
- Mouth, Stomach, Colon
- Uterus, Breasts
• spread by way of the lymphatic system
Sarcoma
• originates in muscle or
connective tissue and lymph
• a fairly rare form of cancer
• certain leukemias are sarcomas

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Routine Medical Examination
•Pap smear
- test for cervical & uterine Ca
•Breast exam
- palpate for lumps in the breast
•Digital rectal exam
- screening for prostate Ca
•Testicular exam
- palpate for tumors in testes

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Blood Tests
Blood Tests
•Carcinoembryonic antigens (CEA)
- detects gastrointestinal tumors
•Prostate-specific antigen (PSA)
- detects prostate Ca
•Alpha-fetoprotein test (AFP)
- detects liver or testicular Ca
•Human chorionic gonadotropin (HCG)
•present with testicular Ca
•Cancer antigen 125 (CA-125)
- protein produced by ovarian cancer cells

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Categorizing Tumors
Tumors are categorized by:
Categorizing Tumors
•Grade (the maturity of the tumor)
•Stage (the degree the tumor has spread)
•Appearance (using a microscope and by visual observations)

Stages of Cancer Spread
• Stage 1 – confined to site of origin
• Stage 2- cancer is locally invasive
• Stage 3 – cancer has spread to regional structures.
• Stage 4- cancer has spread to distant sites

Cancer …..
• Diagnosis
– Screening procedures and blood
tests:
• Tumor markers- substances on
plasma membranes in blood, spinal
fluid or urine, hormones, genes
antigens or antibodies.
– Markers can be used:
• to screen & identify individuals at
high risks
• to help Dx the specific type of tumor
• to follow the course of the cancer
• Symptoms
– depend on the severity & specific
type of Ca.
– Most Ca however are
asymptomatic and will only
produces signs once they are at
advanced stages.
– Early detection & Tx is the key to
Ca survival.
– There are many symptoms of Ca
but some of the potentially-
serious warning signs are
abbreviated as CAUTIONUS

Cancer…..
• Warning Signs – CAUTIONUS
– C – Changes in bladder or bowel habits
– A – A sore that doesn’t heal
– U – Un usual bleeding or discharges
– T – Thickening or lumps
– I – Indigestion or difficulty swallowing
– O – Obvious changes in warts, moles, or the skin
– N – Nagging cough or hoarseness of voice
– U – Unexplained anemia
– S – Sudden loss of weight

Cancer ….
Clinical manifestations
• Pain
– Usually not in early stages
– 60 – 80 % of terminally ill
– Due to pressure, obstruction, stretching, tissue damage or
inflammation
• Fatigue
– sleep disturbances
– biochemical changes
– loss of muscle function
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Cancer ….
Clinical manifestations…..
• Cachexia – wasting
– anorexia
– early satiety
– weight loss
– anemia
– marked weakness
– taste alterations
– altered metabolism
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• Leukopenia and thrombocytopenia
– tumor invasion of bone marrow
– chemotherapy or radiation
• Anemia
– chronic bleeding
– Malnutrition
– Medical therapies
– malignancy in blood forming organs
• Infection
– most significant cause of cxns & death

Cancer ….
Management
• Mgt of Cancer depends on the specific
stage and site of the cancer.
• Treatment may be;-
– Primary (to kill cancer cells),
– Adjuvant (to kill remaining cancer cells),
– Palliative (to treat signs and symptoms).
• Treatment modality
– Chemotherapy
– Surgery
– Radiation therapy
– Stem cell transplants
– Biological therapy to improve
immune function
– Hormone therapy
• Side effects of treatment
– Gastrointestinal tract:
• Oral ulcers
• Malabsorption
• Diarrhea
• Vomiting – caused by effects on CNS
– Hair and skin:
• Alopecia
• Skin breakdown and dryness
– Bone marrow:
• Chemo and radiation suppress bone
marrow
• Decrease in RBC, WBC and Platelets

Oncologic Emergencies
• Increasing incidence of cancer
• Improved survival
• Patients with malignancies may present to EDs and general
medical OPD
• Oncologic emergencies are:
– Those resulting from the disease itself
– Those resulting from cancer therapy

Oncologic Emergencies
• Oncologic Emergency – is a clinical condition resulting from a metabolic,
neurologic, cardiovascular, hematologic, and/or infectious change
caused by cancer or its treatment that requires immediate intervention
to prevent loss of life or quality of life.

Clinical reasoning in evaluating & treating
oncologic emergency
• Is there a previous diagnosis of malignancy?
• Are symptoms due to tumor or complications of treatment?
• What were the patient’s previous treatments?
• How quickly are symptoms progressing?
• What is the interval b/n Tx and onset of symptoms?
• Should Tx be directed at treating the malignancy or the complication?
• What are the pt’s other existing medical conditions?
• These malignancy-related emergencies are broadly categorized as:
– Those due to local physical effects,
– Those secondary to biochemical derangement,
– Those that are the result of hematologic derangement,
– Those related to therapy

Oncologic Emergency…..
1. Related to local tumor effects
1.1. Malignant airway obstruction
1.2. Bone metastases and pathologic fractures
1.3. Malignant spinal cord compression
1.4. Malignant pericardial effusion with tamponade
1.5. Superior vena cava syndrome
2. Related to biochemical derangement
2.1. Hypercalcemia
2.2. Hyponatremia due to inappropriate ADH secretion
2.3. Hypoglycemia
2.4. Tumor Lysis Syndrome

3.Related to hematologic derangement
• 3.1. Febrile neutropenia and infection
• 3.2. Leukocytosis
• 3.3. Hyperviscosity syndrome
• 3.4. Thromboembolism
4. Related to therapy
 Chemotherapy-induced nausea and vomiting
 Chemotherapeutic drug extravasations

Oncologic Emergences …..
1. Related to local tumor effects
1.1. Malignant airway obstruction
1.2. Bone metastases and pathologic fractures
1.3. Malignant spinal cord compression
1.4. Malignant pericardial effusion with tamponade
1.5. Superior vena cava syndrome

1.1. MALIGNANT AIRWAY OBSTRUCTION (MAO)
• Results from a mass originating in the:
– oropharynx, neck, or superior trachea, bronchi, & lungs.
• Mediastinal tumors such as lymphomas and germ cell tumors can
also cause MAO, more commonly in the pediatric population.
• Primary bronchogenic carcinomas
– are the most common cause of MAO, and
– up to 30% of pts with primary lung tumors develop airway obstruction.

1.1. MALIGNANT AIRWAY OBSTRUCTION……
• Pathophysiology
– Airway obstruction may result from
• external compression of the trachea or bronchi by the tumor, or by
an involved lymph node.
• infiltration of the tumor within the oropharynx, trachea, and
bronchi.
– Acute compromise may occur with:
• supervening infection,
• hemorrhage, or
• loss of protective mechanisms, such as muscle tone.

Presentation or S/Sx
• Symptoms
– are nonspecific
– can be mistaken for more common conditions including:
• COPD exacerbations, asthma, or bronchitis.
– usually worsen at night and while lying supine.
• Dyspnea – most common.
• Productive cough,
• Wheezing,
• Stridor
• Hemoptysis is reported in up to 45% of pts w/obstructing neoplasm.
• Tracheal stenosis syndrome
– refers to a constellation of symptoms consisting of:
• dyspnea, cough, wheezing, and stridor
– seen in approx 85% of pts w/primary tracheal tumors.

Diagnosis
• Physical examination
– may show evidence of a mass in the pharynx, neck, or supraclavicular
area.
• Chest X-rays
– may show tracheal deviation or airway narrowing
• CT scan – preferred
• Bronchoscopy
– allows direct visualization of the obstruction,
– allows obtaining tissue for diagnosis.
• Direct laryngoscopy is discouraged

Treatment
• Admin of supplemental humidified oxygen
• Maintenance of the best possible airway through pt positioning.
• Administer Dexamethasone 20 mg IV followed by 4 mg QID or BID.
• Emergency trans tracheal jet ventilation or cricothyroidotomy can be lifesaving if
the obstruction is above the vocal cords.
• Awake fiber optic intubation with a 5-0 or 6-0 ETT.
• Sustained relief - neodymium-yttrium-aluminum-garnet laser photo radiation for
vaporization of obstructing tissue and
• placement of a self-expanding stent at the stenotic site.
• Definitive tumor control – radiation or chemotherapy.

1.2. BONE METASTASES AND PATHOLOGIC FRACTURES
• Commonly affect
– the axial skeleton (calvarium included)
• articulated bones of head, vertebral column, and thorax (i.e., head
and trunk) and
– the proximal aspect of the limbs.
• Most pathologic #s are due to metastases from solid tumors that
localize in areas of bones with high blood flow, identified as
containing red marrow.
– e.g., breast, lung, prostate

1.2. BONE METASTASES AND PATHOLOGIC #s…..
• Presentation
– Localized pain
– benign outward appearance
of the involved area.
• Treatment
– Priorities are pain relief and
restoration or salvage of function
– Parenteral analgesics,
– Palliative radiotherapy,
– Open surgical repair
• Diagnosis
– Plain X-ray
• Malignancy alters the normal
radiographic appearance of bone
– Advanced imaging
• CT scan with IV contrast,
• MRI

1.3. MALIGNANT SPINAL CORD COMPRESSION (MSCC)
• Relatively common
– 2.5-6% of cancer patients
• most cases of MSCC occur in pts w/known dx of malignancy,
• 5-25% of MSCC cases occur as the initial presentation of malignancy.
• Confers poor prognosis overall
• Need urgent Dx & Tx
• all tumor types have the potential to cause MSCC
• Most common are:
– breast,
– lung and each account for approx 15-20% of the cases,
– prostate
– non-Hodgkin lymphoma,
– renal cell carcinoma, and each causing 5-10% of cases.
– myeloma

MSCC …
Pathophysiology
• the compressive indentation, displacement, or encasement of the thecal
sac that surrounds the spinal cord or caudaequina by Ca.
• Compression can occur by;
– posterior extension of a vertebral body mass,
– anterior extension of a mass arising from the dorsal elements, or
– growth of a mass invading the vertebral foramen.
• common locations for MSCC are:
– the thoracic spine (70%)
– the lumbosacral region (20%) and,
– the cervical spine (10%).

MSCC ….
• Presentation
– Vary on severity, location, and duration of
the compression.
– back pain (localized or radicular pain)
• 90% of the cases,
• is the most common initial Sx
• BACK PAIN + MALIGNANCY = MSCC!!
– Motor weakness,
– Sensory impairment – numbness and
– Autonomic dysfunction.
– Lately urinary retention and overflow
incontinence
– bowel/bladder/sexual dysfunction
• Diagnosis
– Plain radiographs:
• may detect vertebral body
metastases but less sensitive
and specific for MSCC.
– MRI:
• modality of choice,
• image entire vertebral column.
– CT myelography:
• used when MRI not available or
accessible.

MSCC ….
Treatment
• Treatment Objectives
– Pain control
– Avoidance of complications
– Preserve or improve
neurological function
• Dexamethasone, 10 mg IV
followed by 4 mg PO or IV QID
• Radiation therapy
– is standard approach,
– is beneficial in approx 70%
• Efficacy of Tx depends most on
– the pt’s neurological function at
presentation
• Definitive Tx depend on:
– spinal column stability,
– degree of compression, and
– radio sensitivity of the tumor.
• If spinal instability is present, surgical
decompression should be considered.

1.4. MALIGNANT PERICARDIAL EFFUSION WITH
TAMPONADE
• Malignant pericardial effusions develop through
– direct or metastatic involvement of the pericardial sac.
• Tamponade physiology can arise from volumes of as little as 100ml if they
accumulate rapidly.
• Direct extension
– is most common in those tumors with sites of origin adjacent to the
heart:
• lung Ca, breast Ca, and mediastinal lymphoma.
• Cancer Tx,
– especially thoracic irradiation, can cause transudative effusions.
• Immunosuppression
– can also allow suppurative infections to develop in the pericardial space.

1.4. MALIGNANT PERICARDIAL …..
Presentation
• Symptoms depend on rapidity of onset
• Most patients complain of dyspnea and chest
discomfort.
• dyspnea, cough,
• chest pain,
• dysphagia,
• hiccups,
• hoarseness
• Tachycardia,
• Distant heart sounds,
• JVD,
• UE and LE edema,
• Pulsus paradoxus
• Tamponade classically
presents with
– the Beck’s triad:
• hypotension,
• elevated JVP, and
• muffled precordium.
– Tachycardia is nearly universal

• Diagnosis
– Echo preferred test
• is the definitive test,
• demonstrates
– RV collapse during early diastole.
– Presence of fluid
– “Tamponade phyiology’’
– Chest X-rays
• may show cardiomegaly and the classic “water
bottle” cardiac silhouette.
– ECG
• can show low voltage and electrical alternans
from the shifting axis of the heart as it moves
like a pendulum within the fluid-filled sac.
– CT and MRI also useful
CT scan showing large pericardial effusion
and bilateral pleural effusions.

• Treatment
– Sonographically guided pericardiocentesis
–Pericardiectomy
–Decompression can produce paradoxical hemodynamic instability
requiring admission to the ICU and pressor support

1.5. SUPERIOR VENA CAVA SYNDROME (SVCS)
• Primary or metastatic tumors can cause
compression.
• Cancers classically associated with SVCS
include:
– lung Ca (particularly rt-sided),
– breast Ca – primary mediastinal lymphoma,
– lymphoblastic lymphoma,
– thymoma, and
– germ cell tumors (either primary or
metastatic to the mediastinum).
• Nononcologic etiologies include:
– syphilitic aortic aneurysms,
– fibrosing mediastinitis (classically
associated w/histoplasmosis),
– substernal hypertrophy of the
thyroid,
– granulomatous ds (such as
tuberculosis and sarcoidosis), and
– thrombosis,
• Tumor obstructs SVC Elevated venous pressure/venous hypertension,
congestion in the upper body.

1.5. SVC SYNDROME …..
• Occurs when blood flow through the SVC
(the major vein that carries blood from
the head, neck, upper chest, and arms to
the heart) is compressed:
– ↓ venous return to heart,
– ↓ cardiac output,
– ↑ venous congestion & edema.

Presentation
• Early signs:
– face edema that improves through day
– Presyncope or syncope
– SOB, cough, chest pain
– Distension of chest, neck veins
– Cyanosis
• In advanced SVC obstruction:
– Headaches
– confusion
– lethargy
– vision changes
• Signs and symptoms from
impedance to flow in the SVC:
– Edema in the arms
– Plethora
– facial edema
– Chemosis
– periorbital edema
– JVD
– dyspnea
– orthopnea
– cough
– Stridor
– Hoarseness

Presentation….
Dilated Chest Wall Veins in Superior Vena Cava Syndrome

Presentation….

Diagnosis
• Most common findings from Radiographic imaging are;
– Mediastinal widening
– Pleural effusion
• CXR
• CT scan –
– remains gold standard for localizing obstruction
• MRI and Venography are usually preferable for their:
– noninvasiveness,
– easier availability, and
– decreased contrast load.
• Transthoracic Echo:
– presence of pericardial effusion

Treatment
• Corticosteroids and loop diuretics are commonly used
• Pts who have neurologic Sx or airway compromise merit immediate Tx;
– endovascular stenting
• Chemotherapy
– may be the only necessary Tx in pts presenting in non-emergent fashion w/small cell:
• lung Ca, lymphoma, or germ cell tumors.
• Intravascular stents, with or without angioplasty,
– can be used to reduce obstruction to SVC flow.
• Initial mgt is with;
– head elevation to decrease venous
pressure in the upper body and
– supplemental oxygen to reduce the
work of breathing.
• do NOT sedate
• do NOT give anxiolytics
• avoid anything which will compromise
– muscular tone
– venous return
– an already compromised
cardiopulmonary state

Oncologic Emergences …..
2.1. Hypercalcemia
2.2. Hyponatremia due to inappropriate ADH
secretion
2.3. Hypoglycemia
2.4. Tumor Lysis Syndrome

2.1. HYPERCALCEMIA
• Occurs in about 20-40% of pts with cancer
• most common life-threatening metabolic disorder.
• the prevailing causes of hypercalcemia are:
– Breast, lung, and renal cell carcinomas;
– multiple myeloma; and adult T-cell leukemia/lymphoma

2.1. HYPERCALCEMIA…..
Pathophysiology
• A variety of mechanisms can explain elevated calcium in cancer patients:
a. systemic release of parathyroid hormone-related peptide (PTHrP) by
the tumor, which does not require the presence of bone metastases;
b. metastases to bone, leading to osteolytic effects;
c. systemic secretion of vitamin D analogues by the tumor, which also
does not require the presence of bone metastases.
• Squamous cell carcinomas from the aerodigestive and genitourinary
tracts commonly cause this type of “humoral” hypercalcemia but this can
also be seen in breast, kidney, cervical, endometrial, and ovarian cancer.

2.1. HYPERCALCEMIA….
• Presentation
– symptoms are nonspecific, and delayed recognition can worsen morbidity and
mortality.
– Usually gradual in onset
– Fatigue, constipation, anorexia, apathy, decreased LOC common manifestations
– The mnemonic “bones, stones, moans, and groans” is used to emphasize:
• skeletal pain, nephrolithiasis, abdominal discomfort, and altered mentation as presenting
symptoms.
– hypercalcemia shortens the QT interval and can produce arrhythmias.
• Diagnosis
– Serum Ca levels >11.0 mg/dl (Normal= 8.5 -10.5mg/dl).
– Serum chloride is a more readily available test,

2.1. HYPERCALCEMIA…..
Treatment
• Normal Saline 1-2 L bolus, to restore intravascular volume, followed by an infusion at a rate of 200-
250 ml/h.
• Furosemide 20–40 mg iv every 12–24 h with heart failure or renal insufficiency to prevent volume
over load.
• Bisphosphonates are the recommended agents to treat malignancy-associated hypercalcemia
(inhibitors of bone resorption)
• Steroids
– Hydrocortisone, 100 mg iv q6h or
– prednisone, 60 mg po daily
• Calcitonin is a naturally occurring hormone that inhibits bone resorption and increased excretion of
calcium.
• Hemodialysis for those with profound AMS or renal failure
• 50% hypercalcemic cancer patients also have hypokalemia.
• Serum potassium levels should be monitored Q4h and potassium chloride (20–40 mEq, IV or PO)
supplemented as necessary to prevent severe hypokalemia

2.2. HYPONATREMIA DUE TO INAPPROPRIATE ADH SECRETION
• hyponatremia means that intravascular water is present in excess relative to sodium, either
through
– water retention and/or sodium loss.
• ADH promotes free water uptake in the distal tubules by binding to the vasopressin 2 (V2)
receptor.
• Compounding the problem is continued free water intake
– b/c the thirst mechanism is not sufficiently inhibited.
• SIADH secretion
– should be suspected if a pt with cancer presents with normovolemic hyponatremia.
– more commonly encountered in diseases originating in or involving the
• lungs, pleura, thymus, and brain.
• 10-45% of pts with small cell lung Ca 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

2.2. HYPONATREMIA................
• Presentation
– Anorexia, nausea, & malaise are the earliest findings, followed by
• headache, confusion, obtundation, seizures, & coma.
– Life-threatening Sx are almost invariably associated with Na conc.
<110mmol/l
– The most concerning Sx of hyponatremia are neurologic, including:
• lethargy, delirium, seizures, and coma, all of which merit urgent Tx.
• Classification
– Hyponatremia can be classified as;
• mild (131-135 mmol/L),
• moderate (126-130 mmol/L), or
• severe (<125 mmol/L).

2.2. HYPONATREMIA.....
Treatment
• Hypovolemic hyponatremic pts have lost Na and mgt involves
– infusing sodium-containing fluids.
• Severe hyponatremia with neurologic Sx can merit very careful use of hypertonic (3%)
saline. Otherwise, normal (0.9%) saline is an appropriate infusate.
• The serum sodium should not be corrected at a rate greater than 0.5 mEq/L/hour to avoid
central pontine myelinolysis, a condition in which rapid, osmotically driven shrinkage of
brainstem cells can result in quadriparesis, pseudobulbar palsy, “locked-in” syndrome,
coma, and death.
• Asymptomatic, euvolemic hyponatremic pts with ca are treated by:
– removing the offending stimulus for ADH secretion, such as
• controlling nausea, lessening pain, and
– treating the underlying malignancy.
• Restriction of free water intake to 500-1000 ml/day
– will increase plasma osmolality and normalize Na level in many pts with SIADH.

2.3. Hypoglycemia
• Some tumors are capable of ectopic production of substances that
affect glucose metabolism.
• Insulin is made in excess by insulinomas and nesidioblastosis.
• Mesenchymal tumors like sarcoma, including
– gastrointestinal stromal tumor and solitary fibrous tumor, can produce
insulin-like growth factors (IGFs) such as IGF-2, which
• increases glucose utilization by tissues and
• blunts the secretion of growth hormone.

2.3. Hypoglycemia……
• Rapidly proliferating neoplasms can consume glucose prodigiously.
• Tumors with high mitotic rates may consume glucose with sufficient
briskness as to induce hypoglycemia; this is most often seen in
aggressive lymphomas (e.g., Burkitt lymphoma)
• Tumors can infiltrate organs that play crucial roles in normal glucose
metabolism, such as
– hepatocellular carcinoma replacing the liver parenchyma or
– pheochromocytoma overtaking the adrenal gland.

• Presentation
– Neurologic manifestations
• range from confusion and blurred
vision to seizures and coma.
– The catecholamine response to
hypoglycemia can result in:
• Diaphoresis,
• palpitations, and
• dilation of the pupils
• DIAGNOSIS
– The Whipple triad, initially developed to
determine eligibility for pancreatic
surgery in pts with insulinoma, includes;
• measured hypoglycemia,
• symptoms attributable to hypoglycemia,
and
• reversal of symptoms when
normoglycemia is restored.

Treatment
• The Tx of cancer-related hypoglycemia include;
– surgical removal of the underlying tumor,
– chemotherapy and radiation for unresectable tumors.
– Interim mgt may include the administration of:
• glucagon at a dose of 1 mg Iv/Im,
• dextrose infusion,
• diazoxide (3 mg/kg/day initially),
– cessation of nonselective beta-blockers that blunt adrenergic response to
low blood sugar.

2.4. TUMOR LYSIS SYNDROME (TLS)
Pathophysiology
• Tumor lysis occurs when cancer cells release their contents into the
bloodstream, either spontaneously or following antineoplastic therapy,
leading to an influx of electrolytes and nucleic acids into the circulation.
• Usually after chemotherapy
• Lysed cells  metabolic changes
• Hyperuricemia: N/V, renal failure due to renal precipitation
• Hyperphosphatemia: N/V, lethargy, seizures, renal impair
– Also binds with Ca+  calcium
• Hypocalcemia: tetany, arrhythmia

2.4. TUMOR LYSIS SYNDROME (TLS)…..
• The sudden dev’t of hyperkalemia, hyperuricemia, and
hyperphosphatemia can have life-threatening end-organ effects on the
myocardium, kidneys, and CNS
• TLS is more common in the rapidly proliferative hematologic
malignancies such as:
– acute lymphoblastic leukemia (ALL),
– acute myeloid leukemia (AML), and
– Burkitt lymphoma
• Treatment-provoked TLS can occur following;
– chemotherapy,
– Tx with single-agent corticosteroids in pts with sensitive tumors,
– radiation, surgery, or ablation procedures.

2.4. TUMOR LYSIS SYNDROME (TLS)…..
Diagnosis
• LABORATORY TLS
– Two or more laboratory changes must be observed within 3 days before or
7 days after cytotoxic therapy.
• Uric acid ≥ 8 mg/dL
• Potassium ≥ 6 mEq/L (≥ 6 mmol/L)
• Phosphorus ≥ 6.5 mg/dL (≥ 2.1 mmol/L)
• Calcium ≤ 7 mg/dL (≤ 1.75 mmol/L)
• CLINICAL TUMOR LYSIS SYNDROME
– Clinical TLS is diagnosed when one or more of 3 conditions arise:
• Creatinine ≥ 1.5 times the upper limit of normal
• Cardiac arrhythmia or sudden death
• Seizure

2.4. TUMOR LYSIS SYNDROME (TLS)……
Treatment
• Reduce the risk of tumor lysis
syndrome developing:
– prophylactic allopurinol and
– maintaining good hydration
• Allopurinol
– inhibits xanthine oxidase, thus
decreasing uric acid production, and
– can be given preventively starting up to
48 hrs before Tx at doses of 100mg/m
Q8h (max daily dose: 800 mg).
• Admission to an ICU with cardiac rhythm
monitoring is indicated.
• Aggressive IV fluid administration to
increase urinary excretion of the released
intracellular solutes is the cornerstone.
• Hyperkalemia can be treated by:
– β-adrenergic agonists,
– sodium bicarbonate, and
– dextrose-insulin therapy.
• Hyperphosphatemia is managed with phosphate
binders like
• aluminum hydroxide (300 mg with
meals),
• aluminum carbonate (30 ml q6h), or
– by the administration of dextrose and
insulin.
• Hemodialysis can correct all biochemical
abnormalities of TLS.

3.Related to hematologic derangement
3.1. FEBRILE NEUTROPENIA and INFECTION
• Absolute neutrophil count (ANC) can decline through
– a cancer's direct interference with hematopoiesis, as in
• leukemia or metastatic replacement of the bone marrow,
• neutropenia is most commonly seen as an effect of cytotoxic
therapy
• exposure to prior chemotherapy or current immunosuppression;
• pretreatment elevations in alkaline phosphatase, bilirubin, or
aspartate aminotransferase levels;
• reduced GFR; and
• cardiovascular comorbidities.

Oral chemo causing neutropenia
• 6-mercaptopurine
• Altretamine
• Busulfan
• Capecitabine
• Carmustine
• Chlorambucil
• Crizotinib
• Cyclophosphamide
• Dasatinib
• Etoposide
• Everolimus
• Hydroxyurea
• Imatinib
• Lenalidomide
• Lomustine
• Melphalan
• Methotrexate
• Pazopanib
• Procarbazine
• Sorafenib
• Sunitinib
• Temozolomide
• Thalidomide
• Topotecan
• Vandetanib
• Vemurafenib

• Organisms
– a variety of organisms can be responsible.
– Gram-positive cocci, which are now responsible for the majority of
culture-positive cases of neutropenic fever, include:
• S.aureus, S.epidermidis (especially in pts with indwelling devices), Strep
pneumoniae, Strep pyogenes, the Strep viridans, and Enterococcus faecalis and
faecium.
– Corynebacterium is the most likely gram-positive bacillus.
– Gram-negative bacilli include:
• E.coli, Klebsiella species, and Pseudomonas aeruginosa.
– Candida is the most common fungal infection, but Aspergillus and
Zygomycetes are more feared for their angioinvasive predilection.

• Factors Predisposing to Infection and Sepsis
– Clinical debilitation, prolonged bed rest
– Nutritional compromise
– Disruption of mucous membranes and skin barriers
– Indwelling catheters
– CNS dysfunction secondary to cancer, sedatives, opiates, or
psychotropic medications.

• Presentation
–Infection is responsible for at least half of the cases of
neutropenic fever.
–Fever is a single oral temperature of 38.3°C (101°F) or
higher, or temperatures of 38.0°C (100.4°F) or higher
measured 1 hour apart.

• Diagnosis
– A careful, thorough physical examination is crucial
– At a minimum, 2 sets of blood cultures should be drawn in each patient.
– Urinalysis and urine culture
• the lack of neutrophils may preclude pyuria.
– Chest x-rays to evaluate respiratory symptoms.
– For clinical decision making:
• neutropenia is defined as an ANC<1000/mm3
• severe neutropenia is defined as an ANC <500/mm3 and
• profound neutropenia is defined as an ANC <100/mm3

• Physical examination
– with attention to three areas typically overlooked in routine
examination:
– the oral cavity,
– the perianal area, and
– The entry sites of intravascular catheters.
– DRE is relatively contraindicated in neutropenic pts —
• withhold until after initial antibiotic administration.
– Evaluate the entry sites of IV catheters for evidence of infection

• Treatment
– Empiric antibiotic therapy
• can be administered in the inpatient or outpatient setting depending upon the pt's initial risk ass’t.
– Monotherapy is acceptable only with a sufficiently broad-spectrum agent such as the fourth-
generation cephalosporin
• cefepime,
• a carbapenem, or
• piperacillin-tazobactam, all of which offer antipseudonomal activity.
– Vancomycin can be added for skin and soft tissue infections, pneumonia, or suspicion of an
infected device.
– Antibiotic therapy should be continued at least until the ANC improves to above 500/mm3.
– The addition of antifungal coverage should be considered in high-risk pts who remain febrile
after 4 to 7 days of broad-spectrum antibiotics with no identified causative organism.

3.2. HYPERVISCOSITY SYNDROME
• Hyperviscosity syndrome (HVS) refers to the clinical sequelae caused
by
– increased blood viscosity.
• Increased serum viscosity (SV) is a result of
– excess proteins, usually immunoglobulins (Igs), most commonly arising from
Waldenström macroglobulinemia (WM) (85%) and multiple myeloma (MM).
• Increased blood viscosity can result from elevated cellular components
seen in
• hyperproliferative states such as leukemia and
• myeloproliferative diseases such as polycythemia vera (PV).
• When hyperviscosity results from elevated WBC, it is referred to as
hyperleukocytosis or, if symptomatic, leukostasis

3.2. HYPERVISCOSITY SYNDROME …..
• Presentation
• Mucosal bleeding and purpura
– are also common clinical
manifestations of HVS, with
proteins coating the platelets
and hindering their function.
• CHF, ischemic ATN, and pulmonary
edema, with MOF and death occurring if
Tx is not promptly initiated.
— Headache,
— AMS,
— Nystagmus,
— Vertigo, due to impaired microcirculation in the brain
— Ataxia,
— Paresthesias,
— Seizures, or
— even coma.
– The “classic triad” of HVS includes
• neurologic abnormalities,
• visual changes, and
• bleeding,

• Thrombocytopenic bleeding
– Petechiae and mucosal bleeding (the
image below) are common but by
themselves don’t require systemic Tx
– Active bleeding with a platelet count
under 50,000/mm3 requires platelet
transfusion regardless of etiology

• Diagnosis
– There is no single definitive test for HVS because it is a clinical diagnosis.
– A detailed history and physical examination are important.
– Laboratory studies including
• an electrolyte panel,
• Serum Viscosity(SV),
• peripheral blood smear,
• coagulation panel, and
• quantitative Ig levels
– Any pt with an SV >4 cP should be evaluated for HVS.
– (normal 1.2-2.8cp centipose)

• Treatment
– Plasmapheresis
• is the fastest, most effective method to reduce plasma viscosity.
– Phlebotomy
• has been used to reduce acute symptoms in ED where
plasmapheresis is not readily available.
– All these actions, however, are temporizing measures.
– Red cell transfusions should be avoided unless critically necessary, as
this can increase SV, thus worsening HVS.

Leukostasis
• is a hematologic emergency
• is associated with
– respiratory failure,
– intracranial hemorrhage, and
– early death.
• If it is not recognized and treated promptly, the mortality rate can be as high as
40%.
• Risk for leukostasis increases with a WBC >100,000/mm3.
• The incidence ranges from 5-13% in pts with AML & 10-30% in adult pts with
ALL.
• Other risk factors include younger age (with presentation in infants being most
common

Leukostasis ….
• Presentation
– Leukostasis can involve any organ system, but the initial symptoms
most commonly are related to the respiratory system and the CNS.
– Pulmonary symptoms can range from exertional dyspnea to severe
respiratory distress, with diffuse interstitial or alveolar infiltrates
often present on chest x-ray.
– Neurologic manifestations span the spectrum from mild confusion to
somnolence.
– MI, limb ischemia, renal vein thrombosis, and DIC.
– Fever is almost always seen and can be greater than 39°C.

Leukostasis ….
• Diagnosis
–is made by the combination of
• pt symptoms and
• the WBC.
–CXR

Leukostasis ….
• Treatment
–Rapid cytoreduction is the initial Tx in these pts.
• Ideally, this is achieved by induction chemotherapy, which can
dramatically reduce the WBC within 24 hours.
–These pts are at very high risk for TLS and require close
monitoring of electrolytes, with prophylaxis by allopurinol
–The use of leukapheresis is a widely accepted initial Tx and
was commonly believed to reduce early mortality.

3.3. THROMBOEMBOLISM
• occurs with all tumor types
• is the second leading cause of death in cancer pts.
• Symptomatic DVT 15% pts with cancer 50% with advanced
malignancies.

3.3. THROMBOEMBOLISM…..
• Risk factors
– The tumor may release procoagulant factors or inflammatory cytokines
that directly activate the coagulation system.
– Large tumors may cause venous obstruction and promote thrombosis.
– Impaired production of proteins C and S and antithrombin can produce a
hypercoagulable state.
– Surgery with attendant postoperative immobilization or long-term central
venous catheterization can incite thrombosis.
– Chemotherapy or hormonal therapy for breast ca increases the risk for
thromboembolism

3.3. THROMBOEMBOLISM…..
• Treatment
– LMWH is recommended as the initial Tx for 5-10 days.
– Continued Tx with LMWH for at least 6 months in preventing
recurrent thromboembolic events.

Increased Intracranial Pressure
• Elevated ICP secondary to malignancy in the brain can cause devastating
neurologic injury.
• Successful mgt requires prompt recognition and therapy.
• The vast majority of all intracranial neoplasms are metastatic with;
– lung cancer (20%),
– breast cancer (5%),
– melanoma (7%),
– renal cancer (10%), and
– colorectal cancer (1%).
• Increased ICP is due to both the mass effect of the tumor as well as
cerebral edema caused by neoplastic disruption of the BBB.

Increased ICP….
• Presentation
– The clinical presentation of brain metastases will vary depending on the location,
size, and rate of growth of the tumor
– Headache – most common
• worsen with bending over
• accompanied by nausea or emesis.
– Seizures range from 10-20%.
– Strokes occur if the tumor embolizes, bleeds, or compresses an artery.
– Melanoma, choriocarcinoma, thyroid ca, and renal cell carcinoma are more
likely to cause hemorrhagic strokes.
– The triad of signs referred to as the Cushing response is a late effect and
indicates impending herniation.
• hypertension with wide pulse pressure,
• bradycardia, and
• an irregular respiratory rate

Increased ICP….
• Diagnosis
–Once an intracranial malignancy is suspected,
• contrast-enhanced MRI
–is the preferred method of Dx
• Noncontract CT scan
–is the preferred scanning technique, however, in an acute
situation when hemorrhage or hydrocephalus is suspected.

Increased ICP….
• Treatment
– Dexamethasone is the standard agent 10-24mg IV bolus followed by 4 mg QID or
8 mg BID.
– In severe cases, mannitol and hyperventilation are used.
• Mannitol can be administered as an IV bolus or as a continuous infusion to
decrease cerebral edema.
– Intubation and controlled hyperventilation
• lead to a rapid decrease in cerebral edema
– Definitive Tx modalities include:
• whole-brain radiation therapy (WBRT),
• surgery
– Chemotherapy can be used in highly chemo sensitive disease such as:
• germ cell tumors, lymphoma, or small cell carcinomas, or
• in cases in which radiation therapy is not an option.

References
• Tintinally emergency medicine
• Rosen’s emergency medicine

Individual Assignment
1. General characteristics of cancer cells
2. The effects of Cancer on nutritional status
3. The use of nutrition for cancer patients
4. Decubitus ulcer

Onco Emergency 2020.pptx

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