This document outlines several oncological emergencies including tumor lysis syndrome, hyperleukocytosis, disseminated intravascular coagulopathy, superior vena cava obstruction, febrile neutropenia, and infection. It provides details on the characteristics, risks factors, signs and symptoms, and management approaches for each emergency. Key aspects of management include hydration, monitoring of electrolytes and blood counts, use of allopurinol or steroids to prevent tumor lysis, platelet transfusions for coagulopathies, and early treatment of febrile neutropenia with antibiotics. The document emphasizes the need for prompt recognition and treatment of these potentially life-threatening oncological complications.
This presentation focuses on main and most common oncological emergencies that are required by any stagiaire or junior doctor.
This presentation based on three books mainly, Davison’s principles and practice of medicine, pocket guide to oncological emergencies and ESMO hand book of oncological emergencies, in addition to some researches.
Tumor lysis occurs when cancer cells release their contents into the blood stream, either spontaneously or following antineoplastic therapy leading to an influx of electrolytes and nucleic acids into the circulation.
The sudden development of hyperkalemia, hyperuricemia and hyperphosphatemia can have life-threatening end-organ effects on the myocardium, kidneys and CNS.
Hypocalcemia is a consequence of hyperphosphatemia in TLS.
Symptoms are variable from the metabolic derangements of TLS.
This presentation focuses on main and most common oncological emergencies that are required by any stagiaire or junior doctor.
This presentation based on three books mainly, Davison’s principles and practice of medicine, pocket guide to oncological emergencies and ESMO hand book of oncological emergencies, in addition to some researches.
Tumor lysis occurs when cancer cells release their contents into the blood stream, either spontaneously or following antineoplastic therapy leading to an influx of electrolytes and nucleic acids into the circulation.
The sudden development of hyperkalemia, hyperuricemia and hyperphosphatemia can have life-threatening end-organ effects on the myocardium, kidneys and CNS.
Hypocalcemia is a consequence of hyperphosphatemia in TLS.
Symptoms are variable from the metabolic derangements of TLS.
Tumor Lysis Syndrome
The most common disease-related emergency encountered by physicians caring for children or adults with hematologic cancers
When tumor cells release their contents into the bloodstream, either spontaneously or in response to therapy-
leading to the characteristic findings of
hyperuricemia, hyperkalemia, hyperphosphatemia, and
hypocalcemia
Electrolyte and metabolic disturbances- progress to clinical toxic effects- including
-renal insufficiency,
-cardiac arrhythmias,
-seizures, and
-death due to multiorgan failure
Laboratory tumor lysis syndrome : Requires that two or more of the metabolic abnormalities occur within 3 days before or up to 7 days after the initiation of therapy
Clinical tumor lysis syndrome: Laboratory tumor lysis syndrome is accompanied by an increased creatinine level, seizures, cardiac dysrhythmia, or death.
IN MALIGNANCIES
–high proliferative rate,
–large tumor burden,
–high sensitivity to treatment-
Initiation of cytotoxic chemotherapy,
Cytolytic antibody therapy,
Radiation therapy,
Sometimes glucocorticoid therapy alone
Rapid lysis of tumor cells!!!!!
Releases massive quantities of intracellular contents:
K+ , phosphate, and nucleic acids
diagnostic criteria and pathophysiology of hellp syndrome. Its anesthetic management both pre-operatively and post operatively. complication and differential diagnosis of hellp
Oncologic emergencies are vital for many healthcare practitioners to note even if they do not take care of cancer patients alone. This slide deck covers malignant spinal cord compression, hypercalcemia of malignancy, and tumor lysis syndrome.
Tumor Lysis Syndrome
The most common disease-related emergency encountered by physicians caring for children or adults with hematologic cancers
When tumor cells release their contents into the bloodstream, either spontaneously or in response to therapy-
leading to the characteristic findings of
hyperuricemia, hyperkalemia, hyperphosphatemia, and
hypocalcemia
Electrolyte and metabolic disturbances- progress to clinical toxic effects- including
-renal insufficiency,
-cardiac arrhythmias,
-seizures, and
-death due to multiorgan failure
Laboratory tumor lysis syndrome : Requires that two or more of the metabolic abnormalities occur within 3 days before or up to 7 days after the initiation of therapy
Clinical tumor lysis syndrome: Laboratory tumor lysis syndrome is accompanied by an increased creatinine level, seizures, cardiac dysrhythmia, or death.
IN MALIGNANCIES
–high proliferative rate,
–large tumor burden,
–high sensitivity to treatment-
Initiation of cytotoxic chemotherapy,
Cytolytic antibody therapy,
Radiation therapy,
Sometimes glucocorticoid therapy alone
Rapid lysis of tumor cells!!!!!
Releases massive quantities of intracellular contents:
K+ , phosphate, and nucleic acids
diagnostic criteria and pathophysiology of hellp syndrome. Its anesthetic management both pre-operatively and post operatively. complication and differential diagnosis of hellp
Oncologic emergencies are vital for many healthcare practitioners to note even if they do not take care of cancer patients alone. This slide deck covers malignant spinal cord compression, hypercalcemia of malignancy, and tumor lysis syndrome.
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The "ICH Guidelines for Pharmacovigilance" PDF provides a comprehensive overview of the International Council for Harmonisation of Technical Requirements for Pharmaceuticals for Human Use (ICH) guidelines related to pharmacovigilance. These guidelines aim to ensure that drugs are safe and effective for patients by monitoring and assessing adverse effects, ensuring proper reporting systems, and improving risk management practices. The document is essential for professionals in the pharmaceutical industry, regulatory authorities, and healthcare providers, offering detailed procedures and standards for pharmacovigilance activities to enhance drug safety and protect public health.
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M Capital Group (“MCG”) predicts that with, against, despite, and even without the global pandemic, the medical technology (MedTech) industry shows signs of continuous healthy growth, driven by smaller, faster, and cheaper devices, growing demand for home-based applications, technological innovation, strategic acquisitions, investments, and SPAC listings. MCG predicts that this should reflects itself in annual growth of over 6%, well beyond 2028.
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There is a movement towards home-based care for the elderly, next generation scanning and MRI devices, wearable technology, artificial intelligence incorporation, and online connectivity. Experts also see a focus on predictive, preventive, personalized, participatory, and precision medicine, with rising levels of integration of home care and technological innovation.
The average cost of treatment has been rising across the board, creating additional financial burdens to governments, healthcare providers and insurance companies. According to MCG, cost-per-inpatient-stay in the United States alone rose on average annually by over 13% between 2014 to 2021, leading MedTech to focus research efforts on optimized medical equipment at lower price points, whilst emphasizing portability and ease of use. Namely, 46% of the 1,008 medical technology companies in the 2021 MedTech Innovator (“MTI”) database are focusing on prevention, wellness, detection, or diagnosis, signaling a clear push for preventive care to also tackle costs.
In addition, there has also been a lasting impact on consumer and medical demand for home care, supported by the pandemic. Lockdowns, closure of care facilities, and healthcare systems subjected to capacity pressure, accelerated demand away from traditional inpatient care. Now, outpatient care solutions are driving industry production, with nearly 70% of recent diagnostics start-up companies producing products in areas such as ambulatory clinics, at-home care, and self-administered diagnostics.
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Defecation
Normal defecation begins with movement in the left colon, moving stool toward the anus. When stool reaches the rectum, the distention causes relaxation of the internal sphincter and an awareness of the need to defecate. At the time of defecation, the external sphincter relaxes, and abdominal muscles contract, increasing intrarectal pressure and forcing the stool out
The Valsalva maneuver exerts pressure to expel faeces through a voluntary contraction of the abdominal muscles while maintaining forced expiration against a closed airway. Patients with cardiovascular disease, glaucoma, increased intracranial pressure, or a new surgical wound are at greater risk for cardiac dysrhythmias and elevated blood pressure with the Valsalva maneuver and need to avoid straining to pass the stool.
Normal defecation is painless, resulting in passage of soft, formed stool
CONSTIPATION
Constipation is a symptom, not a disease. Improper diet, reduced fluid intake, lack of exercise, and certain medications can cause constipation. For example, patients receiving opiates for pain after surgery often require a stool softener or laxative to prevent constipation. The signs of constipation include infrequent bowel movements (less than every 3 days), difficulty passing stools, excessive straining, inability to defecate at will, and hard feaces
IMPACTION
Fecal impaction results from unrelieved constipation. It is a collection of hardened feces wedged in the rectum that a person cannot expel. In cases of severe impaction the mass extends up into the sigmoid colon.
DIARRHEA
Diarrhea is an increase in the number of stools and the passage of liquid, unformed feces. It is associated with disorders affecting digestion, absorption, and secretion in the GI tract. Intestinal contents pass through the small and large intestine too quickly to allow for the usual absorption of fluid and nutrients. Irritation within the colon results in increased mucus secretion. As a result, feces become watery, and the patient is unable to control the urge to defecate. Normally an anal bag is safe and effective in long-term treatment of patients with fecal incontinence at home, in hospice, or in the hospital. Fecal incontinence is expensive and a potentially dangerous condition in terms of contamination and risk of skin ulceration
HEMORRHOIDS
Hemorrhoids are dilated, engorged veins in the lining of the rectum. They are either external or internal.
FLATULENCE
As gas accumulates in the lumen of the intestines, the bowel wall stretches and distends (flatulence). It is a common cause of abdominal fullness, pain, and cramping. Normally intestinal gas escapes through the mouth (belching) or the anus (passing of flatus)
FECAL INCONTINENCE
Fecal incontinence is the inability to control passage of feces and gas from the anus. Incontinence harms a patient’s body image
PREPARATION AND GIVING OF LAXATIVESACCORDING TO POTTER AND PERRY,
An enema is the instillation of a solution into the rectum and sig
Health Education on prevention of hypertensionRadhika kulvi
Hypertension is a chronic condition of concern due to its role in the causation of coronary heart diseases. Hypertension is a worldwide epidemic and important risk factor for coronary artery disease, stroke and renal diseases. Blood pressure is the force exerted by the blood against the walls of the blood vessels and is sufficient to maintain tissue perfusion during activity and rest. Hypertension is sustained elevation of BP. In adults, HTN exists when systolic blood pressure is equal to or greater than 140mmHg or diastolic BP is equal to or greater than 90mmHg. The
4. DEFINITION
• Massive tumour cell death with rapid release of intracellular
metabolites, which exceeds the excretory capacity of the kidneys
leading to acute renal failure. Can occur before chemotherapy is
started.
• Risk factor include large tumor burden/bulky volume, cancers that
rapidly divide or cancers that are extremely sensitive to
chemotherapy .Common in Iymphoproliferative tumours with
abdominal involvement (e.g. B cell/ T cell Iymphoma, leukaemias and
Burkitt’s Iymphoma)
5.
6. CHARACTERISTICS:
• Hyperuricaemia
• Release of intracellular purines increase uric acid
• Hyperkalaemia
• Occurs secondary to tumour cell Iysis itself or secondary to renal failure from uric acid
nephropathy or hyperphosphataemia.
• Hyperphosphataemia with associated hypocalcaemia
• Most commonly occurs in Iymphoproliferative disorders because Iymphoblast phosphate
content is 4 times higher than normal lymphocytes.
• Causes:
Tissue damage from CaPO₄ precipitation. Occurs when Ca X PO₄ > 60 mg/dl.
Results in renal failure, pruritis with gangrene, eye and joint inflammation
Hypocalcaemia leading to altered sensorium, photophobia, neuromuscular
irritability, seizures, carpopedal spasm and gastrointestinal symptoms
8. complication
* Close attention to symptoms of
electrolyte abnormalities:
Abdominal pain
Back pain
Vomiting
Cramps
Diarrhea
Dehydration
Muscle spasms
Tetany, seizures
9. Management (Prevention):
To be instituted in every case of acute leukaemia or Iymphoma prior to induction chemotherapy.
• Hydration : Double hydration - 125ml/m²/hr or 3000ml/m²/day.
- No added potassium.
• Alkalization of urine: Adding NaHCO₃ at 150 - 200 mmol/m²/day (3 mls/kg/day NaHCO₃ 8.4%) into IV fluids to keep urine
pH 7.0 - 7.5.
- Avoid over alkalinization as this may aggravate hypocalcemia and cause hypoxanthine and xanthine precipitation. It can
also cause precipitation of calcium phosphate if pH > 8. Monitor urine pH and VBG 8 hourly. If urine pH < 7.0 , consider
increasing NaHCO₃ infusion. This can only be done if HCO₃ in the blood is below normal range. Otherwise, have to accept
that some patients just cannot alkalinise their urine.
• Allopurinol : 10mg/kg/day, max 300mg/day.
• May have to delay chemotherapy until metabolic status stabilizes.
• Close electrolyte monitoring: BUSE, Ca²⁺, PO₄, uric acid, creatinine, bicarbonate.
• Strict I/O charting. Ensure adequate urine flow once hydrated. Use diuretics with caution. Maintain urine output at least
3 mL/kg/hr
– Lasix 0.5-1 mg/kg
– Mannitol 0.5 g/kg
10. Management (Treatment)
• hyperkalaemia – oral kalimate,lytic cocktail, dialysis in severe cases.
• Diuretics.
• Hypocalcaemia management depends on the phosphate level:
If phosphate is raised, then management is directed to correct the high
phosphate.
If phosphate is normal or if child is symptomatic, then give replacement IV
calcium.
If hypocalcaemia is refractory to treatment, exclude associated
hypomagnesaemia.
• Dialysis if indicated. Haemodialysis most efficient at correcting
electrolyte abnormalities. Peritoneal dialysis is not effective in
removing phosphates.
14. • Occurs in acute leukaemia. Defined as TWBC > 100 000 / mm³.
• Leukostasis - Blasts lack deformability
• Increased viscosity > WBC aggregates > thrombi especially in small
veins causing obstruction
• Excessive leukocytes competes for oxygen; damages vessel wall
causing bleeding.
• Can be fatal (greatest risk at WBC > 300K) CNS hemorrhage, thrombosis
• Pulmonary Leukostasis
- Affects the lungs due to pulmonary infiltrates. May cause dyspnoea,
hypoxaemia and right ventricular failure.
• Affects the central nervous system causing headaches,
papilloedema, seizures, haemorrhage or infarct.
Associated :
- In acute lymphoblastic leukaemia (ALL) with high risk of tumour
Iysis.
- In AML with leucostasis (esp monocytic).
- Seen in 10% ALL and 15-20% AML
15. There are no diagnostic tests or criteria for leukostasis. Clinicians must have a high index of
suspicion in patients who are at risk as defined above. Respiratory and CNS status must be
reviewed regularly. Discuss with PTC consultants early if leukostasis is suspected.
16. MANAGEMENT
A-B-C
• Hydration
To facilitate excretion of toxic metabolites.
To reduce blood viscosity.
Avoid increasing blood viscosity.
• Strict i/o chart
• Daily weight bd/od
• Ix: FBC, ca, po4 ,mg ,uric acid, urea creatinine, LDH
• Cautious in use of packed cell transfusion(increase viscosity) and diuretics – not recommend unless in life
threatening condition.
• During induction in hyperleukocytosis, keep platelet >20 000/mm³ and coagulation profile near normal
Consider platelet transfusion if <20000/mm3 – prevent haemorrhage
• If WBC rises rapidly / does not drop quickly, consider cytoreduction Steroids :
• Hydoxyurea
• Leukopheresis
• Exchange transfusion
*Exchange transfusions and leukopheresis should not be used alone as rapid rebound usually occurs. Concurrent
drug treatment should therefore be initiated soonest possible.
18. >> Pathologic process where there is generalized activation and dysregulation of
the hemostatic system resulting in generation of microthrombi and consumption
of platelets and clotting factors , this consumption result in Thrombosis, organ
failure, Severe Bleeding
• Patients at risk: APML and infection or sepsis
• Causes:
1. Gram negative sepsis
2. Leukemia (AML M3,M5; ALL with high WBC)
3. Metastatic solid tumors
• Signs & Symptoms: Bleeding, petechiae, purpura and laboratory derangements
*AML especially M3 is associated with an initial bleeding diathesis from
consumptive coagulopathy due to release of a tissue factor with procoagulant
activity from cells. However the use of all-trans retinoic acid (Atra) has
circumvented this complication.
19. Supportive Care Protocol version 5.0 (August
2011), NHS foundation
Management by protocol :
• Platelet transfusions: 6 units / m²
should increase platelets by 50,000 /
mm³.
• Fresh frozen plasma (FFP) or
cryoprecipitate.
• Vitamin K.
• +/- Heparin therapy (10u/kg/hr) -
controversial
21. • Superior Vena Cava Syndrome (SVCS): Refers to signs and symptoms from
compression, obstruction or thrombosis of the superior vena cava
• Common in Non Hodgkin Lymphoma / Hodgkin Lymphoma / ALL .
• Rarely: malignant teratoma, thymoma, neuroblastoma,
rhabdomyosarcoma or Ewing’s may present with anterior or middle
mediastinal mass and obstruction.
• 50% associated with thrombosis.
symptoms: facial swelling, upper body edema, cyanosis of the face or upper
body, plethora, conjuctival suffusion, headache , shortness of breath,cough
syncope.
Signs: tacycardia, elevated venous pressure, vocal cord paralysis,dyspnea,
horner syndrome
#Sometimes no signs or symptoms until stressed
23. Investigation:
Diagnosis – History, Physical, CBC, CXR, CT, Echo
1. Recognition of symptoms and signs of SVC obstruction and avoidance of sedation and general
anaesthesia.
• Orthopnea, upper body edema, and dyspnea at rest have been associated with increased anesthesia risk.
2. Tissue diagnosis is important but should be established by the least invasive measure available. Risk
of circulatory collapse or respiratory failure may occur with general anesthesia or sedation.
3. BMA.
4. Biopsy of superficial lymph node under local anaesthesia.
5. Measurement of serum markers e.g. alpha-fetoprotein.
• Management
• IV access (lower limbs if possible-a risk of exacerbation of facial swelling and cerebral oedema in SVC obstruction in
upperlimb cannulae,bleeding due to increased intravascular pressure, aggravate SVC obstruction), keep hydration
• Keep pt calm, minimal handling, no sedation
• Upright, left lateral position with face mask O2
• Monitor and treat TLS
• ECMO on standby if available
• If tissue diagnosis is not obtainable, empiric treatment may be necessary based on the most likely diagnosis. Both
chemotherapy and DXT may render histology uninterpretable within 48 hours, therefore biopsy as soon as possible
• Primary mode of treatment is with steroids and chemotherapy if pathology due to Non-Hodkin Lymphoma
• +/- DXT(adjuvant radiotherapy).
• Intubate only for life threatening obstruction
25. Febrile episodes in oncology patients must be treated with urgency especially if
associated with neutropenia. Nearly all episodes of bacteraemia or disseminated
fungal infections occur when the absolute neutorphil count (ANC) <500 /mm³. Risk
increases maximally if ANC < 100 /mm³ and greatly reduced if the ANC > 1000
/mm³.
Characterized by:
• Fever (definition variable)
• T>38.3° C x1 or
• T>38.0°C x2 in a 24 hour period
• Absolute neutrophil count (ANC)
• < 500 or
• < 1000 with expected decline
• WBC count x (% segs + bands)
26. • Why are cancer pts at risk for life-threatening infection?
• Chemotherapy Decreased number and function of immune cells
• Radiation
-further tissue injury and impairment of the body’s innate immunology
• Surgeries
• Breakdown of mucocutaneous barriers (indwelling catheter, etc)
• Foreign bodies (CVL, grafts, etc.)
29. other considerations:
• If central line is present, culture from central line
(both lumens); add anti-Staph cover e.g.Cloxacillin.
• Repeated physical examination to look for new
clues, signs and symptoms of possible sources.
• Close monitoring of patient’s well-being – vital signs,
perfusion, BP, I/O.
• Repeat cultures if indicated
• Investigative parameters, FBC, CRP, BUSE as per
necessary.
• In presence of oral thrush or other evidence of
candidal infection, start antifungals.
•Try to omit aminoglycoside and vancomycin if on
cisplatinum - nephrotoxic and ototoxic. If required,
monitor renal function closely.
30. references
• PAEDIATRIC PROTOCOLS For Malaysian Hospitals, 3rd edition
• Paediatric Haematology & Oncology: Supportive Care Protocols NHS
Foundation trust, 4th Edition version 1.0
• The Practical Journal of paediatric medical emergency, Volume 16,
Number 5 / May 2011, www.ahcmedia.com
Editor's Notes
Acute Promyelocytic Leukaemia (APML) is a subtype of Acute Myeloid Leukaemia (AML). APML is most commonly associated with a swapping over (translocation) of chromosomes 15 and 17.
However, administrationof steroids may result in tumor lysis syndrome and may impair the
ability to make a diagnosis. Steroids,
therefore, should be given only
in an immediately life-threatening
situation after consultation with a
pediatric oncologist. Even more
rarely, the mass may not be sensitive
to corticosteroids, and emergent
radiation therapy may be considered.
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