Case 1: Upper Gastrointestinal Bleeding

Case 1: Upper Gastrointestinal Bleeding

The upper gastrointestinal tract refers to the portion of the digestive system above Treitz’s ligament, where bleeding occurs. Bleeding from the esophagus, stomach, duodenum, gallbladder, pancreas, and common bile duct all fall under this category. With portal hypertension in liver cirrhosis, the submucosal vessels throughout the entire digestive system become congested and dilated. Esophageal veins and gastric fundal veins are particularly prominent. At this time, the stomach experiences increased stress-induced gastric acid secretion, and the gastric, intestinal, and pancreatic secretory systems are activated. Dietary habits, emotional states, and physical exertion can all trigger enhanced gastrointestinal motility, leading to rupture of esophageal veins and gastric fundal veins and resulting in upper gastrointestinal bleeding. Additionally, due to impaired liver function, the levels and quality of various coagulation factors—such as prothrombin, factor VIII, and thrombin—decline, thereby promoting bleeding. Furthermore, prolonged restriction of fatty foods reduces the absorption of fat-soluble vitamins D and K; vitamin K is a major coagulation factor and a component of prothrombin, while vitamin D plays a role in calcium absorption and utilization—both calcium and vitamin K are important coagulation factors. Consequently, in the entire digestive tract, besides major bleeding from the esophagus and gastric fundal veins, chronic mucosal leakage and small, frequent bleeds are also present. As a TCM and Western medicine physician, I first need to accurately assess the amount of bleeding. When the volume exceeds 5 ml, occult blood begins to appear; when it exceeds 50 ml, black stools of varying degrees of severity may occur; when it exceeds 250 ml, vomiting may occur; and when it exceeds 500 ml, blood pressure drops, leading to shock. Hematocrit is also an important indicator for assessing the amount of bleeding: the lower limit for normal hematocrit is 40%, while a hematocrit of 30% indicates a bleeding volume of 500–1000 ml; a hematocrit of 20% suggests a bleeding volume of 1000–2000 ml. The speed of the pulse is also closely related to the amount of bleeding—pulse rate and blood pressure are generally inversely correlated. When the amount of bleeding exceeds 500 ml, blood pressure begins to drop; let us use systolic blood pressure as a standard to explain this. When systolic blood pressure is around 16.7 kPa (80 mmHg), the pulse rate is 100 beats per minute. When blood loss accounts for about 1/4 of total circulating blood volume, it is considered mild shock; when systolic blood pressure is around 9.3 kPa (70 mmHg), the pulse rate rises to 120 beats per minute, and blood loss accounts for about 1/3 of total circulating blood volume, indicating moderate shock; when systolic blood pressure falls below 8.0 kPa (60 mmHg), the pulse rate becomes irregular, and blood loss is about half of the total blood volume.

Treatment for severe upper gastrointestinal bleeding:

1. Blood transfusion is the most critical measure in rescuing upper gastrointestinal bleeding. Typically, 400 ml of fresh blood can increase hemoglobin levels by 1 g; for blood transfusions of less than 2000 ml, stored citrate blood can be used, but calcium gluconate must be supplemented to prevent hyperkalemia caused by large-volume blood transfusions. The transfusion rate should not be too fast—30–40 drops per minute is ideal. If 2000 ml of blood needs to be transfused within the first hour, both pipelines should be infused simultaneously.

2. Pituitary posterior gland hormone: It can be administered via intravenous push or drip, with a dose of 10 units per administration, dissolved in 5–10% glucose. The drip rate should ideally be 30–40 drops per minute. This medication has been used for decades to treat severe bleeding from ruptured esophageal and gastric fundal veins; due to its proven efficacy, it is often the first choice. However, this medication has many side effects—increased intestinal motility, abdominal pain, and diarrhea are the most common side effects, and it can sometimes cause myocardial ischemia, even angina pectoris—but these occurrences are relatively rare.

3. Good Regulation: Includes octreotide and somatostatin, which belong to the class of growth inhibitors. Octreotide is an 8-peptide growth inhibitor, while somatostatin is a 14-peptide growth inhibitor. The former is administered at 0.3 mg per dose, and the latter at 3 mg per dose, diluted in 10% glucose solution for intravenous infusion. Growth inhibitors originally function by suppressing the secretion of various glands; they were initially used clinically for conditions such as thymoma and gastrinomas. Recently, it has been discovered that their broad inhibitory effect on digestive system glands holds significant therapeutic potential for treating massive upper gastrointestinal bleeding. After initial clinical trials, this drug gained widespread attention from clinicians due to its remarkable efficacy.

4. The use of vasoactive drugs like dopamine and norepinephrine can help restore blood pressure and improve blood flow to organs, but these effects are only achieved when combined with large-volume blood transfusions. Administer 20 mg of dopamine and 40 mg of norepinephrine dissolved in 500 ml of 5% glucose solution, infused intravenously at a rate of 20–30 ml per minute. Dopamine directly stimulates α- and β-adrenergic receptors, while norepinephrine exerts its effect indirectly; together, these two drugs work synergistically to enhance peripheral circulation.

5. Hemostatic Medications: Commonly used hemostatic medications include hemostatic acid, hemostatic敏, hexamethylenetetramine, and Litaixue. These medications can be administered via intramuscular injection or intravenous drip. The recommended dosage for hemostatic acid is 0.6 g per administration, for Hemostatic敏 2 mg, for Hexamethylenetetramine 6 g, and for Litaixue 100 u. Additionally, 500 u of compound thrombin can be dissolved in 40–80 ml of cold saline solution and administered orally, or 100 ml of 0.08% epinephrine diluted in cold saline solution can be given orally—both methods provide localized hemostatic effects.

6. Antacids: Commonly used antacids include methocarbamol 200–400 mg, ranitidine 100–200 mg, and omeprazole 20 mg, taken three times daily. All of these medications effectively reduce stomach acidity. Antacids serve as a prerequisite for hemostasis, as they promote the effectiveness of hemostatic treatments.

7. The once-popular triple-cavity double-bag tube was eventually found to have irreparable flaws—such as causing patients to attempt suicide, and both insertion and removal of the tube could exacerbate bleeding. As a result, it is now rarely used in clinical practice.

The understanding of upper gastrointestinal bleeding in traditional Chinese medicine and herbal medicine dates back to the Eastern Han Dynasty, when the renowned physician Zhang Zhongjing suggested two highly effective formulas.

1. Xu Xin Tang: Contains 10 g of rhubarb, 3 g of coptis, and 10 g of scutellaria, decocted in water and taken orally. According to the "Jin Gui," "When heart qi is deficient, leading to vomiting blood or nosebleeds, Xu Xin Tang is prescribed." The "Jin Jian" states, "Deficiency should be considered excess; when qi is excessive, it becomes fire, and when fire overcomes and causes blood to flow abnormally, vomiting blood occurs." Tang Rongchuan said, "To treat heart deficiency is to clear fire; to clear fire is to stop bleeding." Xu Xin Tang provides a precise definition of hemostasis. Tang believed that vomiting blood is a sign of "a dramatic upheaval," and that without the powerful descending action of rhubarb, the qi in the stomach would rise against its natural downward flow, causing blood to surge upward. He argued that the meridians, skin, and internal organs all experience qi imbalances, and thus must be corrected. Based on Tang's theory, the author developed a formula: 10 g of rhubarb, 3 g of coptis, 10 g of scutellaria, 20 g of raw ochre powder (mixed in), and 3 g of cinnamon, decocted in 200 ml of water and divided into four doses, spaced 30–60 minutes apart. This formula was routinely used in the Integrated Traditional and Western Medicine Ward of the Gansu Provincial Academy of Medical Sciences to treat massive upper gastrointestinal bleeding, yielding varying degrees of efficacy for most patients; it also showed notable effectiveness in treating bleeding caused by esophageal variceal rupture and gastric fundal variceal rupture.

2. Huang Tu Tang: Contains 6 g of licorice, 12 g of rehmannia root, 10 g of atractylodes macrocephala, 6 g of processed aconite, 10 g of donkey-gelatin, and 10 g of scutellaria, decocted in water and taken orally once daily. According to the "Jin Gui," "When blood comes out after bowel movements, first with blood in the stool, this is distant blood; Huang Tu Tang is prescribed." The "distant blood" referred to by Zhang Zhongjing indicates bleeding located far from the anus—specifically, in the upper gastrointestinal tract. This formula proved particularly effective in treating black stools, confirming that Zhang Zhongjing’s observations were correct. When using this formula, the author added 15 g of codonopsis to enhance its effects, aligning it with the principles of Fuzi Lizhong Tang. In cases of severe bleeding accompanied by black stools, the bleeding often subsides, and the primary issue at this stage is often a disruption of the gastrointestinal autonomic nervous system, along with increased intestinal peristalsis—leading to frequent black stools. Traditional Chinese medicine believes that the middle qi is urgently in need of regulation at this time, so Fuzi Lizhong Tang is employed. Patients with black stools may still experience continued bleeding in both the stomach and esophagus, so the author increased the dosage of rhubarb to 3 g, coptis to 3 g, scutellaria to 10 g, pinellia to 6 g, and raw ochre to 20 g.

II. Hepatic Encephalopathy

This condition is commonly known as hepatic coma. In chronic liver disease, hepatic encephalopathy is often the final clinical manifestation. It is more likely to develop during the decompensated phase of cirrhosis under the following circumstances: ① concurrent liver necrosis (chronic severe hepatitis), ② massive upper gastrointestinal bleeding, ③ extensive paracentesis, ④ severe colds or infections, ⑤ renal failure (hepatic renal syndrome), ⑥ severe electrolyte disturbances.

The primary clinical manifestations of hepatic encephalopathy include mental disorders, agitation, coma, and clonic tremors. The earliest symptoms include disrupted sleep patterns—daytime drowsiness, nighttime excitement and agitation. These symptoms indicate the early stages of hepatic coma; clinicians should pay close attention and immediately begin emergency treatment for hepatic encephalopathy. The biochemical characteristics of this condition can be summarized as three highs and three lows: high blood ammonia levels, elevated levels of false neurotransmitters, and elevated levels of aromatic amino acids; low potassium levels, low serum albumin levels, and low blood glucose levels. The key to successful clinical rescue of hepatic encephalopathy lies in correcting the three highs and three lows to achieve the intended therapeutic goals accurately.

1. Elevated blood ammonia levels: Normal blood ammonia levels range from 13 to 57 μmol/L; when levels exceed this range, blood ammonia is considered elevated, which is a direct cause of hepatic encephalopathy. Clinically, lowering blood ammonia is a top priority. Administer 23 g of glutamate in 500 ml of 10% glucose solution via intravenous drip, 25 g of arginine in 500 ml of 10% glucose solution via intravenous drip, and 1 g of acetylglutamine in 500 ml of 10% glucose solution via intravenous drip. While any one of these medications can be selected, acetylglutamine is often the best choice based on experience. Recently, the new drug Abos has also become a viable option—it is a composite preparation of ornithine and aspartate, with a pronounced ammonia-lowering effect, though it is relatively expensive. Potassium magnesium aspartate also has some ammonia-lowering properties and can be used clinically; this medication is especially beneficial when potassium and magnesium levels are low, as it helps improve electrolyte imbalances. Lactulose can be administered orally to block the reabsorption of intestinal ammonia, typically 20–40 ml per day, three times a day.

2. Elevated false neurotransmitters: This refers to an increase in hydroxyphenylethanolamine in brain tissue. This substance shares a similar structure to dopamine and can act as a substitute for dopamine in brain tissue, thereby reducing dopamine levels and accelerating the progression of hepatic encephalopathy. Treatment focuses on replenishing dopamine levels. However, pure dopamine cannot directly cross the blood-brain barrier; it must be administered in the form of levodopa. Yet levodopa can damage the liver, so it must be administered in conjunction with carbidopa to protect the liver. Clinically, 100 mg of levodopa mixed with 20 mg of carbidopa can be infused intravenously in 250–500 ml of glucose solution, once or twice daily.

3. Elevated aromatic amino acids: Under normal circumstances, the ratio of branched-chain amino acids such as glutamate, arginine, and aspartate to aromatic amino acids such as tyrosine, methionine, tryptophan, and phenylalanine in human serum remains stable, maintaining a consistent proportion. When liver function is severely impaired, aromatic amino acids increase, causing a shift in the branched-chain to aromatic amino acid ratio, and hepatic encephalopathy begins to develop. At this point, treatment should focus on supplementing large amounts of branched-chain amino acids. The aforementioned glutamate, arginine, and acetylglutamine not only directly reduce blood ammonia levels but also increase branched-chain amino acid levels, helping to restore the branched-chain to aromatic amino acid ratio. Intravenous administration of aspartate and ornithine also has this effect.

Improving the three lows involves replenishing potassium, replenishing sugar, and replenishing protein. Clinically, 10 ml of 10% potassium chloride can be added to 500 ml of 10% glucose solution for intravenous infusion; this approach also replenishes both potassium and sugar levels. Serum albumin is available in various concentrations—5 g or 10 g—and can be administered according to individual needs.

In cases of hepatic encephalopathy, traditional Chinese medicine and herbal remedies also offer certain therapeutic benefits. The author frequently uses the Da Cheng Qi Tang and the Tao Ren Cheng Qi formula. According to the "Shanghan Lun," "When diarrhea occurs, delirium appears, with bloody stools; Da Cheng Qi Tang is prescribed." "If a Suner’s illness is not resolved, heat accumulates in the bladder, and the patient becomes agitated; blood comes out from below—when the external symptoms are not yet resolved, treatment is not yet appropriate; once the external symptoms have subsided, but if there is still tightness in the lower abdomen, then Walnut Cheng Qi Tang is suitable." Both passages share a common theme: fever accompanied by psychiatric symptoms. The "delirium" in the former passage and the "agitation" in the latter both resemble psychiatric symptoms associated with hepatic encephalopathy. The use of these two formulas to treat hepatic encephalopathy—with their cooling and detoxifying effects—aligns with the TCM principle of clearing heat from the Yangming腑 pattern. By combining this method with modern Western medicine, the author successfully turned critical cases of hepatic encephalopathy into stable ones: 10 g of rhubarb, 10 g of mirabilite (melted), 10 g of jujube fruit, 6 g of magnolia bark, 10 g of peach kernel, 6 g of licorice, 10 g of bupleurum, 10 g of white peony, 10 g of cinnamon twig, 6 g of fresh ginger, 4 jujubes, 10 g of scutellaria, 3 g of coptis, 10 g of wood fragrance, 10 g of grassy cardamom, 10 g of salvia miltiorrhiza—decocted in water and taken once daily, administered in divided doses via nasogastric tube, with each dose ranging from 50 to 100 ml. Once the patient’s mental state is clear, the medication can be gradually consumed. The author believes that the use of large doses of rhubarb and mirabilite promotes the elimination of NH³⁺ and NH⁴⁺ residues in the intestines, thereby preventing further absorption of ammonia. Additionally, the large volume of water expelled through bowel movements helped reduce the progression of cerebral edema.

III. Hepatic Renal Syndrome

As cirrhosis progresses to a certain stage, liver function deteriorates, metabolic waste products accumulate, blood ammonia levels remain high, false neurotransmitter levels rise, and albumin levels decrease—all of which significantly impact and increase the burden on the kidneys. Over time, kidney function is damaged, leading to impaired excretion of non-protein nitrogen, with serum urea nitrogen exceeding normal levels (5.9 mmol/L) and creatinine levels also surpassing normal values (96 mmol/L). A decline in carbon dioxide binding capacity (below the normal range of 21–30 μmol/L) indicates that renal failure has progressed to acidosis. While Western medicine and pharmaceuticals offer several approaches to treat renal failure—such as large doses of albumin infusion and dialysis—there are no other effective options. Dialysis is only a temporary solution, capable of providing relief only temporarily and prone to complications like systemic infections, ultimately leaving patients vulnerable to death. Some say, “Dialysis has no circuit.” Traditional Chinese medicine and herbal remedies also show promise in treating hepatic renal syndrome. Through long-term observation, the author has found that employing methods that soothe the liver and tonify the kidneys can help some patients with hepatic renal syndrome improve. Below, we present a commonly used formula: 10 g of angelica sinensis, 10 g of white peony, 10 g of atractylodes macrocephala, 10 g of poria, 10 g of alisma, 12 g of rehmannia root, 6 g of cornus officinalis, 10 g of Dioscorea opposita, 6 g of peony root, 10 g of rhubarb, 6 g of processed aconite, 10 g of cinnamon twig, 20 g of motherwort, 10 g of red peony, 10 g of plantain seeds, 10 g of two flowers, 20 g of snake tongue grass, 10 g of triangle root, 10 g of turmeric, 6 g of leeches (mixed in), decocted in water and taken once daily, divided into multiple doses. Among the herbs in this formula—triangle root, turmeric, motherwort, leeches, and other ingredients that break up blood stasis—play a crucial role in treating renal failure. In particular, leeches possess the power to “break down walls,” making them a key component in restoring balance. The formula combines Xiaoyao San and Gui Fu Ba Wei to soothe the liver, tonify the kidneys, and strengthen the body’s fundamental defenses. I once reviewed the “Comprehensive Collection of Prescriptions from Famous Modern Doctors in China” (Hebei Science and Technology Press), where the prescription by Zhejiang’s renowned old Chinese medicine practitioner Pan Chenglian, “Xu Changqing’s Formula,” was a well-structured remedy. This formula contains 15 g of Xu Changqing, 10 g of white reed root, 6 g of wood ivy, 10 g of winter melon seeds, 10 g of Qumai, 10 g of Areca catechu, 10 g of talc, decocted in water and taken once daily. This formula was tested in clinical settings and proved effective. In March 2000, Mr. Wang, a 52-year-old man, was hospitalized for more than three months due to hepatic renal syndrome. He had undergone long-term treatments including liver protection, diuretic therapy, and infection prevention; his ascites subsided, liver function returned to normal, but his urea nitrogen level remained at 11.2 mmol/L, and his serum creatinine was 208 μmol/L. After taking the above formula for 10 doses, his urea nitrogen dropped to 9.2 mmol/L, and his serum creatinine fell to 182.5 μmol/L. Since then, the patient continued to take this formula alongside standard treatment for decompensated cirrhosis, and he was even discharged from the hospital, able to manage his daily activities independently. This formula originated from the “Lu Fang,” originally designed to treat qi stagnation and obstruction, resulting in difficulty urinating and abdominal distension. Mr. Pan Chenglian’s insight was unique—he used it to treat renal failure, and the results were truly impressive. This ancient formula is still relevant today, offering a fresh perspective on traditional medicine. Based on my experience, patients with renal failure often experience disruptions in gastrointestinal endocrine function and exocrine function. Given this, the digestive and absorptive functions of the gastrointestinal tract are often severely compromised. Therefore, while taking traditional Chinese medicine, it is advisable to administer 10 mg of domperidone three times a day and 150 mg of ranitidine three times a day—only in this way can we ensure that the traditional Chinese medicine reaches the stomach.

IV. Electrolyte Imbalances

The accumulation of sodium and water due to massive ascites and hypoproteinemia creates an imbalance between sodium and potassium ions, naturally leading to hypokalemia—a fundamental characteristic of the electrolyte status in liver cirrhosis. Moreover, the use of large quantities of diuretics leads to significant potassium loss, further exacerbating potassium deficiency. Therefore, potassium supplementation is a basic treatment strategy for liver cirrhosis; typically, 1 g of potassium chloride is added to 500 ml of 10% glucose solution and slowly infused intravenously, keeping the concentration moderate to avoid cardiac complications. Since calcium and magnesium ions, like potassium ions, also exhibit opposing relationships with sodium ions, hypokalemia often coincides with low levels of calcium and magnesium. Although the body is generally in a state of sodium-water retention due to ascites and edema, sodium ions are concentrated in the interstitial spaces; however, serum sodium levels remain low. Thus, in the early stages of decompensated cirrhosis, the electrolyte status can be summarized as “low.” At this stage, in addition to potassium supplementation, magnesium, calcium, and sodium should also be appropriately replenished. As the disease progresses, patients with cirrhosis may develop renal failure, a condition known as “hepatic renal syndrome.” The breakdown of renal clearance functions leads to elevated levels of urea nitrogen and serum creatinine, as well as decreased carbon dioxide binding capacity, resulting in acidosis. Due to reduced urine output and decreased excretion, serum potassium levels begin to rise; because phosphate excretion is hindered, hyperphosphatemia develops, and the opposing relationship between calcium and phosphorus causes calcium levels to drop. The onset of acidosis causes sodium and calcium ions to be replaced by acidic radicals, making hypokalemia and hypocalcemia even more pronounced. In summary, after renal failure sets in, in addition to high potassium and high phosphorus levels, calcium, sodium, and magnesium remain low. Proper fluid replacement is still essential. In the final stages of decompensated cirrhosis, a small number of patients may develop hyperparathyroidism; in these cases, serum calcium levels rise unexpectedly, while serum phosphorus levels fall.

Once these characteristics are understood, the management of electrolyte imbalances in decompensated cirrhosis becomes much clearer.

In summary, there are only three key points:

① In the early stages of decompensated cirrhosis, potassium, sodium, calcium, and magnesium are all deficient or low; therefore, potassium supplementation should be prioritized, alongside sodium, calcium, and magnesium.

② During hepatic renal syndrome, serum potassium levels rise as urine output decreases; at this point, potassium supplementation should be avoided, as sodium, calcium, and magnesium are also low and can be supplemented as needed.

③ In rare cases where patients develop hyperparathyroidism, serum calcium levels rise while phosphorus levels fall; for high calcium levels, medications containing phosphorus are often used as countermeasures—oral sodium phosphate or potassium phosphate are the most common choices, typically administered at 0.5 g three times daily.

**In addition to the four aspects mentioned above, treatment during the decompensated stage of cirrhosis should still focus on diuresis, liver protection, infection control, immune enhancement, gastrointestinal support, and nutritional support. Diuresis helps eliminate ascites, reduce portal venous pressure, and alleviate the greatest psychological stress experienced by patients with cirrhosis. The use of Western medications such as diuretics like hydrochlorothiazide, furosemide, and spironolactone is well-known and often effective for general ascites; however, when ascites are complicated by infection or in cases of severe hypoproteinemia, these diuretics may fail to provide adequate relief. When combined with renal failure, diuretics become less effective. Given that some patients require peritoneal drainage, various types of ascites drainage devices have been successively adopted in clinical practice. The benefit of ascites drainage is that it allows for the reuse of albumin and other valuable nutrients in the ascitic fluid—but the biggest side effect is that repeated drainage can lead to infection, even accelerating the deterioration of kidney function. In the 1980s, I developed a special drug for liver cirrhosis-related ascites, “Gu Sheng II,” which proved highly effective in treating liver cirrhosis-associated ascites, especially when Western medications like furosemide failed to provide satisfactory results. The main ingredient of Gu Sheng II is the “Nitrate-Ferrite Powder” from the “Jin Gui,” a product that renews the past while staying true to the future, opening up promising prospects for treating liver cirrhosis-associated ascites. After more than 20 years of trial use in Lanzhou, its remarkable efficacy became widely known; people from Shaanxi, Sichuan, Qinghai, Ningxia, Beijing, and many other regions came seeking treatment and purchasing the drug. All diuretics—including Gu Sheng II—while eliminating ascites and edema, also carry the side effect of potassium loss. Therefore, when administering diuretics, it is essential to supplement potassium salts, as the mucous membranes of the gastrointestinal tract in decompensated cirrhosis are often congested and swollen due to portal hypertension, and gastrointestinal digestion and absorption are extremely weak. Thus, oral potassium supplementation should be prioritized; while potassium supplements can also be administered orally, they are best suited for patients with relatively intact gastrointestinal function and mild conditions. Western medicine often uses 500–1000 ml of 10% glucose solution with 1000 mg of vitamin C and an appropriate amount of insulin, along with 1 mg of glucagon, administered once daily. Traditional Chinese medicines such as Xiaoyao San, Qiang Gan Tang, Xiang Sha Liu Jun Tang, and Chai Shao Liu Jun Tang are also valid options—but in my experience, these formulas should always include 30 g of salvia miltiorrhiza, 30 g of astragalus, 10 g of angelica sinensis, 10 g of white peony, 10 g of qian tong, and 20 g of indigo woad root. For liver area pain, add triangle root, turmeric, yuan hu, chuan lian zi, and prepared leeches; for patients with liver damage, add two flowers, forsythia, astragalus, bitter cress, snake tongue grass, half-branch lotus, and five-flavor berry powder (for oral administration); for significant splenic enlargement, add triangle root, turmeric, summer grass, raw oyster, sanqi, and leeches. For jaundice, Western medicine currently lacks specialized treatments; traditional Chinese medicine offers a wide array of remedies. I often combine Da Chai Hu Tang with Yin Chen Hao Tang, Yin Chen Wu Ling San, and other formulas, which have shown good clinical outcomes.

Don’t Be Disappointed, HBV Carriers

Since the outbreak of hepatitis B in the 1960s, its spread has been astonishing, sweeping across Asia, Africa, and Latin America. In China, nearly 150 million people have been infected, and for a time, people spoke openly about hepatitis B, fearing it or even turning pale upon hearing the word. With advances in science and technology, our understanding of hepatitis B has deepened and become more comprehensive. The previously feared issues of contagiousness, treatment resistance, and genetic inheritance have gradually been clarified, and effective preventive measures have emerged. Even those who contract hepatitis B can achieve remission through proper treatment; some patients can even be completely cured. Regarding the contagiousness of hepatitis B, as long as precautions are taken correctly, it is not impossible to prevent infection. As for vertical transmission from infants, the latest three-block technologies have now made it possible to completely eliminate this risk.