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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
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.
How long does the treatment for pulmonary embolism take?
The timing of pulmonary embolism treatment mainly depends on the severity of the pulmonary embolism. The main goals of pulmonary embolism treatment are to save lives by addressing life-threatening right heart dysfunction and obstructive shock caused by the pulmonary embolism, to re-establish pulmonary vascular patency, restore lung tissue perfusion, and prevent the recurrence of pulmonary embolism. Main treatment methods include: respiratory and circulatory support, anticoagulation, thrombolysis, interventional or surgical removal of blood clots, placement of inferior vena cava filters, etc. General management: Patients who are highly suspected or diagnosed with pulmonary embolism should be closely monitored, tracking changes in respiration, heart rate, blood pressure, venous pressure, electrocardiogram, and blood gases to prevent the dislodgement of clots again. Absolute bed rest is required, and care should be taken not to overly bend the lower limbs, maintain bowel regularity, and avoid straining. For patients experiencing anxiety and panic symptoms, reassurance should be provided, along with appropriate use of sedatives. If there is chest pain, analgesics may be administered. For symptoms like fever and cough, corresponding symptomatic treatments should be given. To prevent lung infections and treat phlebitis, antibiotics may be used. Additionally, support treatments for respiratory and circulatory functions, as well as anticoagulation therapy, should be provided.
The impact of hypokalemia on skeletal muscle
In clinical practice, hypokalemia can affect the muscular and nervous conduction systems. The most prominent symptoms of hypokalemia in the neuromuscular system are flaccid paralysis of the skeletal muscles, loss of tension in smooth muscles, and rhabdomyolysis. If the respiratory muscles are involved, it can lead to respiratory failure. Hypokalemia can also lead to insulin resistance, resulting in significantly abnormal glucose tolerance. If hypokalemia occurs clinically, it is crucial to actively treat the primary disease, appropriately supplement potassium, monitor during the supplementation process to avoid hyperkalemia, and closely monitor blood potassium levels with regular reviews.
Causes and Clinical Manifestations of Hypokalemia
Hypokalemia refers to a condition where blood potassium levels are below 3.5mmol/L. The causes can be due to inadequate intake of potassium, such as prolonged inability to eat without sufficient intravenous supplementation of potassium. It can also result from excessive loss of potassium, through external losses such as vomiting and diarrhea, or through renal losses due to the excessive use of diuretics and certain hormonal imbalances. A third cause involves the shift of potassium into cells, such as during episodes of alkalemia and periodic paralysis. Clinically, mild to moderate hypokalemia is characterized by symptoms like muscle weakness, fatigue, cramps, intestinal obstruction, and some abnormalities in electrocardiograms, including the presence of U waves and flattened T waves. Severe hypokalemia can lead to life-threatening arrhythmias, such as ventricular tachycardia and ventricular fibrillation, which require immediate treatment.
Can pulmonary embolism lead to pneumonia?
Pulmonary embolism itself does not cause pneumonia; however, during the treatment of pulmonary embolism, procedures such as oral tracheal intubation and the creation of an artificial airway might be employed. These can lead to nosocomial infections of iatrogenic origin, resulting in pneumonia. Pulmonary embolism often manifests as unexplained respiratory difficulty, pleuritic pain, tachycardia, and decreased oxygen saturation. Other high-risk factors include being over the age of 40, having a history of DVT (Deep Vein Thrombosis), obesity, prolonged immobilization, stroke, congestive heart failure, malignancy, lower limb fracture, anesthesia time exceeding 30 minutes during surgery, pregnancy and childbirth, use of estrogen, and a hypercoagulable state. These are all potential high-risk factors for pulmonary embolism.
Is acute severe pancreatitis serious?
Acute severe pancreatitis is a very serious disease in clinical practice, with a high mortality rate, often requiring comprehensive treatment in the ICU. Acute severe pancreatitis is a disease caused by multiple etiologies that results in localized inflammation, necrosis, and infection of the pancreas, accompanied by a systemic inflammatory response and persistent organ failure. It is divided into three phases. The first phase is the acute response phase, occurring from onset to about two weeks, characterized by systemic inflammatory response; the second phase is the systemic infection phase, occurring from two weeks to about two months, characterized by necrosis and infection of the pancreas or peripancreatic tissues; the third phase is the residual infection phase, occurring two to three months later, with clinical manifestations primarily of systemic malnutrition and persistent fistulas, accompanied by gastrointestinal fistulas.