Social Work in Public Health

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Oncological Emergencies from Pathophysiology

and Diagnosis to Treatment: A Narrative Review

Ameneh Jafari , Mostafa Rezaei-Tavirani , Maryam Salimi , Reza Tavakkol &

Zahra Jafari

To cite this article: Ameneh Jafari , Mostafa Rezaei-Tavirani , Maryam Salimi , Reza Tavakkol &
Zahra Jafari (2020): Oncological Emergencies from Pathophysiology and Diagnosis to Treatment: A
Narrative Review, Social Work in Public Health, DOI: 10.1080/19371918.2020.1824844

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SOCIAL WORK IN PUBLIC HEALTH
https://doi.org/10.1080/19371918.2020.1824844

Oncological Emergencies from Pathophysiology and Diagnosis to

Treatment: A Narrative Review
Ameneh Jafaria,b, Mostafa Rezaei-Taviranib, Maryam Salimic, Reza Tavakkold, and Zahra Jafarie
a
Student Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran;
b
Proteomics Research Center, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences,
Tehran, Iran; cDepartment of Biology and Anatomical Sciences, Faculty of Medicine, Shahid Beheshti University of
Medical Sciences, Tehran, Iran; dDepartment of Nursing, School of Nursing, Larestan University of Medical Sciences,
Larestan, Iran; e9 dey Manzariye Hospital, Isfahan University of Medical Sciences, Isfahan, Iran

ABSTRACT KEYWORDS
Oncological emergencies are defined as any acute possible morbid or life- Oncology; emergency; tumor
threatening events in patients with cancer either because of the malignancy lysis syndrome; diagnosis;
or because of their treatment. These events may occur at any time during treatment
malignancy, from symptoms present to end-stage disease. The aim of this
study is the review of urgent conditions results from cancer or cancer treat­
ment side effects that need to be addressed immediately. In this study,
a comprehensive and in-depth narrative review was carried out by searching
the databases of PubMed, Scopus, Science Direct, Google Scholar with the
keywords of “cancer, emergency, metabolic emergency, neutropenic fever”
along with the words, “tumor lysis syndrome, chemotherapeutic emergency,
diagnosis, treatment “ in last two decades. Patients suffering from cancer
mostly face the challenges that we are classified in different categories,
including metabolic, hematologic, cardiovascular, neurologic, respiratory,
infectious, and chemotherapeutic emergencies. These patients mostly com­
plain of headaches, nausea, pain, and fever. In conclusion, knowledge of
oncology emergencies and palliative care as part of a team approach is
critical for treating cancer patients. In this light, it is pivotal for physicians
to focus on the early detection of oncological emergencies. Moreover, train­
ing programs for cancer patients help them to timely recognize and report
the oncologic emergency symptoms, leading to avoid deleterious conse­
quences and unnecessary healthcare costs as well as improve the quality of
life in these patients.

Introduction
Cancer is the second leading cause of morbidity and mortality after cardiovascular disease worldwide
(Jafari et al., 2020; Nagai & Kim, 2017; Najminejad et al., 2019). The population with a cancer
diagnosis in the United States is expected to rise from about 15.5 million people by 2016 to
26 million by 2040 (Bluethmann, Mariotto, & Rowland, 2016; Howlader et al., 2016; National
Cancer Institute 2018). Emergency departments face overcrowding challenges when addressing the
increasing health needs of patients, such as cardiac attacks, stroke, burn, epileptic and non-epileptic
psychogenic seizures, respiratory diseases, and cancer patients (Jafari et al., 2020; Legramante et al.,
2018). Emergency care is a key part of the comprehensive care of patients with cancer (Miranda et al.,
2016). Currently, cancer-related patients account for 4.2% of all emergency department visits (Bischof,
Presley, & Caterino, 2019). Cancer patients, particularly those with progressive disease, may pose
complications or severe deterioration in their clinical condition requiring emergency care due to the

CONTACT Mostafa Rezaei-Tavirani tavirany@yahoo.com; Ameneh Jafari amenehjafari@gmail.com Proteomics Research

Center, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
© 2020 Taylor & Francis Group, LLC
2 A. JAFARI ET AL.

natural history of their disease, anticancer therapy, and/or lack of control of symptoms (Barbera,
Taylor, & Dudgeon, 2010). Hence, most oncologic patients experience at least one emergency during
their illness (Sadik et al., 2014).
Oncological emergencies are potentially life-threatening situations that should be identified
promptly with rapid intervention because stabilization is often required, in addition to referrals to
manage the underlying malignancy and to initiate palliative measures (McCurdy & Shanholtz, 2012).
Numerous of these situations are gradual and take months to develop, while others occur over hours
and lead to devastating consequences such as paralysis and death (Lewis, Hendrickson, & Moynihan,
2011). Many common oncological emergencies arise from metabolic and hormonal abnormalities,
malignancy treatment, and aggressive tumor compression on vital organs (Higdon, Atkinson, &
Lawrence, 2018). Their signs and symptoms can occur at any time during the course of malignancy
from the time before diagnosis to the end-stage disease (Higdon et al., 2018). A comprehensive,
available educational program about oncology emergencies can help the therapist team to better
manage treatment, provide appropriate services, and ensure timely and effective cure for cancer
patients. This study aimed to review urgent conditions that occur a result of cancer or its treatment
and need to immediate cure. We outline the most common oncological emergencies as metabolic,
cardiovascular, infectious, hematologic, neurologic, respiratory, and chemotherapeutic to facilitate
their recognition during the system-by-system assessment of the patient. In the current paper, the
pathophysiology, presentation, diagnosis, and treatment of commonly encountered emergencies in
oncology, and adverse effects of treatment in cancer patients are also addressed.

Oncological emergencies
In this review, the most common oncological emergencies have been classified to seven categories that
illustrated in Figure 1 and discussed below.

Metabolic emergencies
Tumor lysis syndrome
A specific definition of tumor lysis syndrome (TLS) as a syndrome that may include hyperkalemia,
hyperphosphatemia, hypocalcemia, and hyperuricemia is generally agreed as a series of metabolic
complications that may result from severe tumor cell death.

Pathophysiology. TLS is a rare but potentially fatal metabolic disorder with an estimated mortality of
29–79% unless diagnosed early and appropriately treated (Belay, Yirdaw, & Enawgaw, 2017;
Mirrakhimov, Voore, Khan, & Ali, 2015; Wilson & Berns, 2014). This disorder can occur spontaneously,
but it arises more often after chemotherapy and can also occur after radiation and biologic therapies
(Wilson & Berns, 2014). TLS is characterized by metabolic abnormalities resulting from acute destruction
of neoplastic cells and the liberation of intracellular components into the circulation in amounts beyond
the capacity of the kidney to eliminate (Howard, Pui, & Ribeiro, 2014). The incidence and severity of TLS
depend on numerous factors, including the type of malignancy, tumor mass, type and intensity of
anticancer therapy, the high proliferation rate of cancer cells, the sensitivity of cancer cells to anticancer
therapy, elevated lactate dehydrogenase levels, renal dysfunction, and taking multiple medications
(Howard et al., 2014; Mika, Ahmad, & Guruvayoorappan, 2012). Symptoms may include fatigue, cardiac
dysrhythmia, signs of dehydration, seizures, acidosis, nausea, and vomiting (Montesinos et al., 2008).
Patients commonly present metabolic abnormalities such as hyperphosphatemia, hyperkalemia, hyper­
uricemia, hypocalcemia, quantified by the Cairo-Bishop definitions (Table 1) (Wagner & Arora, 2017).
The secretion and catabolism of nucleic acids caused by tumor cell lysis can lead to hyperuricemia
(Coiffier, Altman, Pui, Younes, & Cairo, 2008). Under conditions of hyperuricemia, crystal formation
and deposition increase, leading to acute obstructive uropathy and renal insufficiency or failure (Cairo &
Bishop, 2004). The clinical manifestations of obstructive uropathy include hematuria, azotemia, acidosis,
 SOCIAL WORK IN PUBLIC HEALTH 3

Figure 1. Classification of most common oncological emergencies.

Table 1. Cairo-Bishop criteria for laboratory and clinical tumor lysis syndrome.
laboratory tumor lysis syndrome
Uric acid ≥8 mg/dL or 25% increase from baseline
Potassium ≥6 mEq/L or 25% increase from baseline
Phosphorous ≥6.5 mg/dL for children or ≥4.5 mg/dL for adults or 25% of increase from baseline
Calcium ≤7 mg/dL or 25% decrease from baseline
Clinical tumor lysis syndrome
Renal involvement Creatinine ≥1.5 times the upper limit of age-adjusted
Cardiac involvement Arrhythmia or sudden death
Neurologic involvement Seizure

low back pain, hypertension, edema, oliguria, anuria, lethargy, and drowsiness (Ly & Winokur, 2019).
Hyperkalemia, the most serious manifestation of acute TLS, may result from an overdose of iatrogenic
potassium during treatment induction, leading to diarrhea, vomiting, anorexia, neuromuscular abnorm­
ality, cardiac arrhythmia, and sudden death. Hyperphosphatemia is due to the extensive release of
intracellular phosphorus (Cairo & Bishop, 2004; Ly & Winokur, 2019). It is hypothesized that malignant
cells may contain up to three times the amount of organic and inorganic phosphorus compared to
normal cells. Secondary hypocalcemia may occur as a consequence of hyperphosphatemia, and phos­
phate and calcium-binding. Hyperphosphatemia and hypocalcemia can result in neuromuscular irrit­
ability, cardiac arrhythmia, hypotension, tetany, and seizures (Cairo & Bishop, 2004; Gemici, 2006).
4 A. JAFARI ET AL.

Presentation. Patients are symptomatic variably from the TLS metabolic derangements. When one or
more of three disorders occur, clinical TLS is diagnosed: acute renal failure, arrhythmias, and seizures
(Lewis et al., 2011). TLS occurs most frequently in rapidly proliferating hematological malignancies
such as non-Hodgkin lymphoma (NHL), acute myeloid leukemia (AML), acute lymphoblastic leuke­
mia (ALL), and Burkitt lymphoma, but has been reported in solid tumors, especially small cell lung
cancer, inflammatory breast cancer, germ cell tumors, and melanoma (Lewis et al., 2011; Vogel,
Pletcher, & Liang, 2010). The initiation of TLS may be delayed days to weeks in patients with severe
malignancy (Gemici, 2006).

Diagnosis. To help diagnose TLS, Cairo and Bishop developed the concept of TLS, which includes
clinical TLS (CTLS) and Laboratory TLS (LTLS), in 2004 (Table 1) (Cairo & Bishop, 2004). According
to this definition, LTLS occurs when there are 2 or more abnormal metabolic rates, or a 25% change
within 3 days before or 7 days after treatment (McBride & Westervelt, 2012). CTLS is specified as the
presence of LTLS along with one or more of the clinically significant complications including renal
failure, cardiac abnormalities, seizures, and sudden death (Coiffier et al., 2008; Ly & Winokur, 2019;
McBride & Westervelt, 2012).

Treatment. To minimize morbidity and mortality from TLS, prevention, and prompt initiation of
appropriate treatment is required. A key factor in the successful management of acute TLS is the
identification of patients by the risk group and the prevention of aggressive preventive strategies for
preventing and/or reducing the severity of clinical symptoms in high-risk patients. Ideally, tumor
therapy should be delayed in patients at risk for TLS until prophylactic measures for TLS are initiated.
Standard supporting care includes monitoring of electrolytes prior to and during cytoreductive
regimens as well as during aggressive hydration, initiated at least 24 hours prior to cytotoxic therapy.
High urine production results in robust hydration that improves urine flow, thereby facilitating uric
acid and phosphate excretion via enhanced intravascular volume, renal blood flow, glomerular
filtration, and reducing the risk of urate crystal accumulation within the genitourinary tract
(Gemici, 2006). Allopurinol inhibits xanthine oxidase and thus decreases the production of uric
acid and can be administered preventively every 8 hours at doses of 100 mg/m2 up to 48 hours before
treatment (Table 2). Urine alkalinization has historically been a general recommendation and stan­
dard practice for the prevention and treatment of TLS, specifically with concomitant use of allopur­
inol, by adding sodium bicarbonate to intravenous (IV) fluid to maintain the urine pH 7. However, the
use of sodium bicarbonate for urine alkalinization is no longer recommended due to a lack of clear
evidence of efficacy (Lewis et al., 2011; Pi et al., 2016). Loop diuretics can treat hyperkalemia. Injecting
10 U of normal insulin, followed immediately by 50 mL of 50% dextrose, and then a 50 to 75 mL of
10% dextrose hour-long infusion to avoid hypoglycemia can accomplish immediate reduction of
serum potassium by intracellular shifting. Inhaled beta-agonists, including 20 mg of nebulized
albuterol, can rapidly and sustainably (Lewis et al., 2011). Hyperphosphatemia is treated by
a phosphorous-restricted diet or by the short-term use of oral phosphate binders, such as aluminum
carbonate, aluminum hydroxide, or calcium acetate (which should be avoided in patients with
hypercalcemia) (Rampello, Fricia, & Malaguarnera, 2006). In the end, dialysis may be required to
treat any refractory, life-threatening electrolyte disruptions, particularly in the context of volume
overload and renal failure (Table 2) (Lewis et al., 2011).

Hyperphosphatemia and hypocalcemia

Tumor cells may contain up to 4 times phosphorous levels compared with normal cells, therefore
hyperphosphatemia may occur consequent rapid tumor lysis. Then, the kidneys attempt to clear
uprising phosphate levels by increasing urinary excretion and reducing tubular resorption.
Nevertheless, transport mechanisms gradually become overwhelmed, leading to the accumulation
of calcium phosphate within the renal tubules with consequent acute kidney damage, increased levels
of serum phosphorus, and decreased levels of calcium. Hypocalcemia presents as tetany, altered
 SOCIAL WORK IN PUBLIC HEALTH 5

Table 2. Treatments for metabolic emergencies.

problem Intervention Dosage
Renal insufficiency Intravenous fluids Normal saline, 3 L/m2 daily
(Use with caution if decreased systolic function)
Dialysis
Hyperkalemia Insulin (regular) 10 U iv
Dextrose 50 mL of 50% dextrose iv push, then
infuse 50–75 mL of 10% dextrose over 1 h
Albuterol 20 mg nebulized
Dialysis
Calcium gluconate 1000 mg iv (If hyperkalemic electrocardiogram changes are
noted)
Hypercalcemia Normal saline 1000–2000 ml iv
Bisphosphonates (pamidronate and
zoledronic acid)
Calcitonin 4 to 8 IU/kg every 12 h
Hypocalcemia Calcium gluconate 50–100 mg/kg or 1–3 g for adults (Use with caution in severe
hyperphosphatemia)
Hyperuricemia Allopurinol 100 mg/m2 per dose orally every
8 h (only effective for prophylaxis)
Rasburicase 0.15–0.2 mg/kg/d iv
Hyperphosphatemia Minimize phosphate intake Minimal consumption of
dairy and bread products
Phosphate binders (aluminum 30 mL orally every 6 h
Hydroxide/carbonate)
Dialysis (If no response to oral therapy)
Hypoglycemia glucagon at a dose of, 1 mg iv/im
dextrose infusion
diazoxide 3 mg/kg/day initially
Exogenous glucocorticoids

mental status, muscle cramps, carpopedal spasm, paresthesias, seizures, hypotension, hallucinations,
and exacerbation of arrhythmias (Cairo & Bishop, 2004; Wagner & Arora, 2017). Hypocalcemia
usually resolves as tumor lysis increases, without any interference. The slow IV administration of
calcium gluconate with electro cardio graph (ECG) monitoring may, however, be given in patients
with symptomatic hypocalcemia (Pi et al., 2016).

Hypercalcemia
Hypercalcemia is a metabolic emergency that occurs in 20–30% of patients with malignancy at some
time throughout the course of their disease (Hoyoux, Lombet, & Nicolescu, 2017; Reagan, Pani, &
Rosner, 2014). It most commonly occurs in advanced malignancies, usually associated with breast
cancer, lung cancer, multiple myeloma, and non-Hodgkin’s lymphoma, although it can be seen with
any malignancy (Sternlicht & Glezerman, 2015; Yeung & Liu, 2016). Hypercalcemia often indicates
poor prognosis regarding malignancy, especially when associated with increased protein levels asso­
ciated with parathyroid hormones (PTHrP) (Hoyoux et al., 2017). PTHrP increases bone resorption
through osteoclast activity and improves the resorption of calcium in the renal tubule (Hoyoux et al.,
2017).

Pathophysiology. Up to 80% of malignant hypercalcemia is caused by the systemic circulation of

PTHrP released by the tumor. The effects of this hormone reflect a true paraneoplastic syndrome with
PTHrP circulating which causes bone resorption and calcium retention in the renal (Goldner, 2016).
Bone metastases can induce a local paracrine effect by generating various factors that stimulate
osteoclasts, resulting in bone resorption with subsequent hypercalcemia and bone destruction. It is
most commonly observed in metastatic breast cancer and multiple myeloma. Despite the frequency of
bone metastases, prostate cancer rarely causes hypercalcemia, underlying that it is not just bone
involvement but the specific interaction of the tumor and bone that releases calcium from the bone
(Lewis et al., 2011; Onalan, 2019). New agents, such as those altering the nuclear factor kappa-B ligand
6 A. JAFARI ET AL.

(RANKL) receptor activator (denosumab) or inhibiting osteoclastogenesis (osteoprotegerin), may be

used to alter the tumor microenvironment to control hypercalcemia and bone resorption (Lewis et al.,
2011). Vitamin D analog tumor production is a less common etiology of malignant hypercalcemia,
with non-Hodgkin lymphoma and Hodgkin lymphoma both capable of producing elevated levels of
calcitriol.

Presentation. The symptoms of hypercalcemia are unspecific, and delayed recognition of this meta­
bolic disorder may exacerbate morbidity and mortality (Walji, Chan, & Peake, 2008). The symptoms
are unclear and often indicate symptoms of significant volume depletion due to hypercalcemia-related
osmotic diuresis (Hoyoux et al., 2017). Anorexia, nausea, vomiting, and constipation are the most
common symptoms but may include malaise, polyuria, polydipsia, lethargy, depression, and even
coma (Rosner & Dalkin, 2012).

Diagnosis. Ionized calcium is the most reliable laboratory test for detecting hypercalcemia, and is
considered to be above 1.29 mmol/L. It is important to correct hypoalbuminemia when measuring
total calcium using the following formula: corrected calcium in mg/dL = measured total calcium
in mg/dL + 0.8 (4-measured albumin in g/dL) (Hoyoux et al., 2017). The assessment of PTHrP has not
been shown to affect the outcome and should not direct the initial administration. Nevertheless,
patients with PTHrP >12 pmol/L may be less responsive to bisphosphonates, and more likely to
develop recurrent hypercalcemia (Lewis et al., 2011; Mirrakhimov, 2015). Serum chloride is a ready-to
-use test and hypocalcemia below 100 mEq/L supports humoral hypercalcemia diagnosis (Lewis et al.,
2011). An ECG may exhibit prolonged PR, widened QRS, shorter QT, and dysrhythmias of the
ventricle (Sternlicht & Glezerman, 2015; Yeung & Liu, 2016).

Treatment. Initial emergent hypercalcemia treatment includes rapid IV hydration with an initial
1000–2000 ml bolus of normal saline accompanied by an infusion rate of 200–300 ml/h to reach
100–150 ml/h urine output (Reagan et al., 2014; Yeung & Liu, 2016). In addition to hydration, IV
bisphosphonates (pamidronate and zoledronic acid), which interact with osteoclast activity and
induce apoptosis of osteoclast, are the cornerstone of treatment for malignant hypercalcemia (Pi
et al., 2016). If the use of pamidronate or zoledronic acid is used to treat renal dysfunction, a long-term
infusion should be considered. The starting time for IV bisphosphonate is 24–72 hours. For persistent
or refractory hypercalcemia, repeated doses of a bisphosphonate should not be administered less than
7 days after previous administration (Pi et al., 2016). Dialysis may be sufficient for treating patients
with renal failure, if excessive hydration and bisphosphonate administration are unsafe or not feasible.
Calcitonin administration lowers calcium faster than bisphosphonates, often producing normalcalce­
mia within 12 to 24 hours, but rapidly loses efficacy through tachyphylaxis. Because of rebound
hypercalcemia it should not be used as a single agent. Calcitonin may be administered intramuscularly
or subcutaneously every 12 hours at a dose of 4 to 8 IU/kg, but intranasal administration is ineffective
to treat hypercalcemia (Table 2). Glucocorticoids such as 60 mg of prednisone daily or 100 mg of
hydrocortisone IV every 6 hours may be useful in mediating the release of osteoclasts-stimulating
cytokines and prostaglandins. Besides their direct lympholytic effect, steroids prevent the production
of calcitriol by macrophages and decrease calcium levels significantly within 3 to 5 days after injection.
Denosumab is a fully-humanized monoclonal antibody with a high affinity and specificity for RANKL
licensed for use in the management of postmenopausal osteoporosis and in the prevention of bone
metastasis skeletal events and has potential application in malignant hypercalcemia (Lee, Saylor, &
Smith, 2011; Lumachi, Brunello, Roma, & Basso, 2009). Osteoprotegerin, a RANKL decoy receptor,
and an osteoclast maturation inhibitor, has been shown to correct hypercalcemia faster and more
sustainably than bisphosphonates (Morony et al., 2005).
 SOCIAL WORK IN PUBLIC HEALTH 7

Hypoglycemia
Pathophysiology. Hypoglycemia can occur in cancer patients via multiple etiologies. Some tumors are
able to produce substances ectopically, which affects the metabolism of glucose (McElroy, Lowy, &
Weidner, 2010). Mesenchymal tumors such as sarcoma, including solitary fibrous tumor and gastro­
intestinal stromal tumor, capable of producing insulin-like growth factors (IGFs), such as IGF-2, that
increase tissue use of glucose and blunts the growth hormone secretion (Bruzzone, Varaldo,
Ferrarazzo, Tunesi, & Mencoboni, 2010). In cancer cells, the glycolysis pathway is very active via
the Warburg effect, even in the presence of oxygen, so high glucose uptake in these cells contributes to
hypoglycemia. This is most often seen in severe lymphomas (e.g., Burkitt lymphoma) but was also
identified in cancer of the small cell lung (Diaz, Antoine, & Azad, 2010). Tumors can penetrate organs
that play an important role in normal glucose metabolisms, such as hepatocellular carcinoma that
replaces hepatic parenchyma or adrenal gland pheochromocytoma (Habra et al., 2010).

Presentation. Neuroglycopenia and antiadrenergic dysregulations are signs and symptoms of hyper­
glycemia, which can occur as neurological manifestations from agitation and blurred vision to seizures
and comas. Diaphoresis, palpitations, and dilation of the pupils are due to hypoglycemic catechola­
mine reactions (Tesfaye & Seaquist, 2010).

Diagnosis. Initially developed to determine eligibility for pancreatic surgery in patients with insuli­
noma, the Whipple triad involves assessed hypoglycemia, symptoms due to hypoglycemia and
symptom recovery when normoglycemia is restored. In the absence of insulin secretagogues, an
otherwise healthy adult will typically maintain a level of glucose above 50 mg/dL over a 72-hour fast
(Van Bon, Benhadi, Endert, Fliers, & Wiersinga, 2009). Insulin and high levels of peptide C indicate
islet cell tumors, whereas high ratio of IGF-2 to IGF-1 indicates a mesenchymal tumor (Lewis et al.,
2011).

Treatment. Treatment for cancer-related hypoglycemia may include surgical resection of the tumor
or chemotherapy underlying, and radiotherapy for unresectable tumors. Temporary treatment may
include prescribing glucagon, dextrose injection, diazoxide, and discontinuing nonselective beta-
blockers that blunt adrenergic reactions to low blood sugar (Arao, Okada, Hirose, & Tanaka, 2006).
Also were suggested exogenous glucocorticoids and regimented daily intake of carbohydrates (Table
2) (Thipaporn, Bubpha, & Varaphon, 2005).

Syndrome of inappropriate antidiuretic hormone

Pathophysiology. In cancer patients with normal or increased plasma volume and hyponatremia, the
syndrome of inappropriate antidiuretic hormone secretion (SIADH) should be suspected (Mentrasti
et al., 2020). This disorder is characterized by the unrestrained release of antidiuretic hormone (ADH)
from the hypophysis or non-hypophysis sources, or by continued activity on receptors of vasopressin.
SIADH is most common in small cell lung cancer and less common in head and neck cancers,
extrapulmonary small cell carcinomas, and olfactory neuroblastomas. In patients with SIADH, levels
of ADH are high that lead to water retention and hyponatremia (Mentrasti et al., 2020).

Presentation. The signs and symptoms of SIADH depend on the rate and severity of hyponatremia.
The earliest clinical manifestations of acute hyponatremia include malaise and nausea (Higdon &
Higdon, 2006). Patients with a more severe and acute fall in sodium concentration may present
lethargy, headache, myalgia, and obtundation. Whenever the serum sodium level falls below 115 to
120 mEq/L, Coma and respiratory arrest can occur (Higdon & Higdon, 2006; Yasir & Mechanic, 2020).

Diagnosis. There is no single best diagnostic method for SIADH. Laboratory testing may reveal
Serum sodium <135 mEq/L (hyponatremia), and Serum osmolality less than 275 mOsm/kg,
8 A. JAFARI ET AL.

concentrated urine. Some tests for SIADH are serum osmolality and serum sodium, BUN and
creatinine, Thyroid profile, Serum cortisol, and Liver function (Higdon & Higdon, 2006).

Treatment. The treatment of SIADH involves slow correction of serum sodium levels. Hypertonic
saline (osmolality 513 mOsm/kg) should be considered for patients with severe neurologic symptoms
symptomatic or resistant hyponatremia. Demeclocycline, conivaptan (IV), and tolvaptan (oral) are
recommended for SIADH (Higdon & Higdon, 2006; Mentrasti et al., 2020).

Hematologic emergencies
Hyperviscosity syndrome
Hyperviscosity syndrome (HVS) refers to clinical sequelae caused by increased blood viscosity due to
excess serum protein, generally Waldenström’s macroglobulinemia (WM), multiple myeloma (MM)
or immunoglobulins (Mazzucchelli, Frustaci, Deodato, Cairoli, & Tedeschi, 2018). Hyperviscosity
syndrome contributes to partial hypotension, and its clinical symptoms suggest end-organ disorder
that can resemble another disease’s pathology. For instance, patients with HVS can complain of
dyspnea (pulmonary embolism mistake or congestive heart failure), visual changes (cerebrovascular
accident mistake), or changed mental status (sepsis mistake) (Wagner & Arora, 2017). As with
cytoreductive agents, regular phlebotomies can be used to reduce the risk of microvascular obstruction
(Lewis et al., 2011).

Pathophysiology. For healthy subjects, hematocrit is the major determinant of blood viscosity.
Because of its combination of large size, asymmetric form, load and concentration, fibrinogen is
the major determinant of plasma viscosity, while albumin is the most abundant protein in the blood
(Porcu et al., 2000). Excessive amounts of circulating immunoglobulins (Igs) are produced in
paraproteinemias, such as the WM and MM. IgG has a positive charge and thus reduces the
repulsive forces between negative red blood cells. Such proteins bind electrostatically to erythrocytes
in the presence of overexpression, resulting in the development of a roll shape as well as a decrease
in the versatility of red blood cells. It eventually leads to the decreased passage of blood cells,
microvascular obstruction, reduced tissue perfusion, and resulting damage to the tissue (Behl,
Hendrickson, & Moynihan, 2010; Mullen & Wang, 2007). The standard relative serum viscosity
(SV) is about 1.4–1.8 centipoise (cP) (Lewis et al., 2011). An SV more than 4 cP suggests
hyperviscosity syndrome (Khan, Shanholtz, & McCurdy, 2017). Many patients have paraprotein
levels range from 5 to 8 g/L, with levels above 8 g/L causing symptoms almost always (Lewis et al.,
2011).

Presentation. The “classic triad” of HVS includes visual changes, neurologic deficits, and skin
bleeding, although not all three need to be present to make the diagnosis (Kwaan, 2013). The
ophthalmological examination can detect hyperviscosity, showing dilated, engorged veins resembling
“sausage links”, a condition known as fundus paraproteinaemicus. If not treated, retinal vein occlusion
and flame-shaped hemorrhages will be developed (Behl et al., 2010). Mucosal bleeding and purpura
are also typical clinical manifestations of HVS, coating the platelets with proteins, and impeding their
operation. Other clinical consequences of HVS include headache, altered mental status, congestive
heart failure, ischemic acute tubular necrosis, pulmonary edema, ataxia, seizures, with multiorgan
system failure, and death occurring if treatment is not undertaken immediately (Mullen & Wang,
2007).

Diagnosis. There is no conclusive HVS test as this is a clinical diagnosis but it is important to have
accurate history and physical examination. A markedly elevated white blood cell count (i.e.,
>100 × 104) or hemoglobin (i.e., approaching 20 g/dl) associated with hypoperfusion symptoms
should be considered. Laboratory studies including an electrolyte panel, SV, CBC with peripheral
 SOCIAL WORK IN PUBLIC HEALTH 9

blood smear, coagulation panel, and quantitative Ig levels should be obtained.178 Blood transfusion
can exacerbate HVS dramatically and should be avoided unless critically necessary (Leblond et al.,
2016; Stone & Bogen, 2012). Each patient with an SV greater than 4 cP for HVS should be tested.
Patients also have pseudo hyponatremia, hyperphosphatemia, and hyperkalemia (Porcu et al.,
2000).

Treatment. The key therapy basics are reducing serum viscosity by the resuscitation of IV fluid,
plasmapheresis, or leukopheresis (Ganzel, Becker, Mintz, Lazarus, & Rowe, 2012). In an emergency
setting, phlebotomy (e.g., polycythemia) or even urgent chemotherapy (e.g., acute leukemia) may also
be indicated to reduce acute symptoms (Chakraborty, Kapoor, Ansell, & Gertz, 2015). Research for
these treatments shows that they do not alter the course of the disorder but rather assist in relieving the
symptoms. Both HVS patients will need hospital admission and merit a good ICU admission
(Klemencic & Perkins, 2019).

Leukostasis
Leukostasis, a hematological emergency most often seen in acute myeloid leukemia patients, is associated
with respiratory failure, intracranial hemorrhage, and early death. Risk factors for leukostasis include
white blood cell count (WBC) greater than 100,000/mm 3, younger age, acute lymphoblastic leukemia
with Philadelphia chromosome, and subtypes M3, M4, and M5 of AML (Majhail & Lichtin, 2004).

Pathophysiology. The leukostasis pathophysiology is not fully understood. The leukemic blasts in the
microvasculature secondary are thought to be a part of’’ sludging’’ to increase whole blood viscosity.
On average, the leukemic myeloblasts have a mean volume of cells nearly twice that of the leukemic
lymphoblasts and therefore the symptoms are more frequent in AML patients rather than ALL (Lewis
et al., 2011). In addition, Leukemic blast/endothelial cell interactions resulting in the destruction of the
vascular wall, as well as complementary aggregation of granulocytes (Porcu et al., 2000). Generally,
whole blood viscosity in leukostasis does not increase dramatically, as the increase in the WBC is often
counterbalanced by a decrease in the number of red blood cells. This is vital to recognize because
packed red blood cell transfusions can rapidly lead to leukostasis in patients with asymptomatic
hyperleukocytosis (Behl et al., 2010).

Presentation. Although leukostasis can involve any organ system, most commonly the initial symp­
toms are associated with the respiratory system and CNS (Porcu et al., 2000). Pulmonary symptoms
can vary from exertional dyspnea to extreme breathing difficulty, and neurologic manifestations span
the spectrum from mild agitation to somnolence. Patients usually have all the same symptoms of
hyperviscosity but also focal neuro deficits, intracranial hemorrhage, hypoxia, pulmonary infiltrates,
chest pain, myocardial infarction, fever, renal failure, and thrombosis been reported. Patients generally
complain of fatigue, headache, dizziness, tinnitus, blurred vision, or deficiencies in the visual field
(Majhail & Lichtin, 2004).

Diagnosis. The leukostasis diagnosis is made by integrating patient symptoms and the WBC (Lewis
et al., 2011).

Treatment. Leukapheresis is a generally accepted initial treatment and was previously believed to
minimize early mortality; however, it lacks randomized controlled trials and longitudinal studies have
not demonstrated a survival benefit. Leukapheresis that quickly lowers the white count and improving
symptoms is typically performed when the blast count is greater than 100,000/m3 or in the presence of
symptoms, regardless of blast count (Chang et al., 2007). Rapid cytoreducing is also the initial
treatment, ideally done by induction chemotherapy, which can reduce the WBC significantly within
24 hours. Hydroxyurea can be administered every 6 hours at doses of 1 to 2 g and can reduce the WBC
within 24 to 48 hours by 50% to 80% (Porcu et al., 2000).
10 A. JAFARI ET AL.

Cardiovascular emergency
Pericardial effusion and cardiac tamponade
Pathophysiology. If stretching occurs over a slow interval, the pericardial sac can be distensible up to
2 liters. Increased intraperitoneal pressure affects all four chambers of the heart, but the right
ventricular wall is much thinner and prone to more pressure. Diastolic pressures adversely affect
cardiac output, at this point, tamponade physiology emerges (Spodick, 2003). Malignant pericardial
effusions develop through direct (in those tumors with sites of origin adjacent to the heart) or
metastatic (in noncontiguous breast and lung cancer, as well as in melanoma) involvement of the
pericardial sac (Maisch, Ristic, & Pankuweit, 2010). Treatment of cancer, especially with thoracic
irradiation, can cause trans dative effusions. Immunosuppression may also allow for the development
of supportive infections in the pericardial region.

Presentation. Pericarditis symptoms may precede the emergence of tamponade, which presents with
the Beck triad: hypotension, elevated jugular venous pressure, and a muffled precordium. The majority
of patients complain of dyspnea and chest pain, which can start suddenly (Jacob, Sebastian, Cherian,
Abraham, & John, 2009).

Diagnosis. Physical examination coupled with appropriate studies utilized for diagnosis. Chest x-rays
and electrocardiography can show the classic “water bottle” cardiac silhouette and right ventricular
collapse during early diastole, respectively (Feusner, Hastings, & Agrawal, 2015).

Treatment. Sonographically directed pericardiocentesis has reduced complication rates by 4-fold

over blind subxiphoid pericardiocentesis, which should be reserved for extrem patients. A catheter
can be put in the sac to remove residual or reaccumulation fluid (Kim et al., 2010). Decompression
may lead to paradoxical hemodynamic instability, which requires admission to the intensive care unit.
Chemotherapy injection into the pericardial space has been investigated as a means of reducing the
risk of recurrence of malignant pericardial effusions (Oida et al., 2010; Wagner et al., 2011).

Superior vena cava syndrome

Pathophysiology. Superior vena cava (SVC) syndrome is obstruction of blood flow through the SVC
because of its thin-wall that returns all blood from the cranial, neck, and upper extremity vasculature
to the right side of the heart. Etiologies include primary or metastatic tumors, syphilitic aortic
aneurysms, substernal hypertrophy of the thyroid, thrombosis, and granulomatous (Cohen, Mena,
Carbajal-Mendoza, Matos, & Karki, 2008).

Presentation. Symptoms may include edema in the arms, cough, dyspnea, dysphagia, chemosis,
swelling or stain of the neck, face and upper extremities, and syncope. When the patient is supine,
all these signs may be more apparent. Cancers that are classically associated with SVC syndrome
include lung cancer, breast cancer, lymphoma, primary mediastinal lymphoma, and tumors of the
germ cells (Khalili et al., 2007).

Diagnosis. Although SVC syndrome is a clinical diagnosis, plain radiography, computed tomography
(CT), magnetic resonance imaging (MRI), and venography are typically favored for their noninva­
siveness, easier availability, and lower contrast load (Ganeshan, Hon, Warakaulle, Morgan, & Uberoi,
2009).

Treatment. Management of SVC syndrome is divided into definitive and supportive therapy. When
SVC syndrome heralds malignancy, the physician usually still takes time to perform a biopsy or other
diagnostic procedures without compromising the patient, although treatment should not be unne­
cessarily delayed (Cohen et al., 2008). A simple therapeutic strategy is to lift the patient’s head in order
 SOCIAL WORK IN PUBLIC HEALTH 11

to minimize the hydrostatic pressure and thus the edema. Glucocorticoid therapy, fibrinolytic therapy,
radiation, and chemotherapy are also used depends on cancer type (Cohen et al., 2008; Wilson et al.,
2007). Intravascular stenting, however, offers symptomatic relief within one to two days and is
becoming more widespread, and sometimes the only treatment option for recurrent obstructive
tumors.

Neurologic emergencies
Malignant spinal cord compression
Malignant spinal cord compression (MSCC) is an oncologic emergency that requires prompt treat­
ment to relieve pain, potential paralysis and preserve neurological function (Pi et al., 2016). MSCC
affects 5% of terminal cancer patients with a mean survival of less than 6 months from diagnosis in the
last 2 years of their life. Around 20% of patients with MSCC present as their initial finding (Pi et al.,
2016). Although all tumor types have the potential to cause MSCC, lung, breast, and prostate cancer
each account for approximately 15–20% of the cases, with non-Hodgkin lymphoma, renal cell
carcinoma, and multiple myeloma each causing 5–10% of cases (Prasad & Schiff, 2005).

Pathophysiology. MSCC is characterized as the compressive indentation, displacement, or enclosure

of the thecal sac surrounding the cancer spinal cord or cauda equina. Compression may occur by the
subsequent extension of a vertebral body mass, by the anterior extension of a dorsal mass or by the
growth of a mass, which invades the vertebral foramen. Many cases arise when the metastatic tumor
reaches the vertebral bodies with retropulsion of bony fragments into the epidural space (Prasad &
Schiff, 2005). Location for MSCC is 60% in the thoracic spine, 30% in the lumbosacral region, and 10%
in the cervical spine (Cole & Patchell, 2008). It is also important to note that metastatic lesions are seen
in nearly half of all patients at multiple levels of the spinal cord.

Presentation. Depending on the severity, location, and duration of the compression, the clinical
presentation of MSCC can vary significantly. The most frequent initial symptom is back pain, which
occurs in approximately 90% of the cases. Cervical compression may occur as subscapular pain,
thoracic compression as lumbosacral or hip pain, and lumbosacral compression as chest pain. Other
symptoms include motor weakness, sensory impairment, bowel, and bladder dysfunction, and
ataxia decreased sensation over the buttocks, posterior superior thighs, and perineal region
(Prasad & Schiff, 2005). Early signs include spasticity, hyperreflexia, and loss of sensation, while
weakness, Babinski sign, and decreased anal sphincter tone can occur late (Abrahm, Banffy, &
Harris, 2008).

Diagnosis. The gold standard for MSCC diagnosis is MRI, with a 93% sensitivity, a 97% precision and
a 95% overall accuracy (Lewis et al., 2011). CT myelography may be used when MRI is contraindicated
or not available (Cole & Patchell, 2008).

Treatment. Management of patients with MSCC includes corticosteroids, surgery, and radiation
therapy. Indeed, the goals of treatment for MSCC patients include pain control, reducing complica­
tions, and maintaining or improving neurological function (McCurdy & Shanholtz, 2012; Ribas &
Schiff, 2012).

Increased intracranial pressure

Elevated intracranial pressure (ICP) develops as a frequent neurologic emergency in patients with
cancer. When not properly managed, elevated ICP quickly leads to irreversible neurological defects
and death (Lin & Avila, 2017). The prognosis depends on Karnofsky’s performance status, systemic
disease involvement and the primary tumor (Tosoni, Ermani, & Brandes, 2004)
12 A. JAFARI ET AL.

Pathophysiology. Most metastases travel to the brain through hematogenous expansion. Tumor
microemboli appear to lodge in distal arteries and narrow capillaries in the “watershed” regions and
junctions of gray-white matter. The increase in ICP is due to the effect of tumor mass as well as
brain edema induced by neoplastic impairment of the blood-brain barrier, partly caused by local
production of vascular endothelial growth factor (VEGF) (Argaw, Gurfein, Zhang, Zameer, & John,
2009).

Presentation. The clinical appearance of brain metastases can differ according to the tumor’s loca­
tion, size and rate of growth. The common presentations are headache, seizures, stroke, and focal
neurologic dysfunction (Lin & Avila, 2017). Other indications of increased ICP include vomiting,
nausea, and diplopia from abducens nerve palsies (Lin & Avila, 2017). The triad of symptoms called
the Cushing response (wide-pulse hypertension, bradycardia, and rapid respiratory rate) is a late result
and signals an imminent herniation (Lewis et al., 2011).

Diagnosis. Imaging techniques such as MRI, especially contrast-enhanced MRI, and Non-contrast
CT scanning can be used (Lin & Avila, 2017).

Treatment. Glucocorticoids are the first treatment of choice and can minimize peritumoral edema
and local compression of the brain in hours by restoring the leaky capillary permeability. Mannitol and
hyperventilation are used in severe cases (Thibault, Billemont, & Rixe, 2008). More specific treatment
methods include radiation therapy of the whole brain, chemotherapy or stereotactic radiation surgery.
Chemotherapy may be used in extremely chemosensitive disorders such as tumors in germ cells,
carcinomas in small cells, or lymphoma, or in cases where radiation therapy is not a choice (Lewis
et al., 2011; Lin & Avila, 2017).

Seizures
Seizures are the presenting symptomes in 20–40% of patients with brain metastases, especially when
there are multiple metastases (Maschio, 2012). Status epilepticus includes emergent treatment, usually
with phenytoin, lorazepam, valproic acid, or fosphenytoin. Patients of brain metastases who have not
had seizures do not benefit from antiseizure drug administration (Behl et al., 2010).

Respiratory emergencies
Malignant airway obstruction
A significant proportion of patients with tongue, thyroid, oropharynx, trachea, bronchi, and lung
cancer may experience obstruction of the central airways at some stage during disease and as many as
40% of lung cancer-related deaths arise directly from the loco-regional disease (Mudambi, Miller, &
Eapen, 2017). Airway obstruction does not appear to adversely affect overall survival, but rapid
diagnosis and treatment can lead to significant quality of life.

Pathophysiology. Airway obstruction by a tumor or lymph node can be caused by external tracheal or
bronchial compression. Tumor intrusion into the larynx, trachea, and bronchi can also reason
obstruction, causing severe narrowing.

Presentation. Symptoms of malignant airway obstruction are nonspecific and can be mistaken for
conditions such as exacerbations of chronic obstructive pulmonary disease, bronchitis, or asthma. The
signs may be mild such as cough and exertional dyspnea but are often severe due to post-obstructive
infections, rest dyspnea hemoptysis, and asphyxiation (Mudambi et al., 2017). The syndrome
“Tracheal stenosis” refers to signs of shortness of breath, cough, wheezing, and stridor, and is present
in about 85% of patients with primary tracheal tumors. Hemoptysis was reported in half of the patients
with occlusion neoplasm (Lewis et al., 2011).
 SOCIAL WORK IN PUBLIC HEALTH 13

Diagnosis. For patients with a history of malignancy who have new respiratory symptoms, chest
x-rays should be obtained rapidly to assess the existence of a tumor or indirect signs of obstruction
such as tracheal deviation or airway narrowing, though CT scanning is preferred. Bronchoscopy
provides easy visualization of the obstruction and offers a tool for acquiring tissue for diagnosis and
immediate treatment (Behl et al., 2010).

Treatment. The main component of treatment is stenting via bronchoscopy because it helps to
diagnose and manage. The mainstay of treatment is because it aids in diagnosis and treatment.
Other treatments include thermal therapies, laser therapy ((e.g., Nd: YAG (neodymium-doped yttrium
aluminum garnet)), electrocautery, cryotherapy, radiation, and chemotherapy (Mudambi et al., 2017).

Infectious emergencies
Neutropenic fever
Pathophysiology. Neutropenic fever (NF) is one of the most well-known oncologic emergencies,
related to cancer treatment, particularly chemotherapy (Rosenberg et al., 2006). Other risk factors
include the rapid decline in absolute neutrophil count (ANC); susceptibility to previous chemotherapy
or current immunosuppression; pretreatment elevations in alkaline phosphatase, aspartate amino­
transferase levels, or bilirubin; cardiovascular comorbidity and decreased glomerular filtration rate
(Lewis et al., 2011).
The causative agents at the highest risk include anthracyclines, taxanes, platinum, topoisomerase
inhibitors, gemcitabine, vinorelbine, and alkylating agents (Lyman et al., 2011). NF can be due to
underlying malignancy (e.g., leukemia), chemotherapeutic drug toxicity, mucositis, or a variety of
other conditions. Neutropenic fever is associated with lower quality of life and higher mortality and
morbidity levels (Klemencic & Perkins, 2019). The majority of culture-positive cases of NF is by gram-
positive cocci include Staphylococcus aureus, Staphylococcus epidermidis Streptococcus pyogenes,
Streptococcus pneumoniae, Streptococci viridans, and Enterococcus faecalis and faecium.
Corynebacterium is the most likely gram-positive bacillus. The responsible gram-negative bacilli
include Escherichia coli, Pseudomonas aeruginosa, and Klebsiella species. The most common infec­
tion of fungi is Candida, but Aspergillus and Zygomycetes are more concerned about their angioin­
vasive tendency (Kanamaru & Tatsumi, 2004).

Presentation. Neutropenic fever symptoms include a single oral temperature of 38.5°C or higher or
a sustained temperature of 38°C or higher for an hour, and an ANC of less than 500 cells/mm3 or
a predicted reduction of ANC to less than 500 cells/mm3 in the next 48 hours. Skin and soft tissue
infections may not be accompanied by erythema or inhalation and abscesses do not accumulate in the
absence of pus-producing neutrophils (Kim et al., 2010).

Diagnosis. Normal initial monitoring will include a complete blood count (CBC) with manual
differential, two blood sample sets, complete metabolic panel (CMP), urinalysis and analysis, and
chest x-ray. When the patient has diarrhea, consider doing examination of stool cultures and C. diff
testing. During the initial assessment, renal and liver function are regularly tested for plasma
creatinine levels, blood urea nitrogen, electrolytes, hepatic transaminase enzymes and complete
bilirubin to prepare supportive care, and appropriate treatment (Klemencic & Perkins, 2019).

Treatment. Patients with FN with a high risk of complications should be initiated with empiric
antibiotics administered intravenously in the hospital setting until they are afebrile for 48 to 72 hours
and ANC levels are at least 500 cells per mm3 for 72 hours (Kim et al., 2010). Monotherapy is only
appropriate with a sufficiently broad-spectrum drug, such as cephalosporin cefepime of the fourth
generation, piperacillin-tazobactam, or a carbapenem, all of which provide antipseudonomic activity.
Vancomycin can be added to infections of the skin and soft tissues, pneumonia or suspected device
14 A. JAFARI ET AL.

infections, not as monotherapy (Lewis et al., 2011). For patients at low risk without serious comorbid­
ities, oral observational treatment with ciprofloxacin and amoxicillin-clavulanate is appropriate.
Patients allergic to penicillin may be given cephalosporin, but either ciprofloxacin and clindamycin
or aztreonam and vancomycin are recommended in cases of immediate hypersensitivity. Empirical
antifungal therapy initiation is recommended for patients with persistent fever of unknown causes
following 4 to 7 days of antibiotic therapy, and those with neutropenia expected to last more than
7 days (Freifeld et al., 2011). High-risk patients, such as those with acute leukemia and those recently
given high-dose cytotoxic chemotherapy, can need antibiotic treatment for up to 10 days or until
neutropenia is resolved (Klastersky et al., 2016).

Chemotherapeutic emergencies
Extravasation of chemotherapy
Pathophysiology. Extravasation is characterized as the inadvertent installation or leakage in the
perivascular space during the infusion of cytotoxic drugs. In recent years, extravasation has gained
growing prominence as a feared risk of chemotherapy (Mader, Fürst-Weger, Mader, Nogler-Semenitz,
& Wassertheurer, 2009). Classified according to their subcutaneous toxicity, three types of cytotoxins
have been established: vesicants, irritants, and nonvesicant drugs. Nonvesicant substances have no
signs of local irritation, and irritant drugs may cause local pain, swelling, and irritations, but no
necrosis. Vesicants are cytotoxic drugs that have the ability to induce tissue damage, ulceration, and
tissue necrosis (Mader et al., 2009).

Presentation. Symptoms vary in their clinical presentation and severity, and may arise immediately
after the incident, or develop in days or weeks that follow. Initial symptoms include pain, induration,
blistering, and discoloration. Necrosis of the skin and underlying tissues may develop in severe cases,
leading to inflammation, scars, infection, delay in treatment, functional impairment, amputation, and
occasionally, death. Symptoms for irritant extravasation include erythema, swelling, and tenderness.
Afterward, phlebitis, hyperpigmentation, and sclerosis may develop along the vein. Such symptoms
usually resolve within weeks, and there are extremely rare long-term sequelae (Langer, 2010).

Diagnosis. Extravasation is usually diagnosed by erythema, local signs of pain, and swelling, or by
fluid leakage around the iv site, but the initial indication may be a change in the rate of infusion or loss
of blood return from exposure to the vascular. When suspected, even if asymptomatic, the infusion
should be stopped and immediate treatment started (Langer, 2010; Schulmeister, 2010).

Treatment. Prevention is the best approach to an extravasation injury. Moreover, the education of
patients about risks and manifestations are essential (Jacobson et al., 2009). Application of ice (cool­
ing), which causes vasoconstriction and reduces pain and the extent of local injury, is recommended
for extravasation of vesicants and irritant drugs, except the vinca alkaloids and epipodophyllotoxins.
However, substances such as topical or injectable dimethyl sulfoxide (DMSO), hyaluronidase, and
corticosteroids are used, only the FDA for anthracycline-induced extravasation therapy has approved
dexrazoxane (Kreidieh, Moukadem, & El Saghir, 2016). Sodium thiosulfate recommended for
mechlorethamine extravasation. It significantly improved recovery time in patients with multiple
chemotherapy-induced injuries to extravasation including doxorubicin, vinblastin, epirubicin and
mitomycin C (Doellman et al., 2009). Other approaches include hyperbaric oxygen therapy and
negative pressure wound healing. The use of nano drugs and the liposomal types of chemotherapeutic
agents is associated with reduced drug diffusion ability and thus less exposure to the surrounding
tissue (Kreidieh et al., 2016).
 SOCIAL WORK IN PUBLIC HEALTH 15

Anaphylactic reactions to chemotherapy

Pathophysiology. Chemotherapy drugs, monoclonal antibodies and small molecules for cancer treat­
ment are intended to improve patients’ quality of life and life expectancy, but an increasing number of
reactions, including anaphylaxis, are preventing their use in targeted populations (Castells, 2017).
Anaphylaxis, well established with platinum drugs and the taxanes, is definite as a serious allergic
reaction that is rapid in onset and may cause death. Other agents are known to cause infusion
reactions to include cyclophosphamide, L-asparaginase, bleomycin, ixabepilone, and monoclonal
antibodies such as rituximab (Sampson et al., 2005).

Presentation. Anaphylactic reactions caused by chemotherapy agents with the same signs and
symptoms as secondary responses to other etiologies. The major symptoms are bronchospasm,
urticarial and angioedema, flushing, hypotension or hypertension, chest pain/tightness, back and
abdominal pain, tachycardia or bradycardia, rush and fever (Syrigou et al., 2010).

Diagnosis. Anaphylaxis should be strongly suspected when there are any of the following three
criteria (Sampson et al., 2005, 2006). The first criterion defines acute illness, which occurs within
minutes to hours of exposure, and should include changes in the skin and/or mucosal tissue as well as
evidence of respiratory compromise or hypotension. The second criterion requires that the following
two or more symptoms and/or the following symptoms are likely to grow rapidly after exposure to the
allergen. These symptoms include: 1) involvement of cutaneous/mucosal tissue; 2) Hypertension or
related symptoms (such as syncope); 3) Respiratory compromise; and/or 4) persistent gastrointestinal
symptoms (such as abdominal pain, amnesia, or diarrhea). The third requirement includes decreased
blood pressure after having been exposed to that patient’s identified allergen (Sampson et al., 2005,
2006).

Treatment. Management depends on the severity of infusion reactions. In mild cases, in case of low
blood pressure, the infusion should be immediately withdrawn without any anaphylaxis features, and
IV fluids should be given (Robinson et al., 2001). Diphenhydramine can help relieve mild symptoms at
a dosage of 50 mg.iv. For cases of anaphylaxis, the injection should be promptly stopped, with
subsequent treatment similar to the control of other anaphylaxis causes. A similar examination of
the airways, respiration, and ventilation will take place. Epinephrine, antihistamines, vasopressors and
glucocorticoids can be administered. Oxygen should be administered to counteract shortness of breath
and decreased saturation (Syrigou et al., 2010). Desensitization has been used in situations where the
antineoplastic agent is generally used with curative intent, even with an anaphylactic reaction from
patients (Robinson et al., 2001; Syrigou et al., 2010).

Side effects of treatment

Extravasation injuries secondary to chemotherapy
Extravasation refers to a liquid that mistakenly escapes into surrounding tissues, rather than remain­
ing as intended in the blood vessel. Toxic chemotherapies may lead to a variety of extravasation
injuries (Fidalgo et al., 2012). In this situation pain, erythema, discoloration, blistering, necrosis, and
swelling that progress to blanching of the skin can occur. Early treatment is crucial and involves
stopping the infusion immediately, along with oncology, dermatology, and plastic surgery advice
(Kreidieh et al., 2016).

Radiation therapy problems

It is common to have radiation-related dermatitis, cardiovascular disease, esophagitis, cystitis, sexual
dysfunction and depression (Berkey, 2010). The type of cancer, radiation level, patient age and overall
16 A. JAFARI ET AL.

radiation dose obtained affects complications. Oncology consultation helps the care team of each
patient decide whether the communication should be limited and how long (Higdon et al., 2018).

Gastrointestinal problems
Approximately 17% of patients with cancer are attributable to gastrointestinal problems such as
abdominal pain, nausea, vomiting, diarrhea, constipation, and dehydration, which are increasingly
associated with opioid or immunologic therapy (Mayer, Travers, Wyss, Leak, & Waller, 2011). Testing
for Clostridium difficile infection, cytomegalovirus infection, reactivation of latent hepatitis, and the
use of probiotics containing Lactobacillus is recommended. Based on the gastrointestinal issue and
imaging findings, consultation with oncology, gastroenterology, general surgery, and infectious dis­
ease may be helpful (Andreyev, Davidson, Gillespie, Allum, & Swarbrick, 2012; Gibson et al., 2013).

Immunotherapy problems
Despite rapid advances in cancer research, there is a growing availability of new immunologic agents.
Depending on the method of treatment used (vaccines, cytokines, adoptive cell therapy, or checkpoint
inhibitors), multiple toxic expressions may occur with immunotherapy for cancer and are commonly
referred to as immune-related adverse effects (Abdollahpour-Alitappeh, S, Lotfinia, Amanzadeh, &
Habibi-Anbouhi, 2018; Gedye, Van der Westhuizen, & John, 2015; Gharibi et al., 2020; Michot et al.,
2016; Weber, Yang, Atkins, & Disis, 2015). The clinical spectrum of these events ranges from
a nonspecific, ambiguous disease, like rheumatoid arthritis to life-threatening pneumonitis and
pancreatitis. It is necessary to have high levels of suspicion with prompt oncology and targeted
subspecialty consultation (Morrissey, Yuraszeck, Li, Zhang, & Kasichayanula, 2016).

Conclusion
Oncological emergencies are often etiologically complex and often occur in the acute setting. These
events can endanger the health of virtually every malignant patient and cover ranging from initial
presentation to late recurrence to end-stage disease. If physicians are familiar with how these condi­
tions occur, the main types of cancer identified in emergencies can be prevented, diagnosed early,
treated, and cure. Initial evaluation of the patients in the emergency department, knowledge of
oncologic emergencies and their proper management is of utmost importance for patient outcome,
and crucial in achieving predefined treatment goals and improving patient quality of life. In this
manner, even in cases with advanced stages, the pain could have been reduced and the family assisted
in order to cope with the disease. Overall, emergency physicians in collaboration with the related
disciplines, such as oncologists, can develop consensus protocol to address the frequently encountered
problems and provide opportunities to overcome the challenges of cancer patients. Observing this
protocol can increase patients’ life expectancy, improve their quality of life, reduce medical costs for
patients, save time for doctors, and facilitate hospital affairs.

Acknowledgments
This study is related to the project NO 1397/68924 From Student Research Committee, Shahid Beheshti University of
Medical Sciences, Tehran, Iran. We also appreciate the “Student Research Committee” and “Research & Technology
Chancellor” in Shahid Beheshti University of Medical Sciences for their financial support of this study.

Disclosure statement
No potential conflict of interest was reported by the authors.
 SOCIAL WORK IN PUBLIC HEALTH 17

Authors’ contributions
AJ designed the study and writing manuscript. MRT supervised the study. MRT and MS revision of the manuscript. AJ,
MS, RT and ZJ edited the manuscript. All authors read and approved the final manuscript

Authors orcids
Ameneh Jafari: 0000-0002-8165-5978
Mostafa Rezaei Tavirani: 0000-0003-1767-7475

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