0:00 Hello, in this video, we're going to talk about tumor lysis syndrome. 0:10 Tumor lysis syndrome is caused when tumor cells release their intracellular 0:14 content into the 0:15 bloodstream, either spontaneously or as a result of treatment, leading to 0:21 increased 0:21 DNA, purine and pyrimidines, hypercalemia, hyperphosphatemia, leading to hyp 0:33 ocalcemia 0:33 and also elevated lactic acid. 0:40 Now our body cells, including the tumor cells, our main cations intracellularly 0:46 inside the 0:46 cells are potassium and the main anion that negatively charged are phosphate. 0:54 The DNA within the nucleus of the cells are made up of the building blocks, pur 0:58 ines and 0:58 pyrimidines, which under normal regulatory control can get recycled or removed 1:04 from the 1:04 body safely. 1:09 In tumor lysis syndrome, the tumor cells through chemotherapy treatment, for 1:15 example, die in 1:16 high numbers and they release these intracellular contents into the bloodstream 1:27 . 1:28 So purineucleic acids can actually be broken down to hypoxanthine and then x 1:34 anthine and 1:35 from xanthine to uric acid via the enzyme xanthine oxidase, and this will 1:40 result in hyper uracemia. 1:46 Overproduction and over excretion of uric acid in tumor lysis syndrome can lead 1:52 to crystal 1:52 precipitation and deposition in the renal tubules, resulting in acute kidney 2:03 injury. 2:05 Liquid phosphate in the blood acts as a calcium chelating agent. 2:11 The phosphates in the bloodstream will bind to calcium, lowering calcium level 2:20 stores. 2:21 When you have low calcium, hypocalcemia, you can develop symptoms such as ting 2:26 ling, numbness, 2:28 muscle spasm, in severe cases tetany, seizures and arrhythmias. 2:42 Chvostex or Trozus sign can be observed in some people with hypocalcemia. 2:54 The hypercalemia seen in tumor lysis syndrome is dangerous and can lead to life 2:58 -threatening 2:59 arrhythmias. 3:06 Not all cancer patients are at equal risk of developing tumor lysis syndrome. 3:13 Patients with a large tumor burden of cancer cells and/or tumors that typically 3:16 have rapidly 3:17 dividing cells such as acute leukemia or high-grade lymphomas, as well as 3:23 tumors that are highly 3:24 responsive to therapy are at the greatest risk of developing tumor lysis 3:30 syndrome. 3:31 Tumil lysis syndrome can occur spontaneously before cancer treatment, but is 3:36 more common 3:36 within weeks of starting treatment. 3:42 Tumil lysis syndrome is not limited to patients receiving traditional 3:45 chemotherapy. 3:46 It can occur in patients receiving hormonal therapy, targeted therapy, 3:50 radiation therapy, 3:52 steroids as well. 3:54 Patients who are dehydrated and those with existing kidney dysfunction at a 3:58 higher risk 3:58 of developing tumor lysis syndrome. 4:03 And therefore, the management really is to prevent it from occurring by 4:07 identifying the 4:08 patients at risk of tumor lysis syndrome. 4:12 And these are often the highly proliferative hematological malignancies 4:16 mentioned. 4:17 Tumil access in these patients include vigorous intravenous hydration, 3 liters 4:23 in 24 hours. 4:24 On top of intravenous hydration, allopurinol is used. 4:29 Allopurinol is a zanding oxidase inhibitor, commenced about two days pre-chema 4:33 therapy 4:34 at lowest serum urate levels, and help reduce complications of hyper urecemia. 4:41 In the very high risk patients, rasburocase, a urate oxidase enzyme can be used 4:47 instead 4:47 of allopurinol. 4:49 Again, 48 hours before treatment and with intravenous hydration. 4:55 Rasburocase is a uricolitic agent that catalyzes enzymatic oxidation of uric 5:01 acid into allantoin, 5:04 a water-soluble product, more easily excreted by the kidney in the urine. 5:13 Close monitoring of electrolytes and renal function is important throughout 5:16 this whole 5:16 process. 5:19 However, despite prophylaxis, tumor lysis syndrome may still occur. 5:25 Each hospital has their own local guidelines for management of tumor lysis 5:29 syndrome, and 5:29 can include rasburocase to help clear uric acid. 5:34 But really, for people who have tumor lysis syndrome, managing the 5:38 complications with 5:39 the electrolyte abnormalities is very important, because these can lead to 5:45 renal failure, cardiac 5:46 arrhythmias, seizures, and even death. 5:49 Rapid acute renal failure with rapid electrolyte disturbance may likely require 5:56 temporary 5:56 dialysis. 5:59 To diagnose tumor lysis syndrome, we can use the chiro and bishop definition, 6:06 which involves 6:07 two things. 6:11 It can be a laboratory tumor lysis syndrome definition, or clinical tumor lysis 6:16 syndrome 6:16 definition. 6:17 For the laboratory, it's essentially the presence of two or more of the 6:23 metabolic abnormalities 6:25 listed below, or a change of 25% from baseline. 6:31 These metabolic abnormalities include uric acid, greater or equal to 0.476 mill 6:37 imoles per 6:38 liter, potassium greater than or equal to 6 millimoles per liter, phosphate 6:42 greater than 6:43 or equal to 1.45 millimoles per liter, and the corrected calcium less than or 6:49 equal to 6:49 1.75 millimoles per liter. 6:53 The clinical tumor lysis syndrome definition is essentially the presence of one 6:58 of the laboratory 6:59 findings, plus one or more of the following clinical complications, such as the 7:06 acute 7:07 kidney injury, cardiac arrhythmias, or sudden death, and/or seizures. 7:16 In summary, tumor lysis syndrome is a condition whereby the intracellular 7:22 components are released 7:23 into the bloodstream, resulting in hyperkalemia, increase in uric acid levels, 7:30 hyperphosphatemia, 7:32 and hypocalcemia.
