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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
Severe pancreatitis symptoms
Severe pancreatitis, due to different stages of pathological changes, presents diverse systemic responses. Generally, mild symptoms of pancreatitis include abdominal pain, nausea, vomiting, and fever. In severe pancreatitis, apart from these symptoms, due to bleeding, necrosis, and autolysis of the pancreas, additional symptoms such as shock, high fever, jaundice, abdominal distension, and paralytic ileus, peritoneal irritation signs, and subcutaneous ecchymosis may also occur. Abdominal pain is the earliest symptom, while nausea and vomiting are manifestations due to inflammatory factors stimulating the vagus nerve. The likelihood of jaundice is relatively low in acute edematous pancreatitis but is more common in severe pancreatitis. Extensive inflammatory exudation in the pancreas can lead to pancreatic necrosis and localized abscesses, which may cause varying degrees of fever increase.
Severe Pancreatitis Criteria
Acute pancreatitis with persistent organ failure lasting more than 48 hours is considered severe pancreatitis. In the early stages of the disease, organ failure starts with a systemic inflammatory response produced by the activation of a cytokine cascade, involving the continuous failure of single or multiple organs. Such patients often have one or more local complications, with organ failure that can persist for several days after onset. The mortality rate can reach 36% to 50% once organ failure occurs. Infections in such patients can dramatically increase the mortality rate. CT imaging may show gas bubbles in peripancreatic necrotic tissue and fluid collections. Diagnosis is confirmed by positive results from either a smear of aspirate obtained via image-guided fine-needle aspiration or from bacterial cultures.
Clinical manifestations of hyperkalemia
The clinical manifestations of hyperkalemia mainly affect the cardiovascular system, often presenting with slowed heart rate and various arrhythmias. When the blood potassium level is between 6.6 and 8.0 mmol/L, a tent-shaped T-wave can be observed. Rapid increases in blood potassium can lead to ventricular tachycardia, and even ventricular fibrillation. A gradual increase in blood potassium can cause conduction blocks, and in severe cases, cardiac arrest. Sudden death in severe hyperkalemia is mainly due to ventricular fibrillation and cardiac arrest. The second aspect is symptoms related to the neuromuscular system. As the concentration of potassium ions in the extracellular fluid increases, the resting membrane potential drops, leading to muscle weakness and even paralysis, typically more pronounced in the lower limbs and extending upward along the trunk. In severe cases, some patients may experience difficulty in swallowing and breathing difficulties. Symptoms involving the central nervous system mainly include restlessness, confusion, and fainting.
Precautions for intravenous potassium supplementation in patients with hypokalemia
Patients with hypokalemia should closely monitor their blood potassium levels when receiving intravenous potassium supplementation, rechecking potassium levels within 1-4 hours after supplementation. Continuous electrocardiogram monitoring is necessary to closely observe any changes in the electrocardiogram and prevent life-threatening hyperkalemia. In patients with renal impairment, the potassium supplementation should be 50% of that for normal patients, and it is generally considered that the daily potassium supplementation should not exceed 100-200 mmol. For patients with severe hypokalemia, the total daily potassium supplementation can reach 240-400 mmol, but blood potassium levels should be closely monitored to prevent hyperkalemia. Peripheral administration of high-concentration potassium can irritate the vein wall, causing pain and phlebitis. Generally, it is considered that the rate of potassium supplementation through peripheral veins should not exceed 40 mmol/L.
What are the symptoms of hyperkalemia?
The effects of hyperkalemia on the body mainly include the following aspects: First, the impact on muscle tissue: mild hyperkalemia can cause slight tremors in muscles. If the potassium levels continue to rise, this can lead to decreased neuromuscular excitability, resulting in limbs becoming weak and flaccid, and even leading to delayed paralysis. Second, the impact on the cardiac system: it can cause a decrease in myocardial excitability, conductibility, and automaticity. The electrocardiogram shows a depressed P wave, widened QRS complex, shortened QT interval, and peaked T waves. Third, hyperkalemia affects acid-base balance and can lead to metabolic acidosis during hyperkalemia.
The effects of hyperkalemia on the body
Hyperkalemia affects the body mainly in three aspects. Firstly, hyperkalemia impacts muscle tissues, clinically manifesting as symptoms such as muscle tremors. Secondly, the effect of hyperkalemia on the heart primarily manifests as decreased excitability, conductivity, and automaticity of the myocardium. It affects electrocardiograms, characterized by a depressed P wave, widened QS wave, reduced R wave, and elevated T wave. Thirdly, hyperkalemia affects acid-base balance; during hyperkalemia, potassium efflux from cells can lead to metabolic acidosis, resulting in alkaline urine.
What can be eaten with severe pancreatitis?
Patients with severe pancreatitis should not eat orally. Historically, suppressing pancreatic enzyme secretion by resting the intestines has been considered an important means of controlling the progression of acute pancreatitis. Currently, the implementation of early enteral nutrition is proposed. Early enteral nutrition should be administered via a jejunal tube, which is safer. The nutritional formulation should be chosen based on the patient's condition and intestinal tolerance. Initially, only glucose water may be used to allow the intestines to adapt to the nutrition. Early nutrition should use low-fat preparations containing amino acids or short peptides, because whole proteins entering the intestine directly without being digested by stomach acid can cause indigestion. As the condition enters the recovery phase, the feeding amount and rate can be gradually increased, and preparations containing whole proteins may be given.
The effect of hyperkalemia on the myocardium
The primary mechanism by which hyperkalemia causes arrhythmias is due to dysfunction of myocardial conduction, which is also related to various other factors such as other myocardial lesions, failure, and ionic states. The main impact on the myocardium is on its excitability; myocardial excitability can decrease or even disappear, and its conductivity is also affected, causing a reduction in conductivity. The effect on myocardial automaticity is a decrease in automaticity. Electrocardiographically, there are manifestations such as a low P wave, prolonged PR interval, and widened QRS complex without disappearance; these are some of the presentations of hyperkalemia.
The difference between hyperkalemia and hypokalemia
Potassium ions are one of the essential electrolytes necessary for human life. Their physiological functions include maintaining cell metabolism, regulating osmotic pressure and acid-base balance, and preserving cell emergency functions, among others. The normal concentration of serum potassium is between 3.5 and 5.5 millimoles per liter. If it falls below 3.5 millimoles per liter, it is categorized as hypokalemia. If it exceeds 5.5 millimoles per liter, it is categorized as hyperkalemia. Common causes of hypokalemia include insufficient potassium intake, excessive potassium excretion, and the shifting of potassium from outside to inside the cells. The main causes of hyperkalemia include increased intake or reduced excretion of potassium, as well as substantial movement of potassium from inside the cells to the outside. Whenever hyperkalemia or hypokalemia occurs, it should be actively managed.
Treatment of Hyperkalemia with Drugs
Hyperkalemia primarily affects the conduction of the heart and muscle nerves, with typical clinical manifestations including severe bradycardia, atrioventricular block, and even sinus arrest. Once hyperkalemia occurs clinically, immediate treatment should be administered. The first approach to treatment is promoting the excretion of potassium, using furosemide or other diuretics to increase renal potassium excretion, and taking a small dose of sodium polystyrene sulfonate orally to eliminate potassium. For life-threatening severe hyperkalemia, if serum potassium is greater than 6.5 mmol/L, hemodialysis treatment is necessary. The second aspect involves shifting potassium into cells, using calcium to alter cell excitability, which can protect the heart from the damage to the conduction system caused by hyperkalemia. Additionally, using glucose with insulin and administering sodium bicarbonate can be effective. It is important to note that all the above medications should be used under the guidance of a doctor.