Tumor lysis syndrome is an oncologic emergency characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia due to the rapid breakdown of tumor cells. It occurs after initiation of chemotherapy or other cytotoxic treatments in cancers with a high proliferative rate or large tumor burden. Prophylaxis includes aggressive hydration and use of urate-lowering agents like allopurinol or rasburicase to prevent uric acid crystal formation and preserve kidney function. Early recognition and treatment are important to prevent complications such as acute kidney injury or life-threatening cardiac arrhythmias.
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
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
Oncologic emergency
Abrupt release of intracellular contents in high quantity
Prophylaxis and treatment aimed at assisting body to rid electrolyte excess
May be spontaneous or as a result of anti- cancer therapy
Characterized by: elevated K+ ,PO4 and uric acid with resultant decrease in calcium.
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.
Oncologic emergency
Abrupt release of intracellular contents in high quantity
Prophylaxis and treatment aimed at assisting body to rid electrolyte excess
May be spontaneous or as a result of anti- cancer therapy
Characterized by: elevated K+ ,PO4 and uric acid with resultant decrease in calcium.
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.
The all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
Cirrhosis of liver is the end result of the hepatocellular injury
characterized by the presence of extensive fibrosis,
regenerative nodules and loss of liver architecture.
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. Introduction
Tumour lysis syndrome (TLS)
• Metabolic Derangements
• Rapid Tumour breakdown
• Associated with the initiation of cytotoxic therapy of malignancy
• Affects both Children and Adults
3. • It is an oncologic emergency , which is characterized by a tetrad of abnormalities
1. Hyperuricemia
2. Hyperkalaemia
3. Hyperphosphatemia
4. Hypocalcaemia
• Abrupt release of intracellular ions, nucleic acids, proteins, and their metabolites results
from the rapid destruction of malignant cells and the release of their intracellular
contents into the extracellular space after the initiation of therapy
4.
5.
6. Incidence
• The overall incidence of TLS is not well established
• Primarily - Acute lymphocytic leukaemia and high-grade non-Hodgkin's lymphomas, in
particular Burkitt's lymphoma.
• Also recognized in a variety of other malignancies, both hematologic and solid.
• Hematologic malignancies -- AML, CLL, CML, and low-grade and intermediate-grade
NHL.
• Solid tumours -- Breast cancer, Ovarian and Testicular cancer, neuroblastoma, and small
cell carcinoma of the lungs.
7.
8. Risk Factors
In malignancy with
• High proliferative rate,
• Large tumor burden, -bulky disease >10 cm in diameter and/or
-WBC >50,000 per microL,
- pretreatment serum LDH >2 times UNL,
• Initiation of cytotoxic chemotherapy,
• Cytolytic antibody therapy,
• Radiation therapy,
• Glucocorticoid therapy alone can result in the rapid lysis of tumor cells.
9. • The elevation of the serum LDH level before the initiation of therapy has also
been associated with the recognition of patients at risk for TLS.
• Other predisposing conditions
– Pre treatment hyperuricemia (serum uric acid >7.5 mg/dL or hyperphosphatemia
– Pre existing nephropathy or exposure to nephrotoxins
– Oliguria and/or acidic urine
– Dehydration, volume depletion, or inadequate hydration during treatment
10. Does TLS occur only with i/v chemo?
• TLS is not limited to systemic administration of agents;
• It has been observed with intrathecal administration of chemotherapy and with
chemo-embolization.
Does TLS occur only with chemo?
• Not limited to the administration of chemotherapy alone.
• TLS has been associated with the administration of radiation therapy, corticosteroids,
hormonal agents, biologic response modifiers, monoclonal antibodies, and more recently,
the low-molecular-weight inhibitor, imatinib mesylate, better known as Gleevec
• Spontaneously, before the initiation of any intervention.
13. Hyperuricemia
• Hyperuricemia and its associated complications are most frequently recognized
manifestations of TLS
• Cause of Hyperuricemia -results from rapid release and catabolism of intracellular
nucleic acids.
• Purine nucleic acids are catabolized to hypoxanthine, then xanthine, and finally to uric
acid by xanthine oxidase.
• In humans, who lack urate oxidase, uric acid is the final endpoint of purine catabolism
15. Hyperuricemia
• Uric acid clearance - renal, and in normal circumstances approximately
• Excretion – 500/day.
• pKa of 5.4 to 5.7 and is poorly soluble in water.
• At normal concentrations and at physiologic blood pH, more than 99% of uric
acid is in the ionized form
• The concentration of uric acid has been noted to be elevated in patients with acute
leukemias and lymphomas before the initiation of therapy.
• The high concentrations of uric acid increase the risk for urate crystal precipitation
in the renal collecting ducts and distal tubules, which are sites of urinary
acidification
16. Clinical manifestations of hyperuricaemia
• General clinical manifestations of hyperuricemia include nausea, vomiting,
diarrhea, and anorexia.
• Uric acid crystal precipitation within renal tubules results in a decline in
glomerular filtration and the subsequent development of acute renal failure.
• The risk of acute renal failure caused by uric acid precipitation may be increased
by
• -dehydration, which is often present at the time of diagnosis;
• -ureteral obstruction by tumor;
• -a history of renal insufficiency;
• - possible need for nephrotoxic antibiotics, such as aminoglycosides, in patients
with active infections.
17. • If the hyperuricemia results in acute obstructive uropathy, other clinical
manifestations may include hematuria, flank pain, hypertension, azotemia, acidosis,
edema, oliguria, anuria, lethargy, and somnolence
18. Hyperphosphatemia
• Hyperphosphatemia results from the rapid release of intracellular phosphates from
malignant cells, which may contain as much as four times the amount of organic
and inorganic phosphates as normal cells
• Initially , the kidneys are able to respond to the increased concentration of
phosphorus from tumor lysis by increased urinary excretion and decreased tubular
absorption of phosphorus.
• Eventually, however, the tubular transport mechanism becomes saturated and is
unable to maintain normal serum phosphorus concentrations.
19. • The development of hyperphosphatemia may be further exacerbated by acute renal
insufficiency associated with uric acid precipitation, resulting in obstructive uropathy
or other complications of tumor therapy.
• Hyperphosphatemia can lead to the development of acute renal failure after
precipitation with calcium in renal tubules during TLS.
20. Clinical manifestations of Hyperphosphatemia
• Nausea, vomiting, diarrhoea, lethargy, and seizures.
• More importantly, it may result in tissue precipitation of calcium-phosphate
crystals, resulting in
1. Hypocalcaemia,
2. Metastatic calcification,
3. Intrarenal calcification,
4. Nephrocalcinosis,
5. Nephrolithiasis,
6. Acute obstructive uropathy.
21. Hypocalcemia
• The serum concentration of calcium rapidly decreases as precipitation with phosphate
occurs.
• Hypocalcemia is one of the most serious clinical manifestations of TLS and has been
associated with the development of
1. Paresthesia and tetany with positive Chvostek and Trousseau signs
2. Anxiety
3. Carpal and pedal spasms
4. Bronchospasm
5. Seizures
6. Cardiac arrest
22. • Deposition of calcium phosphate in various tissues may be responsible for the following
signs and symptoms:
•Pruritus
•Gangrenous changes of the skin
•Iritis
•Arthritis
23. Hyperkalemia
• life-threatening
• Hyperkalemia results from the kidneys’ inability to clear the massive load of
intracellular potassium released by lysed tumor cells.
Clinical manifestations of Hyperkalemia
Cardiac manifestations
1. Asystole,
2. Ventricular tachycardia or fibrillation,
3. Syncope,
4. Sudden death.
Neuromuscular signs and symptoms
1. Muscle weakness,
2. Cramps,
3. Paresthesias,
4. Paralysis.
24. Uraemia
• Increases in blood urea nitrogen and creatinine levels occur as a result of renal impairment
• Acute clinical manifestations - nausea, vomiting, and lethargy
• Oliguria or anuria leading to fluid retention; edema, hypertension, congestive heart failure,
metabolic disturbances, and exacerbations of hyperphosphatemia and/or hyperkalemia
• flank or back pain; hematuria; and severe acidosis.
Complications of uremia
• Uremic pericarditis Seizures, and/or coma
• Platelet function defect Acute obstructive uropathy
• Cellular immunodeficiency Confusion/ somnolence
25. Prophylaxis
• Maintain hydration (>100 ml/hr)
• R/O cardiac disease and Renal insufficieny
• Rasburicase - 0.2 mg/kg i/v
• Screen for Hyperkalemia and treat if preexisting hyperkalemia is present
• Treat hypocalcemia – if symptomatic
• Regular Monitoring of renal function and electrolyte
• The LDH concentration serves as an excellent marker for tumor proliferation and
response to therapy.
26. Initial Management of Patients at Risk for Tumor Lysis
Syndrome
1.Identification of the patient at risk
2. Admit to intensive care or hematology/oncology unit
3. Alert dialysis team of existence of patient and potential emergent need of assisted
renal support.
4. Establish adequate venous access.
5. Perform baseline electrocardiogram and continuous cardiac monitoring.
27.
28. Hypouricemic agents
• It is necessary to administer a hypouricemic agent, either allopurinol or
rasburicase, before the initiation of therapy.
29. Allopurinol
• Allopurinol is a potent inhibitor of xanthine oxidase and blocks the conversion of
hypoxanthine and xanthine to uric acid.
• Hypoxanthine is more soluble than uric acid is at physiologic pH, xanthine is less soluble
than uric acid. This may result in the formation of xanthine crystals in the kidney and
lead to obstructive uropathy.
• Allopurinol prevents new uric acid formation, it does not reduce the amount of uric acid
already present.
• Thus allopurinol requires administration for 2 to 3 days before the serum uric acid
concentration begins to fall and therefore needs to be initiated 2 to 3 days before the
initiation of cytotoxic therapy.
30. • It is usually given orally at 600 mg daily for prophylaxis and 600-900 mg daily
(up to a maximum of 500 mg/m2 daily) for treatment of tumor lysis syndrome.
Patients unable to take oral medications can be given IV allopurinol.
31. Cautions for Allopurinol
• Allopurinol is known to interfere with the degradation of 6- mercaptopurine, 6-
thioguanine, and azathioprine through inhibition of the P450 pathway; thus, the dose of
allopurinol should be reduced 50% to 75% in patients receiving these chemotherapeutic
agents.
• Should be used with caution in patients with underlying renal insufficiency, because it can
cause a syndrome consisting of rash, hepatitis, eosinophilia, and worsening renal function
• Previously, urine alkalinization was recommended to increase uric acid solubility and
promote uric acid excretion in patients treated with allopurinol.
• However, it is not currently recommended because of the risk of decreasing ionized
calcium concentrations, decreasing phosphate excretion, and increasing serum phosphate
concentration
32. Rasburicase
• Concept- promote the catabolism of uric acid to allantoin by uric acid oxidase.
• Allantoin is 5 to 10 times more soluble in the urine than uric acid.
• Urate oxidase is an endogenous enzyme commonly found in many mammalian
species but not in humans .
• Urate oxidase, extracted from Aspergillus flavus, has been demonstrated to rapidly
and significantly reduce uric acid levels in patients at high risk for TLS.
• Recently, the gene encoding urate oxidase was identified and expressed in yeast to
yield large quantities of the pure recombinant form of urate oxidase Rasburicase.
33. • Rasburicase is administered by intramuscular injection or IV infusion at dosages ranging
from 50-100 U/kg daily.
• It is contraindicated in glucose-6-phosphate dehydrogenase (G6PD) deficiency and
pregnancy.
• In G6PD deficiency, excess hydrogen peroxide accumulates as rasburicase breaks down
uric acid and accelerates catabolism of its precursors xanthine and hypoxanthine; this
accumulation places patients at risk for hemolytic anemia and methemoglobinemias.
• Some authorities recommend screening for G6PD deficiency prior to administration of
the drug.
34. Allopurinol vs Rasburicase
• In a multicenter trial, 52 pediatric patients with hematologic malignancy at high
risk for TLS were randomly assigned to receive allopurinol or rasburicase.
• Uric acid levels
• Pui and colleagues administered rasburicase IV at doses up to 0.2 mg/kg in 131
pediatric patients with newly diagnosed leukemia or lymphoma.
Rasburicase Allopurinol
Dec by 85% Dec by 12%
Initial uric acid 4 hours 24 hours
9.7 mg/dl 1mg/dl 0.5 mg/dl
35. • Serum phosphorus and creatinine concentrations also decreased significantly within 1 to 3
days
• There were very few adverse reactions after administration, and all of these were mild,
making this an excellent therapeutic option.
• Coiffier and associates investigated the safety and efficacy of rasburicase in 100 adult
patients with non-Hodgkin's lymphoma over a 1-year period.
• Of these patients, 66% had elevated LDH levels and 11% were hyperuricemic with
concentrations higher than 7.56 mg/dL.
• Rasburicase was given to all subjects and uric acid levels then measured at 4 hours. All of
the patients responded to rasburicase with normalization of uric acid, and none exhibited
increased creatinine levels or required dialysis
36.
37. Febuxostat
• Febuxostat is a novel xanthine oxidase inhibitor that does not appear to have the
hypersensitivity profile of allopurinol.
• Does not require dosing modification for renal impairment.
• Initial studies suggested that febuxostat is effective and safe for preventing tumor
lysis syndrome.
38. • Hyperkalemia
1. I/V calcium gluconate
2. Insulin neutralizing drip
3. Beta agonist ( nebulization with salbutamol )
4. Sodium polystyrene sulfonate, a potassium binding resin, at a dose of 15 to 60 g/day
given orally or rectally.
• Hyperphosphatemia.
• Aluminum hydroxide, given orally or through a nasogastric tube at a dose of 15 mL
(50–150 mg/kg/24 hr) every 4 to 6 hours, should be used to treat
• Serum LDH level serves as an excellent marker for a decrease in tumor lysis ( 48-
72 hours)
39. Hypocalcemia
• Treat if symptomatic
• Intravenous calcium gluconate (50–100 mg/kg per dose) may be administered to
correct the clinical symptoms; however, this may increase the risk of calcium and
phosphorus deposition and acute obstructive uropathy.
• Uremic pericarditis
• Hypotensive – C/I Haemodialysis
• First – Pericardial drain
• F/B HD when BP normalizes
40. Haemodialysis
• ARF , significant uremia, or severe electrolyte abnormalities - initiated as soon as
possible.
• Children - Continuous hemofiltration
• The failure to promptly initiate hemodialysis for acute renal failure may turn a potentially
reversible clinical situation into an irreversible one
• Among the indications for renal replacement therapy in patients with TLS are :
– Severe oliguria or anuria
– Intractable fluid overload
– Persistent hyperkalemia
– Hyperphosphatemia-induced symptomatic hypocalcemia
– A calcium-phosphate product ≥70 mg2 /dL