Clinical case analysis report template 1 general data
Name: Liu Gender: Male
Age: 38 years old Occupation: Freelancer
Native place: Xianfeng, Hubei Ethnic Group: Tujia Nationality
Date of admission: April 3, 2000 * * Record date: April 3, 2000 * *
Marriage: statement of married medical history: the patient himself and his family.
Chief complaint: tortuous dilatation of abdominal vein 10 years, progressive aggravation.
Current medical history: the patient complained of abdominal vein dilatation more than 10 years ago, showing earthworm-like changes, appearing above the umbilicus but not below it. Mild abdominal distension, no abdominal pain, no fatigue, poor appetite, no hematemesis, black stool, no fear of colds and fever, and no change in stool habits and characteristics. Without out-of-hospital treatment, the abdominal vein dilates, and the tortuosity is worse than before, and it progresses to the chest wall and is partially tortuous. No redness, swelling, pain and discomfort. Seven months ago, I saw a doctor in our department and was diagnosed as posthepatitic cirrhosis, portal hypertension, hypersplenism, esophageal and gastric varices and abdominal varices. It is planned to be treated by surgery. Because of high bilirubin and abnormal coagulation function, he was discharged without surgery. He continued to protect his liver and was given symptomatic treatment outside the hospital. Now he comes to our hospital for further treatment. Outpatient service is the income department of liver cirrhosis.
Since the onset, the patient's spirit is acceptable, his appetite is poor, his sleep is acceptable, his stool is normal, his urine is normal, and his weight has not changed significantly.
Past medical history: healthy and normal, with a history of hepatitis.
History of surgery and trauma: none.
Blood transfusion history: none.
Allergy history: None.
Personal history: smoking history, drinking history, no contact history.
Marriage and pregnancy history: married, healthy spouse.
Family history: parents are alive and have no history of heredity and infectious diseases.
physical examination
Temperature 37℃, pulse 76/min (normal), respiration 20/min (normal), blood pressure 128/70mmHg. Liver disease, dark skin, slightly yellow sclera, tortuous and dilated veins can be seen on the upper umbilical abdominal wall, extending upward to the chest wall, and some of them are tortuous and clustered. The blood flow in the abdominal wall flows from top to bottom, the abdomen is flat and soft, without tenderness and rebound pain, the costal margin of the liver cannot reach, the costal margin of the spleen is below 3 fingers, the boundary is clear, without tenderness, the surface is smooth, the bowel sounds can reach, the moving dullness (-) can be seen, and the skin pigmentation of both lower limbs is not swollen.
Auxiliary examination before admission: blood routine examination: platelet 230× 10∧9/L, liver function examination: AST 134u/l, DBIL24.8u/l, TBIL53.6umol/l, r-gt188u. There is no obvious abnormality in ECG.
Preliminary diagnosis:
Liver cirrhosis, portal hypertension, hypersplenism, abdominal varices.
Diagnostic basis:
1. Male patient, 38 years old.
2. Have a history of hepatitis, hospitalized in our department before July, with high bilirubin and abnormal coagulation function.
3. Abdominal vein tortuous dilatation 10 years, progressive aggravation.
4. Abdominal veins dilate, showing earthworm-like changes, appearing above the umbilicus but not below it. 1 month, the abdominal vein was dilated, the tortuous vein mass increased, and it expanded to the chest wall.
5. Blood routine: platelet 230× 10∧9/L, liver function test: AST 134u/l, DBIL24.8u/l, TBIL53.6umol/l, R-GT188u/L. ..
Diagnosis and treatment before admission: The patient received lamivudine and propranolol to protect his liver and prevent bleeding complications. At present, the degree of abdominal varicose veins is aggravated, the tortuous veins expand to the chest wall, and the tortuous vein masses increase, so they are admitted to our department for further treatment.
Improve relevant auxiliary examinations after admission;
Routine blood examination showed that red blood cells were 4.02× 10∧ 12/L, white blood cells were 5.08× 10∧ 12/L, hemoglobin 124g/L and neutrophils.
Urine routine bilirubin 2+, occult blood 1+, protein 2+, epithelial cell 57.0ul, cast 1 1.80ul, stool routine has no obvious abnormality.
Coagulation function: prothrombin time 19.3 seconds, plasma prothrombin ratio 1.56, PT international standardized ratio 1.64, and fibrinogen content of 4.78 g/L.
Biochemical analysis: AST 135u/l, ALT 1 15u/l, TP53.0g/l, ALB25.4g/l, A/G0.92, TBIL 20.1umol/L. ALP 197.5u/l, GGT32.2u/l, BUN 7.388 mmol/L, CREA54.2 umol/L, BUN/CREA 136, uric acid 7 16 umol/L, k+3.3 mmol. There was no obvious abnormality in myocardial zymogram. Two halves of hepatitis B: HBsAAg(-), HBV-DNA replication level is not.
Serum tumor markers: CEA, CA 199, AFP, CA 153 are all in the normal range.
Electrocardiogram: No obvious abnormality was found. Chest X-ray showed that the cardiac shadow was slightly enlarged, and the right diaphragm and costal diaphragm angle could not be clearly displayed. Abdominal CT: A small amount of ascites was found, and multiple calcification was found in the right lobe of liver.
X-ray of esophageal barium meal: varicose veins in the middle and lower esophagus were found.
B-ultrasound: The 5th intercostal space on the upper margin of the liver was detected, but the liver under the ribs and xiphoid process was not detected. The spleen is 85mm thick, the ribs are 80mm×50mm, the portal vein is 65,438+08 mm, and the abdominal wall is 5mm away from the body surface. Many tortuous blood vessels with different widths can be detected, with an inner diameter of 7-65,438+08 mm, and a dark area can be seen in front of the liver at night.
Further diagnosis:
Liver cirrhosis, portal hypertension, hypersplenism, esophageal and gastric varices, abdominal varices. Diagnostic basis:
1. Male patient, 38 years old.
2. Have a history of hepatitis, hospitalized in our department before July, with high bilirubin and abnormal coagulation function.
3. Abdominal vein tortuous dilatation 10 years, progressive aggravation.
4. Abdominal veins dilate, showing earthworm-like changes, appearing above the umbilicus but not below it. 1 month, the abdominal vein was dilated, the tortuous vein mass increased, and it expanded to the chest wall.
5. Blood routine showed platelet 2 10× 10 ∧ 9/L, urine routine showed bilirubin 2+, occult blood 1+, protein 2+, epithelial cells 57.0ul, cast11.80. Blood biochemistry: AST 135u/l, ALT 1 15u/l, K+3.3mmol/L, na+132.2mmol/l.
6. CT findings of abdomen: a small amount of ascites, multiple calcification in the right lobe of liver. X-ray examination of esophageal barium meal showed varicose veins in the middle and lower esophagus. B-ultrasound detected the 5th intercostal space on the upper margin of the liver, but did not reach the liver under the ribs and xiphoid process. The spleen is 85mm thick, 80mm×50mm under the rib, the portal vein is wide 18mm and the abdominal wall is 5mm deep from the body surface, which can reach many twists and turns.
The blood vessels of different thickness are coiled and overlapped into a mass, with an inner diameter of 7- 18 mm and a dark area of 9mm in front of the liver at night. Diagnosis and treatment after admission:
After admission, the patient was told to eat soft food with high calorie, high protein, low salt and limited drinking water. Lamivudine was given to improve liver function, diuretics were used to treat and improve ascites symptoms, and * * * * was given to control variceal bleeding. Nursing monitors the changes of patients' daily urine volume, weight and abdominal circumference, and pays attention to the relief of patients' abdominal distension symptoms, and adjusts treatment at any time.
Clinical discussion and analysis:
Characteristics of patient's medical history: 1. Male patient, 38 years old. 2. The tortuous expansion of abdominal vein 10 years, and it was gradually aggravated. 3. Abdominal veins dilate, showing earthworm-like changes, appearing above the umbilicus but not below it. 1 month, the abdominal vein was dilated, the tortuous vein mass increased, and it expanded to the chest wall. 4. Have a history of hepatitis, hospitalized in our department before July, with high bilirubin and abnormal coagulation function. 5. Blood routine showed platelet 2 10× 10 ∧ 9/L, urine routine showed bilirubin 2+, occult blood 1+, protein 2+, epithelial cells 57.0ul, cast11.80. Blood biochemistry: AST 135u/l, ALT15U/L, K+3.3mmol/L, Na+ 132.2 mmol/L 6. Abdominal CT findings: a small amount of ascites, multiple calcification in the right lobe of the liver. X-ray examination of esophageal barium meal showed varicose veins in the middle and lower esophagus. B-ultrasound detected the 5th intercostal space on the upper margin of the liver, but did not reach the liver under the ribs and xiphoid process. The spleen is 85 mm thick, 80 mm× 50 mm under the rib, and the portal vein is 65,438 08 mm wide. Many tortuous blood vessels with different widths can be found in the abdominal wall 5 mm deep from the body surface. The inner diameter is 7-65,438+08 mm, and the dark area at night is 9mm in front of the liver.
According to the characteristics of the patient's condition, the following conclusions can be drawn:
1. Cirrhosis is characterized by diffuse fibrosis, regenerative nodules and pseudolobular formation, and liver function decline and portal hypertension are formed in the late stage of the disease. Its epidemiological characteristics are: the peak age of onset is 35-50 years old, which is more common in men. The patient is a 38-year-old male. Increase the susceptibility of liver cirrhosis.
2. There are many causes of cirrhosis, including viral hepatitis, chronic alcoholism, nonalcoholic steatohepatitis, cholestasis, obstruction of hepatic venous return, hereditary metabolic diseases, industrial poisons or drugs, autoimmune hepatitis evolving into cirrhosis, schistosomiasis and cryptogenic cirrhosis. In China, viral hepatitis is the main infection, mainly hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis D virus (HDV), accounting for about 60%-80%. Hepatitis A virus (HAV) and hepatitis E virus (HEV) will not develop into cirrhosis. The patient has a history of hepatitis B and was hospitalized in our department before July. He has high bilirubin, abnormal coagulation function, a history of drinking and is prone to liver cirrhosis.
3. The liver is the largest gland in the human body, and it participates in many functions such as digestion, metabolism, excretion, detoxification and immunity. The liver is also the largest metabolic organ. Almost all substances absorbed from the gastrointestinal tract enter the liver, where they are synthesized, decomposed, transformed and stored. In the late stage of liver cirrhosis, due to liver damage, the decline of liver function makes its digestion, metabolism, excretion, detoxification and immune function decline. For example, vomiting and loss of appetite lead to electrolyte and acid-base balance disorder and malnutrition; Due to the decline of anabolism, the body's immunity is low, and it is easy to be complicated with infection, which leads to corresponding symptoms of respiratory tract, gastrointestinal tract, urinary tract and other systems. Portal hypertension leads to long-term congestion and swelling of the spleen, which makes the spleen hyperfunction, thus leading to the decrease of white blood cells, red blood cells and platelets in peripheral blood. The patient has symptoms and signs such as loss of appetite, abdominal distension and emaciation. , as well as electrolyte decline and coagulation dysfunction such as portal hypertension and hypersplenism in liver cirrhosis.
4. The clinical manifestations of liver cirrhosis mainly include: (1) compensatory liver cirrhosis: fatigue, loss of appetite, abdominal distension, slightly hard liver, palpable swelling of costal margin, splenomegaly, normal liver function test or slight abnormality of enzymes. (2) Compensatory cirrhosis: manifested as obvious decline of liver function and portal hypertension,
There are mainly portal collateral circulation opening (esophageal and gastric varicose veins, abdominal varicose veins, hemorrhoidal vein dilatation and retroperitoneal vein dilatation), splenomegaly leads to hypersplenism and ascites formation. The patient's abdominal vein tortuous dilatation 10 years, gradually aggravated. Abdominal vein dilates, showing earthworm-like changes, appearing above the umbilicus but not below it; 1 month, the abdominal vein was dilated, the tortuous vein mass increased, and it expanded to the chest wall. Liver disease, dark skin, slightly yellow sclera, 3 fingers under the costal margin of liver and spleen, and skin pigmentation can be seen in both lower limbs. The clinical manifestations of this patient are consistent with cirrhosis, portal hypertension, abdominal varicose veins and splenomegaly.
5. Relevant auxiliary examination: routine blood examination: platelet 2 10× 10 ∧ 9/L; routine urine examination: bilirubin 2+, latent.
Blood 1+, protein 2+, epithelial cell 57.0ul, cast 1 1.80ul. Coagulation function showed prothrombin time 19.3 seconds; Blood biochemistry: AST 135u/l, ALT 1 15u/l, K+3.3mmol/L, Na+ 132.2mmol/L Abdominal CT manifestations: a small amount of ascites, multiple calcification in the right lobe of liver. X-ray examination of esophageal barium meal showed varicose veins in the middle and lower esophagus. B-ultrasound detected the 5th intercostal space on the upper margin of the liver, but did not reach the liver under the ribs and xiphoid process. The spleen is 85 mm thick, 80 mm× 50 mm under the rib, and the portal vein is 65,438 08 mm wide. Many tortuous blood vessels with different widths can be found in the abdominal wall 5 mm deep from the body surface. The inner diameter is 7-65,438+08 mm, and the dark area at night is 9mm in front of the liver.
According to the etiology, clinical manifestations and related auxiliary examinations, the patients can finally be diagnosed as cirrhosis, portal hypertension, esophageal and gastric varices, abdominal varices and hypersplenism. It should be differentiated from the following diseases:
1. Differentiate from hepatomegaly and splenomegaly. For example, chronic hepatitis, with a history of hepatitis infection, needs to check the hepatitis B halves and HBV-DNA replication level; Primary liver cancer needs to be differentiated by immunological examination of serum alpha-fetoprotein (AFP) and liver CT. Some metabolic diseases involving the liver can also lead to hepatomegaly, which needs to be carefully differentiated from clinical manifestations and various auxiliary examinations. Hematological diseases, such as chronic leukemia, are often accompanied by splenomegaly, so bone marrow examination is needed to distinguish them from splenomegaly caused by cirrhosis. There is no obvious abnormality in the peripheral blood picture of the patient. It is feasible to check the peripheral blood picture regularly and observe the changes of the peripheral blood picture after symptomatic treatment such as liver protection.
2. Differentiate from diseases that cause ascites and abdominal distension. Ascites and abdominal distension caused by liver cirrhosis complicated with portal hypertension are due to (1) the increase of portal vein pressure, which makes the hydrostatic pressure of visceral vascular bed increase and the fluid enters the interstitial space to form ascites. (2) Due to the damage of liver function, the function of synthesizing albumin is weakened, which leads to hypoproteinemia and the decrease of plasma colloid osmotic pressure, so that the intravascular fluid enters the stroma and forms ascites.
(3) During portal hypertension due to liver cirrhosis, a large amount of blood stays in visceral vessels, which reduces the effective circulating blood volume, thus activating the renin-angiotensin-aldosterone system, resulting in a decrease in glomerular filtration rate and an increase in water and sodium reabsorption, resulting in water and sodium retention and promoting the formation of ascites. It should be differentiated from ascites caused by constrictive pericarditis, tuberculous peritonitis, abdominal tumor and chronic nephritis. Ascites can be distinguished according to whether it is leaking or oozing, and whether it is cancerous or non-cancerous. Patients with small ascites can exclude cancerous ascites, and ascites caused by heart and kidney diseases can also be excluded according to the clinical manifestations of other systems.
3. Diseases differentiated from complications of liver cirrhosis. Upper gastrointestinal bleeding caused by esophageal varices rupture should be differentiated from peptic ulcer, acute and chronic gastric mucosal lesions, gastric cancer, esophageal cancer and other diseases, and blood pressure should be stable. When the bleeding stops, it is feasible to diagnose by gastroscope. Hepatic encephalopathy caused by toxic substances directly entering the brain through systemic circulation due to the degradation and detoxification function of the liver should be differentiated from consciousness disorder and coma caused by hypoglycemia, diabetes, uremia, drug poisoning and cerebrovascular accident. Because severe liver disease can involve the kidney, resulting in no organic renal damage, it is called functional renal failure, which should be distinguished from acute renal failure caused by chronic nephritis, chronic pyelonephritis and other reasons.
According to the patient's clinical manifestations, auxiliary examination, etc. , made a diagnosis, and made a careful differential diagnosis. According to the various conditions of patients, the following treatment schemes can be arranged:
1. Ask patients to reduce activities appropriately, avoid fatigue, ensure rest to reduce consumption and reduce the chance of infection; The diet is high in calories, high in protein, rich in vitamins and easy to digest. Patients with esophageal and gastric varices should avoid eating rough and hard food. Patients with less ascites should appropriately limit the intake of water and salt.
2. Symptomatic support therapy, according to the patient's diet and nutritional status, adjust the electrolyte acid-base balance, supplement protein, and improve the patient's physical condition.
3. Prevention of complications, feasible conservative treatment, liver protection treatment, treatment to prevent recurrence of primary disease, and prevent the occurrence and development of liver inflammation and necrosis. Lamivudine, long-term oral administration, improves liver function; Adefovir dipivoxil, taken orally for a long time, has a good effect on patients with aggravated illness. Because the patient's hepatitis has been cured, there is no sign of virus replication, and the patient has symptoms of liver decompensation, interferon treatment is not allowed, which will accelerate liver failure, so the application should be very cautious.
4. Patients with a small amount of ascites should limit the intake of water and sodium, and do not use diuretics at the same time for the time being. It is necessary to closely observe the changes of ascites, prevent its aggravation as soon as possible, and avoid electrolyte disorder caused by careless use of diuretics. It can improve colloid osmotic pressure of plasma, properly infuse albumin and plasma, improve nutritional status and promote ascites regression.
5. Patients with esophageal and gastric varices should actively prevent varicose rupture. Conservative treatment can take * * * to reduce the pressure gradient of hepatic vein to
6. Patients with portal hypertension have no effective conservative treatment, and surgical treatment is effective. The main surgical methods are non-selective portosystemic shunt, selective portosystemic shunt and devascularization However, the patient has esophageal and gastric varices and abdominal varicose veins, but the varicose veins are not ruptured and bleeding, so preventive surgery for bleeding can be performed. In view of the severe liver function damage of this patient with posthepatitic cirrhosis, surgery will increase the burden on the body and even cause liver failure. Moreover, according to the data in recent years, such patients should be treated with internal medicine to protect their liver. If it is severe esophageal and gastric varices, especially if the surface of varices has a "red sign" under the microscope, preventive surgery, mainly devascularization, can be considered as appropriate to prevent the first acute bleeding.
7. Due to severe splenomegaly and hypersplenism, splenectomy should be performed. However, after splenectomy, we should pay close attention to the related complications such as abdominal hemorrhage, subphrenic infection and long-term dangerous infection after splenectomy.
8. Comprehensive analysis of the disease, patients with liver cirrhosis, portal hypertension, hypersplenism, esophageal and gastric varices and abdominal varices, the most ideal method is liver transplantation, which can not only replace the diseased liver, but also restore the hemodynamics of portal vein system to normal. However, according to the current medical development, liver transplantation is still limited by the shortage of liver source, high surgical risk and high cost, which needs further research and promotion.
Prognostic analysis: The prognosis of liver cirrhosis is related to etiology, degree of liver function compensation and complications. Liver cirrhosis caused by alcoholic cirrhosis, cholestatic cirrhosis and hepatic congestion. If the cause of liver cirrhosis can be eliminated before the decompensation stage, the lesion can tend to be static, which is better than viral hepatitis cirrhosis and cryptogenic cirrhosis. The causes of death are often hepatic encephalopathy, hepatorenal syndrome, esophageal and gastric variceal bleeding and other complications. Liver transplantation can obviously improve the prognosis of patients with liver cirrhosis. The patient has a history of viral hepatitis for many years, but he was cured at an early age, and the cause was eliminated early with little influence. However, due to the long course of the patient's illness and unreasonable self-care, the symptoms are portal hypertension, splenomegaly, esophageal and gastric varices, abdominal varices, etc., which have a great impact on its poor prognosis. Moreover, patients are generally in poor condition and have poor tolerance for liver transplantation, so transplantation treatment needs careful consideration.
Clinical case analysis report template 2 drinking can cause vasodilation and vasodilation regulation disorder, and cause vascular endothelial damage and lipid deposition, which makes the vascular condition worse and prone to cerebral hemorrhage. In addition, frequent overwork and lack of physical exercise can also increase blood viscosity, destroy vascular conditions and lead to cerebral hemorrhage.
Not all patients have to have these motives. Due to the long-term effects of various basic diseases, some patients can also have cerebral hemorrhage in a quiet state. The pathological mechanism of cerebral hemorrhage is complex, especially patients who often have the above incentives need to be cautious to prevent serious complications.
1. Clinical manifestations
The symptoms of cerebral hemorrhage are related to the bleeding location, bleeding volume, bleeding speed, hematoma size and the general situation of patients. The usual symptoms are sudden headache, nausea and vomiting, slurred speech, urinary incontinence, different degrees of physical activity disorder and consciousness disorder. A small amount of hemorrhage in non-functional areas can only be manifested as headache and mild neurological dysfunction, while a large amount of hemorrhage, deep brain hemorrhage, thalamic hemorrhage or brain stem hemorrhage can lead to rapid coma or even death within hours and days. Typical basal ganglia hemorrhage may cause sudden limb weakness, numbness, slurred speech or aphasia, disturbance of consciousness, severe pain when staring at the bleeding side, nausea, vomiting and urinary incontinence; Thalamic hemorrhage often breaks into the ventricle, and patients suffer from unilateral facial and limb sensory disturbance, apathy and unresponsiveness; However, when a small amount of pontine hemorrhage occurs, facial paralysis and contralateral limb paralysis may occur on the bleeding side, and when a large amount of pontine hemorrhage occurs, consciousness disorder, quadriplegia and eyeball fixation may occur, which is life-threatening; Cerebellar hemorrhage is mainly manifested as headache, dizziness, vomiting, dysarthria and other cerebellar signs. There are generally no typical symptoms of limb paralysis. When there is a large number of hematoma, it can invade the brain stem, causing rapid coma and death.
2. Complications
There are many complications of cerebral hemorrhage, and the human brain is the headquarters of life.
It will affect the normal operation of brain function more or less. Complications of cerebral hemorrhage are often multiple, and all organs in the body can be organs with complications. Therefore, while treating cerebral hemorrhage, we should pay attention to the treatment of complications. Common complications mainly include the following:
2. 1 Pulmonary infection: Pulmonary infection is the most common complication in patients with cerebral hemorrhage, and patients with cerebral hemorrhage are often accompanied by dyskinesia. Long-term bed rest is the most common cause of pulmonary infection. One of the most important complications of cerebral hemorrhage and one of the main causes of death is pulmonary infection. Within 3-5 days after cerebral hemorrhage, coma patients are often complicated with pulmonary infection, which is characterized by excessive phlegm and respiratory disorder, which needs attention and tracheotomy if necessary.
2.2 Upper gastrointestinal bleeding: also known as stress ulcer, is one of the serious complications of cerebrovascular disease. Cerebral hemorrhage combined with upper gastrointestinal bleeding is mostly mixed bleeding and internal capsule bleeding, accounting for 45% and 40% respectively. After cerebral hemorrhage, systemic blood vessels contract, gastrointestinal function declines, gastrointestinal barrier to bacteria weakens, and local blood supply is insufficient, which can lead to massive hemorrhage of digestive tract and even fatal blood loss leading to shock, which is a serious complication.