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Wei Shi Liang
Intensive Care Unit
About me
Graduated from Shanxi Medical University with a degree in Clinical Medicine in 2006, and has been working in the field of Critical Care Medicine ever since.
Proficient in diseases
Treatment of severe infections, ARDS, severe trauma, MODS, and other diseases.
Voices
Prevention and Treatment of Bronchial Asthma
The prevention and treatment of bronchial asthma mainly involve the following aspects: First, eliminating the causes and triggers of the disease; second, preventing diseases and pests such as allergic rhinitis and gastroesophageal reflux disease; third, immunomodulation; fourth, routinely checking if inhaled medications are used correctly; fifth, education and management of asthma patients, mainly allowing them through long-term, appropriate, and sufficient treatment to fully and effectively control asthma attacks. Additionally, understanding individual differences in asthma triggers to avoid occurrences, learning patient self-monitoring of disease progression, mastering the use of inhalers and peak flow meters, and educating patients on simple self-help methods are essential. It's important for patients and doctors to jointly develop a plan to prevent asthma attacks and maintain long-term stability. These are the basic elements of the prevention and treatment of bronchial asthma.
Why does hyperkalemia cause acidosis?
The concentration of potassium ions in serum is 3.5 to 5.5 millimoles per liter, and concentrations above 5.5 millimoles per liter are considered hyperkalemia. In the state of hyperkalemia, potassium ions in the extracellular fluid move into the intracellular fluid, while hydrogen ions in the intracellular fluid move to the extracellular fluid. At this time, through a compensatory mechanism, there is an increase in hydrogen ions in the extracellular fluid, significantly higher than normal levels, resulting in acidosis. Therefore, hyperkalemia often accompanies metabolic acidosis, which in turn affects the renal tubular epithelial cells, causing an abnormal alkaline urine. This is the main reason why hyperkalemia leads to acidosis.
Is hyperkalemia acidosis?
Hyperkalemia is not acidosis, but during acidosis, the hydrogen ions of the gastric fluid within cells enter the cells, causing the potassium ions inside the cells to move to the extracellular fluid, resulting in hyperkalemia. Clinically, it is commonly seen in organic acidosis, lactic acidosis, diabetic ketoacidosis, and acute renal failure causing acidosis. Once hyperkalemia occurs and is diagnosed, immediate treatment should be administered. First, the primary disease should be treated; next, serum potassium should be reduced. In particularly severe cases, bedside hemofiltration can be administered, and the cardiotoxic effects of hyperkalemia should be mitigated.
Can a pulmonary embolism be detected by a CT scan?
CT can detect acute pulmonary embolism, using CT angiography, which is the preferred imaging method for diagnosing pulmonary embolisms. It mainly shows central filling defects, as well as eccentric and abdominal wall filling defects, and complete filling defects. A diagnosis of pulmonary embolism can be made through the visualization of these filling defects on a CT scan. Additionally, some indirect signs, such as pulmonary hypertension, right ventricular enlargement, and the common mosaic sign, can also be observed. These are characteristic CT manifestations of acute pulmonary embolism.
Severe pancreatitis is what disease
Acute severe pancreatitis is a disease caused by various etiologies, characterized by local necrosis, inflammation, and infection of the pancreas, accompanied by systemic inflammatory response and persistent organ failure. The current mortality rate is still as high as 17%. The course of acute severe pancreatitis can generally be divided into three periods. First, the acute response period, occurring up to about two weeks after onset, is characterized by a systemic inflammatory response. Second, the systemic infection period, from two weeks to about two months, is characterized by infection of pancreatic or peripancreatic necrosis. Third, the residual infection period, occurring two to three months later, where the main clinical manifestation is systemic malnutrition.
What are the symptoms of hyperkalemia?
Mild hyperkalemia can affect muscle tissues, causing mild muscle tremors, while severe hyperkalemia may reduce the excitability of neuromuscular functions, leading to weakness and even flaccid paralysis in the limbs. Hyperkalemia can also impact the heart, mainly resulting in decreased myocardial excitability, decreased myocardial conductivity, and decreased myocardial automaticity. The effects on the electrocardiogram (ECG) primarily manifest as low and widened P waves, widened QS complexes, decreased R waves, and elevated T waves. Regarding myocardial contractility, hyperkalemia mainly causes a decrease in contractility and can lead to metabolic acidosis.
Common Causes of Hyperkalemia
Hyperkalemia is when the serum potassium concentration exceeds 5.5 millimoles per liter. Common causes include excessive potassium intake and large doses of potassium salts, which can lead to hyperkalemia, as well as the use of stored blood. Another cause is reduced potassium excretion; in patients with renal insufficiency, reduced urine output or anuria leads to decreased renal potassium excretion. If potassium supplementation is inappropriate at this time, or if potassium-sparing diuretics are used, severe hyperkalemia can occur. Another scenario is the leakage of intracellular potassium during respiratory and metabolic acidosis, where sodium ion exchange occurs in cells, hydrogen ions enter the cells, and potassium ions leak out to the extracellular space, which can lead to increased blood potassium. These are the common causes of hyperkalemia.
Rescue of severe pancreatitis
Severe pancreatitis involves severe illness impacting multiple systems and organs across the body. The rescue of severe pancreatitis should be based in the ICU, with multidisciplinary cooperation. The first step is early fluid resuscitation, with crystalloid solution preferred, and it should be rapidly completed within 48 hours of onset. The second step involves support for circulation and respiration. The third step involves the maintenance of organ functions and the use of blood purification treatments. Early use of blood purification in acute pancreatitis can remove inflammatory mediators, regulate immune dysfunctions, and protect organ functions, potentially extending the survival time of patients with severe pancreatitis. The fourth step includes monitoring intra-abdominal pressure and preventing and treating abdominal compartment syndrome. Further treatments mainly include the use of agents to inhibit pancreatic enzymes and platelet activation, as well as early jejunal nutrition. Additionally, prophylactic use of antibiotics is required, and in cases of biliary acute pancreatitis, ERCP or sphincterotomy should be performed. The final approach is surgical treatment, which is reserved for patients who do not respond to or have poor results from conservative treatment.
Which department to go to for hypokalemia?
Hypokalemia is defined as having a blood potassium level below 3.5 mmol/L. In hospitals, when treating mild hypokalemia, it is essential to identify and treat the primary disease in the corresponding department, such as endocrinology, internal medicine, or gastroenterology. Additionally, timely oral potassium supplementation is necessary to correct the hypokalemia. If severe hypokalemia occurs clinically, with blood potassium levels less than 2.5 mmol/L, treatment in the intensive care unit is required. It is crucial to establish an intravenous access for potassium supplementation immediately. The rate of potassium supplementation should be slow, and blood potassium levels must be monitored continuously.
When supplementing potassium for hypokalemia, what should be paid attention to?
When supplementing potassium for hypokalemia, the following should be noted: 1. Closely monitor the blood potassium levels. Supplement 60-80 mmol/L of potassium, or recheck the blood potassium level within 1-4 hours after supplementation. 2. If the rate of potassium supplementation exceeds 10 moles per hour, continuous ECG monitoring should be maintained, closely observe the changes in the ECG, and prevent the occurrence of life-threatening hyperkalemia. 3. The rate of potassium supplementation for patients with regenerative dysfunction should be 50% of that for patients with normal kidney function. 4. The daily amount of potassium supplementation should not exceed 100-200 millimoles. 5. Try not to use peripheral veins for high-concentration potassium supplementation. 6. Use sodium chloride solution to dilute potassium-containing solutions, and it is not recommended to use glucose or low molecular weight dextrorotatory sugar as the carrier.