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Hemorrhagic fever with renal syndrome mind map
This is a mind map about hemorrhagic fever with renal syndrome, including laboratory tests, pathophysiology, clinical manifestations, etc. The scope is wide, the condition is critical, the mortality rate is high, and the harm is great. Hope this helps!
Edited at 2023-11-05 21:22:37
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Hemorrhagic fever with renal syndrome mind map
- bacteria
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
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- Outline
Hemorrhagic fever with renal syndrome (HFRS)
The scope is wide, the condition is critical, the mortality rate is high, and the harm is great. my country is the hardest hit area.
Hantavirus (RNA virus)
Pathogenesis
Direct effect: Entering the bloodstream causing damage to tissue and cell functions and structures throughout the body
Immune damage: triggering immunity leading to tissue damage
Our country mainly has type I and type II
rat type
November to January/May to July
Rural and forested areas
Serious condition
Type I virus
Hybrid
rural small towns
Mixed prevalence of types I and II
Laboratory infection type
Some are light and some are severe, and severe ones lead to death.
House mouse type
March to May
The condition is mild
Type II virus
City
Afraid of acid, heat, ultraviolet rays, and iodine
Type I, II, III, and IV are recognized by WHO
Can be divided into more than 20 types
Acute onset, fever, congestion, hemorrhage, hypotensive shock and acute renal failure
Vascular disease
Segmental or asymmetric contraction and dilation of small blood vessels throughout the body, fibrous necrosis and disintegration
Vascular endothelial cells become swollen and loose, leading to necrosis and collapse in severe cases
The capillaries are dilated and congested, and microthrombi form in the official cavity.
Organ lesions
cardiogenic pulmonary edema
Caused by damage to pulmonary capillaries, large amounts of fluid in the alveoli, high blood volume, too much fluid infusion too fast, or damage to the myocardium
Acute left heart failure
Kidney disease is most obvious
Renal tubules: degeneration and necrosis, compression, narrowing, and occlusion
Renal medulla: extremely congested with hemorrhage and edema
Glomerulus: congestion, basement membrane thickening
Renal fat sac: edema, hemorrhage
Renal interstitium: congestion, edema
brain lesions
Pituitary enlargement, marked congestion, hemorrhage and coagulative necrosis of the anterior lobe
Brain parenchymal edema and hemorrhage
Causes encephalitis and meningitis
nerve cell degeneration
gliosis
heart disease
Right atrial endometrium: inferior bleeding
Myocardial fibers: There are varying degrees of degeneration and necrosis, etc.
Congestion and hemorrhage of the adrenal cortex and medulla, cortical necrosis and microthrombi may be seen
Splenic disease
There is peptone-like edema in the posterior membrane and mediastinum.
Splenic body compression and atrophy
Splenic medullary congestion
cell proliferation
Splenomegaly
Liver disease
Hepatomegaly
Hepatocellular degeneration, focal necrosis and confluent necrosis
laboratory tests
Immunological examination
Specific antibody test
A 4-fold or above titer increase after 1 week has diagnostic value
Specific | gM antibody 1:20 is positive
IgG antibody 1:40 is positive
Can be detected on the second day of illness
Specific antigen test
Commonly used ELISA, immunofluorescence assay (IFA), and colloidal gold method are more sensitive
Early stage: Viral antigens can be detected in blood and urine
Routine urine examination
(A few) Membranous objects (blood clots, mixed aggregates of large amounts of urinary protein and exfoliated epithelial cells) appear in the urine. Red blood cells, white blood cells and casts can be seen.
Urinary protein often reaches (-) on days 4-6
Generally increases as the disease progresses
Proteinuria appeared on the 2nd day of the disease
Oliguria reaches its peak
coagulation function test
Consumptive hypocoagulation phase: decreased fibrinogen and prolonged thrombin time
Fever period: thrombocytopenia, reduced adhesion, aggregation and release functions
Hyperfibrinolytic phase: increased fibrin degradation products (FDP)
DIC occurs: hypercoagulable stage, clotting time shortened
Hypocoagulation stage: platelets drop significantly
Blood test
leukocyte
(Severe patients) Bacterial cells can be seen showing leukoderma-like reaction
In the early stage, neutrophils are mainly increased
The nucleus is shifted to the left and there are poisonous particles
The course of disease is normal for 1-2 days
Increased on day 3
Hemoglobin and red blood cells
Increased hemoconcentration due to plasma extravasation
platelets
Decrease in 2nd sick days
Atypical platelets can be seen
Lymphocytes
increase
Atypical lymphocytes appear
Other tests
Electrocardiogram: There may be arrhythmia and myocardial damage, high peak T wave in hyperkalemia, and abnormal U wave in hypokalemia.
Chest X-ray examination: pulmonary edema, pleural effusion and other manifestations
liver function test
blood biochemistry test
Blood gas analysis during fever period
respiratory alkalosis
The shock phase and oliguric phase are dominated by metabolic acidosis.
Blood BUN, Scr
Increase in hypotensive shock stage (a few in late stage of fever)
Migration reaches its peak
polyuria decreases later
serum potassium
Low levels during the febrile stage and shock stage
Increased oliguria
Decreased period of polyuria
Serum sodium, chloride, calcium
Mostly reduced
Phosphorus, magnesium
rise
Virus isolation
The virus can be isolated from serum, blood cells, urine, etc. after inoculation with Vero-E6 cells or A549 cells.
Molecular Biology Examination
RT-PCR (reverse transcription-polymerase chain reaction) method can detect viral RNA
Rats are the main source of infection (the urine and blood of early patients contained infectious viruses, but they were not the main source of infection)
Contact transmission: blood, excrement and secretions of host animals, the virus can invade from damaged skin and mucous membranes
Respiratory tract transmission: aerosols formed by contaminated dust can cause respiratory tract infection
Gastrointestinal transmission: oral transmission through contaminated food
Vertical transmission: from pregnant woman to fetus through the placenta
Insect-borne transmission: infected dermestid mites and chiggers
Pathophysiology
shock
primary shock
The increased viscosity of plasma extravasated blood promotes the occurrence of DIV, leading to circulatory stasis and blood flow obstruction, and the effective blood volume further decreases.
Course of disease 3 to 7 days
hypotensive shock
secondary shock
Shock that occurs after the oliguric period
Massive bleeding, secondary infection, insufficient effective blood volume
acute renal failure
Immune damage to glomerular and tubular basement membranes
Glomerular microthrombosis and ischemic necrosis
The lumen of the renal tubules is blocked by proteins, casts, etc.
Activation of renin and angiotensin II
Renal interstitial edema and hemorrhage
renal blood flow disorder
Bleeding
Thrombocytopenia or abnormal function
DIV causes abnormal coagulation mechanism
Increased heparin substances
blood vessel wall damage
clinical manifestations
The incubation period is 4-46 days, usually 1-2 weeks
fever period
capillary damage sign
Mucous membrane "three reds" (mucosal congestion): conjunctiva (flaky bleeding), soft palate (pinpoint-like bleeding spots), pharynx
(A few patients): visceral bleeding, such as vomiting blood, melena, hemoptysis (massive hemoptysis can cause suffocation), hematuria
Skin "three reds" (skin congestion and flushing): face, neck, chest, severe adult appearance
Large patches of skin or massive bleeding in the cavity (severe symptoms, D|C may be present)
Characteristics: Skin bleeding occurs mostly in the armpits, chest and back, such as scratching and streaking.
Parts: eyelids, facial edema, ascites
bulbar conjunctival edema
Symptoms of systemic poisoning
Symptoms of digestive tract poisoning: loss of appetite, nausea, vomiting, abdominal pain, diarrhea (severe abdominal pain can easily be misdiagnosed as acute abdomen)
Nervous system symptoms: drowsiness, excitement, delirium, confusion, convulsions (most of these are severe)
Three pains: headache, low back pain, and orbital pain (caused by congestion in the corresponding parts)
Body aches
Weakness
fever
The higher the body temperature, the longer the time, and the more serious the condition
Body temperature 39-40 (residual fever or relaxation fever)
Lasts 3-7 days, rarely more than 10 days
Chills and fever
acute onset
kidney damage
Proteinuria, hematuria, cast urine
Discharge of membrane-like material in urine
Percussion pain in kidney area
treat
antiviral treatment
Adults can use ribavirin (ribavirin), 1g per day, add 500ml of liquid for intravenous infusion, and use it for 3-5 days.
alpha-interferon intramuscular injection
If necessary, use high-potency immunoglobulin intramuscular injection or high-potency convalescent plasma intravenous infusion
Reduce extravasation
bed rest early
Give rutin, vitamin C (reduces vascular permeability)
Daily infusion of about 1000ml of balanced salt solution or glucose saline (can be increased appropriately in cases of high fever, profuse sweating, vomiting and diarrhea)
Improve poisoning symptoms
Mainly physical cooling
In severe cases, dexamethasone 5-10mg can be used
If vomiting is frequent, metoclopramide (metoclopramide) 10 mg intramuscularly can be administered
Prevent DIC
The hypercoagulable stage of DIC usually occurs from the late stage of fever to shock and the oliguric stage.
In the late stage of fever, the coagulation time (test tube method) does not increase with heparin within 3 minutes. Give a small amount of heparin.
Anticoagulant treatment with Dansan injection or intravenous infusion of low molecular weight dextran
hypotensive shock phase
Usually lasts 1 to 3 days
4 to 6 days (fever subsides at the end and blood levels drop)
Main manifestations: hypotension, shock
It may not occur in mild patients
Severe patients may suffer from refractory shock
Cyanosis occurs due to poor tissue perfusion
DC, hemorrhage, acute renal failure, cerebral edema (caused by shock, abnormal coagulation mechanism, electrolyte imbalance and hypervolemia syndrome), (acute respiratory distress syndrome) ARDS [caused by pulmonary capillary damage, permeability The increase causes a large amount of interstitial fluid in the lungs/due to the formation of microvascular thrombosis in the lungs and the reduction of alveolar surfactant production// manifests as shortness of breath and cyanosis, bronchial breath sounds and dry and wet rales can be heard in the lungs, and the X line shows Bilateral spotty or flaky shadows, ground glass-like appearance, etc.
treat
Replenish blood volume
Based on the principle of early, fast and appropriate amount
Plasma leakage of 600-800ml is hypotension, and 800-1200ml is shock (rapid expansion in shock is 1.5-2 times of plasma leakage in shock: first pressurize and infuse rapidly at a rate of 800-1200ml per hour, usually 30 minutes The internal blood pressure can rise by 100/70mmHg. After the blood pressure stabilizes, it will be changed to regular speed for 12-24 hours)
The volume expansion liquid is based on the principle of crystal glue bonding, and the crystalloid is mainly balanced salt solution.
Colloidal fluids can be low molecular weight dextran (daily input should not exceed 1000ml), 20% mannitol, plasma or albumin
Proper heating of liquids in winter
Adjust acid-base balance
Based on dynamic blood gas test results
For acidosis, use 5% sodium carbonate 5ml/kg intravenously or intravenously.
cardiac
The blood volume is replenished and the heart rate is above 140 beats/min.
The cardiotonic drug Trichoside C (Cedilan) or Trichoside K can be given intravenously
Vasoactive drugs and adrenocortical hormones
Dopamine, metahydroxylamine intravenous infusion
Anisodamine dilates capillaries and relieves vascular acne.
Dexamethasone 10-20 mg intravenously
oliguric phase
Various degrees of visceral bleeding: hemoptysis, hematemesis, hematochezia, hematuria, vaginal bleeding, intracranial hemorrhage (intracranial hemorrhage can cause convulsions, coma or even death), myocardial damage and liver damage, intra-abdominal hemorrhage or spontaneous renal rupture and bleeding (which can easily cause shock and acute renal function failure), hypertensive encephalopathy
Characteristics: Oliguria or anuria (generally considered oliguria when urine output is less than 400ml/d, and anuria when less than 100ml/d), uremia, water, electricity, and acid-base balance disorders
Hypervolemia syndrome: edema, venous filling on the body surface, strong pulse, elevated blood pressure, increased pulse pressure, and increased heart rate
Electrolyte disorders commonly include hyperkalemia, hyponatremia and hypocalcemia. (In a few cases, hypokalemia and hypermagnesemia may occur.
Psychiatric symptoms: dizziness, headache, salivation, irritability, delirium, coma, convulsions
Gastrointestinal symptoms: anorexia, nausea, vomiting, bloating, diarrhea, refractory hiccups
(A few) there is azotemia without obvious oliguria, which is called renal insufficiency
Tachypnea or Kussmaul breathing suggest metabolic acidosis
Lasts 1 to 3 days, more than 10 days in the elderly
Occurs on days 5 to 8 of the disease course
The ultimate stage of the disease
treat
Stabilize the internal environment of the body
Control azotemia
High sugar, high vitamin, low protein diet
For those who cannot eat, daily intravenous injection of glucose should be no less than 200g, and an appropriate amount of insulin should be added
Maintain water, electrolyte and acid-base balance
Rapidly infuse 500-1000ml of electrolyte solution, and at the same time intravenously inject 100-125ml of diuretic 20% mannitol, and observe diuresis for 3 hours (if the urine output does not exceed 100ml, it means renal parenchymal damage). The input amount can be based on the urine volume and vomiting and diarrhea of the previous day. Add 500-700ml
Limit or moderate potassium supplementation
According to CO₂CP examination, give 5% sodium bicarbonate intravenously.
Promote diuresis
In the initial stage, use 125ml of 20% mannitol for intravenous injection (repeat once if the effect is obvious, and stop if it is not obvious)
Furosemide (furosemide), 40-100ml each time, intravenous injection (if the urine output does not increase, the dosage can be increased to 100-300mg/time, repeated every 4-6 hours)
Vasodilator phentolamine 10 mg or anisodamine 10-20 mg intravenously, 2-3 times a day
Catharsis and bloodletting
No gastrointestinal bleeding
Mannitol 25g, 50% magnesium sulfate 40mg, rhubarb 10-30g boiled in water orally.
Oliguria and hypervolemia syndrome causes acute heart failure and pulmonary edema, phlebotomy 300-400ml
Dialysis
hemodialysis or peritoneal dialysis
Significant azotemia, blood BUN>28.56mmol/L, severe uremia
Highly catalytic renal insufficiency, daily blood BUN elevation >7.14mmol/L
Hyperkalemia＞6mmol/L, ECG has high peak T wave
Severe acidosis that is not easily corrected
hypervolemic syndrome
Extreme irritability or cerebral edema and no urine for more than 24 hours or continuous oliguria for more than 4 days
polyuria period
Lasts 7 to 14 days
Days 9 to 14 of the disease course
A urine output of more than 2000ml/d is the polyuria stage
Most of them enter after the oliguric period, and a few enter this period from the fever or hypotension period.
Transition stage: urine output is 400 to 2000ml/d. Blood urea nitrogen (BUN) and creatinine (Scr) can still increase during this period. Many people die during this period.
Early polyuria: urine output exceeds 2000ml/d, but azotemia does not improve and symptoms remain severe
Late polyuria: urine output exceeds 3000ml/d and increases day by day, azotemia decreases, mental improvement occurs, and urine output can reach 4000 to 8000ml/d (note secondary shock, secondary infection, acute renal failure, electrolyte imbalance [Hyponatremia, hypokalemia])
treat
Principle: Treatment in the transitional phase and early polyuria is the same as in the oliguric phase. In the later phase of polyuria, it is important to maintain water and electrolyte balance and prevent and treat secondary infections.
Maintain water and electrolyte balance: provide semi-liquid and potassium-containing foods, and appropriate amounts of fluids (mainly orally) to properly supplement sodium and potassium
Prevention and treatment of infections: prevention and treatment of secondary respiratory and urinary tract infections
recovery period
(A few) remaining hypertension, renal dysfunction, myocardial strain, hypopituitarism, etc.
Urine output is 2000ml/d, or less
Lasts 1 to 3 months
treat
Nutritional supplements
Rest for 1-3 months after discharge from hospital
Regular review of kidney function, blood pressure and pituitary function
identify
Influenza: no bleeding tendency, low blood pressure, normal urine routine, short course of disease, low white blood cells
Epidemic cerebrospinal meningitis: more common in children under 15, without skin and mucosal congestion, extravasation, or obvious kidney damage
Sepsis: There is a primary lesion, no conjunctival edema, extravasation, bleeding tendency and renal damage are not obvious, the course of the disease is not staged, and there are no atypical lymphocytes
Acute glomerulonephritis: more common in children, no abnormality in urine test, no poisoning symptoms such as fever and bleeding tendency
Thrombocytopenic purpura: no fever, characteristic changes in bone marrow smear
Treatment of complications
Major bleeding from the digestive tract or internal organs
Treatment due to illness, transfusion of fresh blood
Transfusion of fresh platelets if platelets are significantly reduced
Yunnan Baiyao, norepinephrine 4-5mg added to 100ml of water or thrombin 4000U added to 100ml of normal saline orally
DIC consumption hypocoagulation period: supplement coagulation factors and platelets
Secondary hyperfibrinolysis: intravenous infusion of 6-aminocaproic acid or toluic acid (p-carboxylamine)
Those with increased levels of heparin substances: intravenous injection of protamine or toluidine blue
Renal rupture and bleeding should be treated surgically
central nervous system complications
Convulsions, spasms: diazepam (valium), sodium amobutal and other sedatives
Intracranial hypertension caused by cerebral edema or intracranial hemorrhage: 20% mannitol intravenous injection, or catharsis and dialysis for dehydration
acute respiratory distress syndrome (ARDS)
High-dose epinephrine glucocorticoids such as dexamethasone 20-30 mg, intravenously infused every eight hours
Limit water intake and perform high-frequency ventilation
Positive end-expiratory pressure ventilation using a ventilator
Treat pulmonary edema aggressively
heart failure and pulmonary edema
Stop or control infusion
Oxygen inhalation, semi-recumbent position
Add 10 mg of the vasodilator phentolamine into the liquid and infuse slowly intravenously
Trichoside C or trichoside K, aminophylline, furosemide are cardiotonic and diuretic
In specific cases, blood pressure reduction, catharsis, bloodletting, dialysis, etc.
Prevent secondary infection
Pay attention to skin and mucous membrane hygiene
Indoor air circulation and disinfection
Use antibacterial drugs that are not harmful to the kidneys when complicated by bacterial infection
prevention
Anti-rodent and anti-rodent
Devices and drugs for rodent control
Prevent rat excrement from contaminating food and utensils
For outdoor accommodation, choose a high place with sleeping bunks at least 0.6 meters above the ground, and dig trenches around to prevent rats.
Cut off transmission routes
Skin wounds: bandage them promptly to avoid contamination
Improve environmental sanitation: avoid pollution
food stamping
Tie your clothes and pants tightly when working outdoors in epidemic areas
Wear multiple layers of masks when cleaning grain storage warehouses
Animal experiments to prevent being bitten by experimental rats
Kill mites
In endemic areas, use % dimethoate or 2% dichlorvos to kill mites every 7 to 10 days.
Straw should be dried before being put into the house
Protect susceptible populations (mainly vaccines)
Gerbil kidney cell inactivated vaccine (type |)
Hamster kidney cell inactivated vaccine (|| type)
Purified Han virus inactivated vaccine from suckling mouse brain (type |)