Keywords:专著资料, 全文在线浏览, 一、传染性
Section Index
IV. Electrolyte Disturbances
The accumulation of sodium and water due to massive ascites and hypoproteinemia creates a positive ion counterbalance between sodium and potassium. Naturally, hypokalemia is a fundamental characteristic of the electrolyte imbalance in liver cirrhosis. Moreover, the extensive use of diuretics leads to significant potassium loss, exacerbating potassium deficiency. Therefore, potassium supplementation is a basic treatment strategy for liver cirrhosis. Typically, 1g of potassium chloride is added to 500ml of 10% glucose solution and slowly infused intravenously; the concentration should not be too high, otherwise cardiac events may occur. Given that calcium and magnesium, like potassium, share a similar counterbalancing relationship with sodium, hypokalemia often results in low levels of calcium and magnesium as well. Although the body is in a state of sodium-water retention due to ascites and edema, sodium ions are still concentrated in the interstitial spaces; however, the sodium levels in the blood remain low. Thus, in the early stages of decompensated cirrhosis, the electrolyte balance 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, liver cirrhosis patients may develop renal failure, which is clinically referred to as “hepatic-renal syndrome.” The breakdown of renal clearance function leads to elevated levels of urea nitrogen and serum creatinine, as well as decreased carbon dioxide binding capacity, resulting in acidosis. Due to oliguria and reduced excretion, blood potassium levels begin to rise; because phosphate excretion is hindered, hyperphosphatemia develops, and the opposing relationships between calcium and phosphorus cause a decline in blood calcium levels. The onset of acidosis causes sodium and calcium ions to bind with acidic radicals, making hypokalemia and hypocalcemia even more pronounced. In summary, after renal failure occurs, in addition to high potassium and high phosphorus levels, calcium, sodium, and magnesium remain in a state of deficiency and should still be appropriately supplemented through fluid infusion. In the final stages of decompensated cirrhosis, a small number of patients may develop hyperparathyroidism; at this point, blood calcium levels rise unexpectedly, while blood phosphorus levels fall.
With a thorough understanding of these characteristics, the electrolyte supplementation strategies for decompensated cirrhosis are clearly supported. In general, there are only three key points: ① In the early stages of decompensated cirrhosis, potassium, sodium, calcium, and magnesium are all deficient or below normal levels; therefore, potassium supplementation should be prioritized, alongside sodium, calcium, and magnesium. ② During hepatic-renal syndrome, blood potassium levels rise as urine output decreases; at this point, potassium supplementation should be avoided, as sodium, calcium, and magnesium are also below normal levels and can be supplemented as needed. ③ In some patients with hyperparathyroidism, blood calcium levels rise while blood phosphorus levels fall; for high calcium levels, it is advisable to use phosphorus-containing medications for treatment, with oral sodium phosphate or potassium phosphate being the most common options—typically 0.5g is administered three times a day.
In addition to these four aspects, treatment during the decompensated stage of cirrhosis should still focus on diuresis, liver protection, anti-infection measures, immune enhancement, gastrointestinal support, and nutritional support. Diuresis helps eliminate ascites, reduce portal pressure, and alleviate the greatest psychological stress experienced by patients with cirrhosis. The use of Western medications such as diuretics like hydrochlorothiazide, furosemide, and indapamide is well-known and often effective for treating common ascites; however, when ascites are complicated by infection or in cases of severe hypoproteinemia, these diuretics often fail to provide adequate relief. When combined with renal failure, diuretics become even less effective.
Given that some patients require paracentesis for fluid 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; however, 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-induced ascites, “Gu Sheng II,” which proved highly effective and reliable in treating liver cirrhosis-associated ascites—especially when Western medications like furosemide were ineffective. The main ingredient of Gu Sheng I was “Niu Shi Ji Shi San” from the Jin Gui, a product that revitalized the past and made it relevant today, opening up promising prospects for the treatment of liver cirrhosis-associated ascites. After more than 20 years of trial use in Lanzhou, its remarkable efficacy became widely known, attracting patients from Shaanxi, Sichuan, Qinghai, Ningxia, Beijing, and other regions who 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 the digestive and absorptive functions of the gastrointestinal tract are extremely weak. Thus, intravenous potassium supplementation is the preferred method for potassium supplementation; potassium salts can also be administered orally, but they are only suitable for patients whose gastrointestinal function is still relatively good and whose condition is mild. Western medicine often uses 500–1000ml of 10% glucose solution mixed with 1000mg of vitamin C, a moderate amount of insulin, and 1mg 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 viable options—but in my experience, the formula should always include 30g of salvia miltiorrhiza, 30g of astragalus, 10g of angelica sinensis, 10g of white peony, 10g of qing tiao, and 20g of indigo woad. For liver area pain, add three-edged polygonum, curcuma, yuan hu, chuan lian zi, and prepared leeches; for patients with liver damage, add two flowers, forsythia, astragalus, bitter wormwood, white flower snake tongue grass, half-branch lotus, and five-flavor berry powder (for oral administration); for significant splenomegaly, add three-edged polygonum, curcuma, summer savory, raw oyster, sanqi, and leeches. For jaundice, Western medicine currently lacks specialized drugs; 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 relatively good therapeutic effects in clinical practice.
Don’t Be Afraid of Hepatitis B Patients
Since its emergence in the 1960s, hepatitis B has spread at an astonishing rate, sweeping across Asia, Africa, and Latin America. In China, the number of infected individuals has reached nearly 1.5 billion, and for a time, people spoke openly about hepatitis B, fearing it or even turning pale upon hearing the word. With the advancement of science and technology, people’s understanding of hepatitis B has deepened and become clearer. The previously feared issues of contagiousness, difficulty in treatment, and genetic inheritance have gradually been elucidated, and effective preventive measures have been developed. 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 entirely unavoidable. As for vertical transmission from infants, the latest three-block technologies have now achieved complete resolution.
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