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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
How is subarachnoid hemorrhage treated?
The treatment of subarachnoid hemorrhage primarily aims to prevent rebleeding, vasospasm, hydrocephalus, and other complications, reducing mortality and disability rates. During the acute phase, keep the patient's head in a raised position, lying on their side, and provide dehydration, sedation, and pain relief; absolute bed rest; monitor blood pressure; and when bleeding is significant, undertake ventricular puncture for drainage. Patients with subarachnoid hemorrhage should generally be admitted to the ICU, monitoring vital signs and changes in neurological signs, ensuring airway patency, maintaining stable respiratory and circulatory functions, resting quietly, avoiding emotional agitation, ensuring smooth bowel movements, and for patients with increased intracranial pressure, appropriately restricting fluid intake.
The role of calcium agents in hyperkalemia
Change the excitability of autonomic cells to protect the heart. Hyperkalemia mainly affects the conduction of the heart and neuromuscular system. Typical clinical manifestations include severe bradycardia, atrioventricular block, and even sinus arrest. By using calcium agents to change the excitability of autonomic cells, we can protect the heart from the damage to the conduction system caused by hyperkalemia. This allows the potassium ions to move from outside the cell to inside the cell. While protecting the myocardium, it is also necessary to use some medications to lower blood potassium. If the blood potassium is particularly high, dialysis or continuous bedside blood filtration can be used to reduce the blood potassium to a normal range.
Severe pancreatitis complications
Complications of severe pancreatitis primarily include: 1. Acute peripancreatic fluid collection and interstitial edematous pancreatitis, where fluid accumulates around the pancreas without necrosis. This can be diagnosed with enhanced CT. 2. Pancreatic pseudocysts, characterized by fluid encapsulated by a clearly defined inflammatory cyst wall around the pancreas, with no or minimal necrosis, commonly occurring around four weeks after an episode of interstitial edematous pancreatitis. 3. Accumulation of acute necrotic material, involving necrotic tissue and liquids from necrotizing pancreatitis, including the parenchyma and peripancreatic tissues, also diagnosable through enhanced CT. 4. Encapsulated necrosis, observable as a clearly defined inflammatory encapsulation of the pancreas and peripancreatic tissues, commonly occurring four weeks post an episode of necrotizing pancreatitis.
Hypokalemia is a condition.
Potassium is one of the essential electrolytes for life. Its physiological functions mainly include maintaining cellular metabolism, regulating osmotic pressure, acid-base balance, and maintaining cell stress functions. The human body intakes about 100 millimoles of potassium each day, of which 90% is excreted through the kidneys, and the remainder is excreted through the gastrointestinal tract. Potassium mainly exists inside cells, with serum potassium accounting for only 2% of the total potassium in the body. The concentration of potassium in serum is between 3.5 to 5.5 mmol/L. If the concentration of serum potassium is below 3.5 mmol/L, it is considered hypokalemia, which is often due to insufficient potassium intake or excessive potassium excretion.
Is pulmonary embolism related to pneumonia?
If unexplained shortness of breath, pleuritic chest pain, tachycardia, and decreased oxygen saturation occur, one should be highly vigilant about pulmonary embolism. Generally, pulmonary embolism has no direct relationship with pneumonia. High-risk factors for pulmonary embolism include obesity, prolonged immobilization, stroke, congestive heart failure, malignant tumor, inflammatory bowel disease, lower limb fracture, anesthesia time exceeding 30 minutes, and acquired or genetic hypercoagulable state. It usually manifests as difficulty breathing, rapid breathing, and pleuritic chest pain.
Symptoms of hypokalemia
The clinical manifestations of hypokalemia are diverse, and the most life-threatening involve the cardiac conduction system and neuromuscular system. Mild hypokalemia is characterized on the electrocardiogram by flattened or absent T waves and the appearance of U waves. Severe hypokalemia can lead to fatal arrhythmias, such as ventricular tachycardia, ventricular fibrillation, or sudden death. In the neuromuscular system, the most prominent symptoms of hypokalemia are skeletal muscle relaxation, paralysis, and loss of tone in smooth muscles, leading to rhabdomyolysis. When respiratory muscles are involved, it can lead to respiratory failure. Hypokalemia can also cause insulin resistance or hinder insulin release, leading to significant glucose intolerance. A decrease in potassium excretion results in a reduced ability of the kidneys to concentrate urine, causing polyuria and low specific gravity urine.
What are the causes of hyperkalemia?
Hyperkalemia, with blood potassium levels greater than 5.5 mmol/L, commonly occurs due to decreased potassium excretion or abnormal potassium transport within cells, as well as other reasons such as excessive intake. Decreased potassium excretion can commonly be due to renal failure, the use of potassium-sparing diuretics, renal tubular acidosis, and reduced secretion of corticosteroid aldosterone. Abnormal potassium transport includes conditions such as acidosis, rhabdomyolysis, extensive burns, severe trauma, intestinal necrosis, and peritoneal bleeding, among other diseases. Excessive potassium intake can be due to sample hemolysis or an elevation in white blood cells, both of which can lead to hyperkalemia. Therefore, it is crucial to be vigilant in clinical settings and address the condition promptly and appropriately.
Principles of Treatment for Severe Acute Pancreatitis
The treatment of severe pancreatitis requires care in an ICU, involving a multidisciplinary team. Early treatment of severe pancreatitis focuses on non-surgical management centered on organ function support, and sterile necrosis is preferably treated non-surgically. Surgical treatment is applied once necrotic infection occurs. Non-surgical treatment principally involves intensive care monitoring and mainly consists of fluid replacement, maintenance of electrolyte and acid-base balance, energy support, and prevention of local and systemic complications. Additionally, current non-surgical treatments for severe pancreatitis include bedside blood filtration, abdominal lavage, etc. Moreover, minimally invasive treatments are supplementary methods for managing severe pancreatitis, including biliary drainage, minimally invasive techniques, and treatment of infected pancreatic necrosis. Surgical intervention, involving the removal of necrotic tissue, is necessary during the infection phase.
Clinical manifestations of hypokalemia
The clinical manifestations of hypokalemia are diverse, with the most life-threatening symptoms affecting the cardiac conduction system and the neuromuscular system. Mild hypokalemia on an electrocardiogram presents as flattened T waves and the appearance of U waves, while severe hypokalemia can lead to fatal arrhythmias such as ventricular tachycardia and ventricular fibrillation. In the neuromuscular system, the most prominent symptoms of hypokalemia are skeletal muscle flaccid paralysis and sustained smooth muscle tension, which can involve the respiratory muscles and lead to respiratory failure. Hypokalemia can also cause insulin resistance or hinder insulin release, leading to significant glucose tolerance abnormalities. Reduced potassium excretion decreases the kidney's ability to concentrate urine, resulting in polyuria and urine with low specific gravity.
The difference between hyperkalemia and hypokalemia.
Hypokalemia refers to a serum potassium concentration lower than 3.5mmol/L, and its clinical manifestations are diverse. The most life-threatening symptoms involve the cardiac conduction system and the neuromuscular system. Mild hypokalemia shows on an electrocardiogram as flattened T waves and the appearance of U waves, while severe hypokalemia can lead to fatal arrhythmias, such as torsades de pointes and ventricular fibrillation. In terms of the neuromuscular system, the most prominent symptom of hypokalemia is the loss of tone in smooth muscles and flaccid paralysis in skeletal muscles, which, when involving respiratory muscles, can lead to respiratory failure. Hyperkalemia, on the other hand, refers to a serum potassium concentration exceeding 5.5mmol/L, mainly presenting clinical symptoms in cardiac and neuromuscular conduction. Severe cases can cause bradycardia, atrioventricular conduction block, and even sinus arrest. Mild hyperkalemia, with levels between 5.5 to 6.0mmol/L, shows on an electrocardiogram as peaked T waves. As hyperkalemia continues to increase, it can lead to lengthening of the PR interval or disappearance of the P wave, QRS widening, and eventually cardiac arrest. Regarding the neuromuscular system, the clinical manifestations of hyperkalemia are very similar to those of hypokalemia, including weakness and paralysis of skeletal and smooth muscles.