Encephalopathy, ranging from mild confusion to coma, is the most striking clinical manifestation of metabolic emergencies. In cancer patients, this presentation is second only to pain and is the most common symptom. The main pathophysiological mechanisms of these metabolic and toxic emergencies associated specifically with cancer are: (i) dysfunction of vital organs such as lung, liver, kidney and urinary tract due to the spread of tumor cells, and these complications are more common in advanced stages of the disease; (ii) dysfunction of vital organs associated with intensive antitumor therapy, especially in patients with extensive spread; (iii) production of biologically active substances by tumor cells causing paraneoplastic syndrome, which is not related to the stage of tumor disease and often appears before the diagnosis of the underlying carcinoma. Hypercalcemia occurs in 10%-20% of patients with solid tumors, depending on whether the cancer can be diagnosed in time. It is most common in multiple myeloma, breast cancer, lung cancer, kidney cancer and head and neck cancer. Hypercalcemia results from increased migration of calcium from bone and decreased renal tubular calcium secretion. The mechanisms are: ① Tumors produce parathyroid hormone-related protein (, PTHrP) to promote osteoclast activity and renal tubular reabsorption of calcium. Patients with epidermoid carcinoma have high concentrations of PTHrP in the blood and therefore have a low response to diphosphate; ② tumor cells or non-tumor cells present at metastatic sites release many mediators, including PTHrP, leading to local osteolysis. Most of these patients (80%) present with extensive osteolytic bone metastases and rarely osteogenic bone metastases; (iii) increased production of osteotriol can be observed in most cases of Hodgkin’s disease and some cases of non-Hodgkin’s lymphoma. Hypercalcemia caused by this mechanism is usually effective with corticosteroids. A retrospective analysis of the medical records of 212 patients with hypercalcemia admitted between 1998 and 2002 at the San Diego VA Medical Center, USA, was performed to be able to determine the main etiology of hypercalcemia. The median age of the patients was 63 years, and 28% (59/212) had malignant neoplasms, of which lung cancer was the main cause (29%); 18% (38/212) had primary hyperparathyroidism, mainly due to parathyroid adenoma; and 54% had various other causes, with acute renal failure being the most common. Most patients had nonspecific clinical manifestations such as fatigue (70%), anorexia (60%), nausea, constipation (60%), weight loss (60%), bone pain (60%), polyuria, thirst, and dehydration. Neurological symptoms include muscle weakness, drowsiness to confusion, delirium or coma; multiple calcific metastases may be present in the brain. The most important renal manifestations are nephrogenic diabetic uremia (mainly polyuria, thirst, dehydration, and abnormal electrical mediators) and acute and chronic renal failure. 2. Hyponatremia Serum sodium below 130 mEq/L is defined as hyponatremia and is one of the most commonly seen metabolic disorders in hospitalized patients, accounting for about 4% of patients with medical carcinoma. The causes are multiple: (1) tumor or drug-induced syndrome of inappropriate anti-diuretic hormone secretion (SIADH). Many tumors ectopically secrete vasopressin (VAP) or vasopressin-like peptides, and inappropriate secretion of anti-diuretic hormone causes excessive water absorption by the kidneys and progressive loss of urinary sodium as volume expansion aldosterone secretion decreases. SIADH is seen in small cell lung cancer, but also in pancreatic cancer, lymphoma, mesothelioma, and primary and metastatic brain tumors. SIADH can also be complicated by many drug treatments, such as the vincristine vincristine, alkylating agents such as high-dose cyclophosphamide (less common in small doses), nitrogen mustard phenylbutyrate, opioids, antidepressants, and combination chemotherapy such as the use of cisplatin. Chemotherapy-induced nausea can strongly stimulate AVP release, as well as excessive hydration after injection of chemotherapeutic agents, which has a role in the development of SIADH. (2) SIADH associated with hypovolemia. insufficient tissue perfusion stimulates AVP release, and hyponatremia may be accompanied by true volume depletion (as in patients with severe vomiting and diarrhea), but may also be associated with an edematous state (peripheral edema or/and ascites). The former has clinical manifestations of hypovolemia, such as postural hypotension, tachycardia and acute weight loss, as well as oliguria and trace amounts of urinary sodium; the latter has oliguria, weight gain, urinary concentration and low urinary sodium concentration. (3) Salt loss nephropathy, possibly secondary to cisplatin therapy (hypomagnesemia may also be present), adrenocortical insufficiency (reduced aldosterone secretion) and cerebral salt depletion (seen in intracranial surgery and cerebral subarachnoid hemorrhage). Patients show hypovolemia without oliguria and high urinary sodium concentration. Signs and symptoms of hyponatremia are related to the degree and speed of onset of hyponatremia. Hypotonicity and hyponatremia cause water intoxication, which mainly manifests as neurological symptoms and cerebral edema leading to neurological dysfunction. If the hyponatremia is only mild, it manifests as fatigue, anorexia, nausea, diarrhea and headache. If the blood sodium is drastically (1-3d) reduced or below 115 mmol/L, confusion, drowsiness, epileptic seizures, coma, or even death can occur. Depending on the etiology, or hypovolemia or normal blood volume, plasma osmolality, urinary osmolality and urinary sodium levels are recommended to help in the differential diagnosis. In patients with hypovolemia-associated SIADH, there are clinical manifestations of hypovolemia, oliguria, but minimal urinary sodium content; in tumor or drug-associated SIADH, as it is hypotonic (150 mmol/Kg) with increased urinary sodium content (>20 mEq/L). 3. Tumor lysis syndrome Acute tumor lysis syndrome can be caused by massive lysis of malignant cells during radiotherapy or chemotherapy, or spontaneous release of intracellular products into the bloodstream, characterized by rapid onset of hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, azotemia or acute renal failure, and these biochemical abnormalities can occur individually or simultaneously. Hyperkalemia can cause lethal arrhythmias, hyperphosphatemia leads to deposition of calcium phosphate crystals in the renal tubules and induces acute renal failure, and hypocalcemia is secondary to hyperphosphatemia. Hyperuricemia and hyperuricuria are associated with high cell turnover, and patients present with spontaneous renal failure (acute uric acid nephropathy) due to deposition of uric acid crystals in the renal tubules; also, uric acid stones at the renal pelvis may lead to ureteral obstruction. Calcium phosphate deposits in the tissues may cause muscle spasms, cardiac arrhythmias and hand and foot convulsions. It is recommended that blood electrolytes, uric acid, calcium and creatinine be measured every few hours for 3-4 d while the tumor patient is receiving cytotoxic drugs to detect and correct these abnormalities in a timely manner. Tumor lysis syndrome is most commonly seen in patients with a high tumor load but who are very sensitive to chemotherapy or radiotherapy, such as acute or chronic leukemia with massive leukocytosis and high-grade lymphomas. Tumor lysis syndrome may also be observed, although rarely, in patients with solid tumors or after the use of non-cytotoxic agents such as alpha-interferon, tamoxifen, or intrathecal methotrexate. The presence of prior renal insufficiency or extensive lesions (e.g., large retroperitoneal or intraperitoneal tumors, elevated blood lactate dehydrogenase, blood leukocytosis, etc.) can increase the severity of tumor lysis syndrome, and preventive measures such as avoidance of nephrotoxic drugs, volume correction, and appropriate chemotherapeutic agents should be taken to reduce the occurrence of the syndrome. 4. Hypoglycemia Hypoglycemia specifically associated with cancer is rare. The following mechanisms may exist to cause hypoglycemia: (1) islet cell tumors produce insulin, and malignant insulinomas account for about 10% of all insulinomas; (2) large non-islet cell tumors, such as mesenchymal tumors (including hemangioepithelial cell tumors, fibrosarcomas, smooth muscle tumors, mesotheliomas, neurofibromas, etc.) and other tumor types (large cell carcinoma of the lung, liver tumors, neuroblastoma, etc.), can secrete and produce insulin like growth factors; (iii) large tumors that consume large amounts of glucose, making it more than the liver can produce; and (iv) end-stage liver failure or pituitary failure. The classic symptoms of hypoglycemia include neurogenic symptoms, i.e. physiological changes caused by the autonomic response to hypoglycemia such as tremor, palpitations, anxiety, sweating, hunger, abnormal sensation, etc., and the consequent symptoms of hypoglycemic neurological dysfunction such as confusion, fatigue and weakness, cognitive decline, epileptic seizures and coma. These symptoms may appear slowly or worsen early in the morning and improve after meals, but in some patients they are acute and severe. Biochemical tests suggest lower blood glucose, but the glycemic threshold for symptoms varies among individuals. Patients with recurrent episodes of hypoglycemia tolerate abnormally low blood glucose concentrations better and often do not show warning symptoms. It is reasonable to perform a hyperglycemia provocation test. Patients with insulinoma or non-islet cell tumors that secrete insulin-like substances respond to hyperglycemia with elevated blood glucose levels, indicating adequate glycogen stores; blood glucose does not rise if liver glycogen stores are lacking or if the liver is in failure. 5. Hyperammonemia The liver is the most common site of metastasis for tumors originating from the gastrointestinal tract, lung or breast. Liver failure occurs when 70% or more of the liver parenchyma is destroyed, therefore, liver failure is often seen in the late stage of tumor. However, some patients are confirmed to have primary or metastatic cancer only when acute liver failure has occurred. Altered liver function is often seen in patients receiving chemotherapy, but severe liver failure and hyperammonemia due to chemotherapy is rare unless treated with L-mentholase. The incidence of spontaneous hyperammonemia after intensive chemotherapy for leukemia has been reported to be about 2.5% in the last 15 years, and the incidence of hyperammonemia after bone marrow transplantation is about 0.5%-1%, usually occurring 2-4 weeks after treatment, with a mortality rate of 70%-80%. Liver failure secondary to fluorouracil infusion in patients with sclerosing cholangitis has also been reported after hepatic artery infusion. Hepatic dysfunction due to increased central venous pressure has also been seen in superior vena cava syndrome. However, clinically significant hepatic necrosis is rarely seen. Severe hyperammonemia is accompanied by metabolic encephalopathy, presenting with lethargy, confusion, disorientation, agitation, and rapid evolution to coma and epileptic seizures. These patients have respiratory alkalosis, abnormal liver function with progressive liver disease, and normalization after bone marrow transplantation. 6. Lactic acidosis is a life-threatening metabolic acidosis characterized by a decrease in arterial pH due to the accumulation of lactic acid in the blood (>2 mEq/L)