Eczema (eczema) and dermatitis (dermatitis) are the most common diseases in dermatology, which are allergic inflammatory reactions of the skin caused by a variety of causes, clinically characterized by erythema, papules, exudation and pruritus, and can be acute, subacute and chronic in course.
Treatment principles
Search for and avoid contact with suspected allergic substances, active treatment of infected foci or suspected underlying diseases, reasonable use of topical glucocorticoids and/or calcium-regulated neurophosphatase inhibitors, oral antihistamines and symptomatic treatment.
Application of glucocorticoids
In principle, glucocorticosteroids should not be applied systemically, but mainly locally. Topical glucocorticosteroids should be used reasonably according to the condition, patient status, lesion location and area. Generally, glucocorticosteroids should be used twice a day for mild eczema dermatitis, and moderately strong glucocorticosteroids for moderate to severe eczema dermatitis; moderately strong glucocorticosteroids for adults, and moderately weak glucocorticosteroids for children and the elderly; moderately weak glucocorticosteroids should be used for eczema dermatitis of the head, face and vulva, and moderately strong glucocorticosteroids for eczema dermatitis of the trunk of the limbs; strong glucocorticosteroids for eczema dermatitis of the hands and feet. Corticosteroids; hair areas should be used in solution, chronic hypertrophic rash can also be used in encapsulation therapy or with hard cream preparations. For maintenance treatment of chronic eczema (2 to 3 times a week), a weak glucocorticosteroid can be used and gradually overtaken to non-hormonal drugs.
For those with secondary self-sensitizing dermatitis or extensive exudation that is difficult to control rapidly with other drugs, systemic glucocorticoids can be considered for a short period of time and gradually reduced after the rash is controlled.
Psoriasis
Psoriasis is a common inflammatory skin disease characterized by red papules, plaques and silvery-white scales, and some patients may have joint and visceral lesions in combination, with a chronic course. It is clinically divided into common, pustular, arthritic and erythrodermic types.
Treatment principles
Actively search for and treat suspected causative factors, and generally do not advocate systemic glucocorticoids for common psoriasis. In the acute stage, systemic medication and local emollients are the mainstay. In the chronic stage, topical glucocorticoids, vitamin D3 derivatives and other topical medications can be chosen, and those with larger areas can be treated with ultraviolet light (narrow-wave NUVB) irradiation, and bathing therapy and other symptomatic treatments can also be chosen. Pustular, arthritic and erythrodermic psoriasis can be systematically treated with retinoic acid, methotrexate, biological agents and glucocorticoids.
[Application of glucocorticoids
Psoriasis vulgaris is not treated with systemic glucocorticoids. Topical glucocorticoids are one of the basic therapies for psoriasis and are mostly applied in combination with other drugs or methods. They should be used reasonably according to the type of skin lesion, lesion site and area. In the acute stage, lesions with inconspicuous infiltration, head, face and vulva, moderate to weak glucocorticoids or emollients are mostly used. For plaque lesions, medium- and strong-acting glucocorticoid creams can be used. Strong glucocorticoid creams can be used for lesions on the extremities and hands and feet. Tinctures or solutions are recommended for hair areas, and encapsulation therapy is also available for chronic hypertrophic rashes. It is important to avoid the side effects of long-term topical glucocorticoid therapy.
Patients with pustular, arthritic and erythrodermic psoriasis can consider systemic glucocorticoids if other treatments are ineffective and the disease is still progressing, with the dose depending on the disease. When the disease is stable and the symptoms are relieved, the dosage can be gradually and slowly reduced to discontinuation. Pay attention to the side effects of glucocorticoid therapy.
Intensive medical treatment for critically ill patients
Shock
Shock is a clinical syndrome of insufficient tissue perfusion and cellular oxygenation caused by various pathogenic factors. Regardless of the causes of shock, all of them have common pathophysiological changes, namely tissue hypoxia, anaerobic metabolism, activation of inflammatory waterfall response and organ dysfunction caused by insufficient tissue perfusion. Theoretically, glucocorticoids can enhance the stress capacity of the organism, and pharmacological doses of glucocorticoids have anti-inflammatory, anti-toxic, anti-shock and anti-allergic effects, so they can be used for various causes of shock and help patients to pass the dangerous period; however, the primary causes of shock are diverse and the pathogenesis is complex, so multi-linked comprehensive treatment is needed.
Infectious shock
Infectious shock (septic shock) is a syndrome of systemic inflammatory response caused by severe systemic infection. Infectious shock should be defined when severe systemic infection has obvious acute microcirculatory perfusion deficit, i.e., persistent hypotension or blood lactate concentration ≥4 mmol/L even after initial fluid resuscitation.
Principles of treatment
Early fluid resuscitation, intravenous antibiotics and organ function support should be started as soon as the presence of inadequate tissue perfusion is established. Treatment should be carried out as closely as possible under close supervision and in a sequential manner as required by the goals of intensive care.
Early resuscitation of patients with persistent hypotension or blood lactate concentration ≥4 mmol/L after initial fluid resuscitation is performed according to early goal-directed therapy (EGDT).
2.On the basis of active circulating volume supplementation, norepinephrine or dopamine was administered promptly to maintain mean arterial pressure (MAP) at ≥65 mmHg to ensure perfusion.
3.When the volume load is appropriate, but the cardiac output still cannot meet the tissue perfusion needs, dobutamine can be applied intravenously.
4. Administer effective antibiotics intravenously as soon as possible (preferably within 1 hour of diagnosis) and obtain appropriate specimens to identify the source of infection before applying antibiotics.
5.Actively search for and identify the foci of infection and use targeted therapeutic measures to control the source of infection.
6.Aggressive supportive therapy, including mechanical ventilation, renal replacement therapy, and blood glucose control if necessary.
7.Other adjuvant therapy: including the application of glucocorticoids as indicated, and the use of recombinant human activated protein C (rhAPC) in adult patients with organ insufficiency and high risk of death if there is no contraindication.
Application of glucocorticoids
1.For patients with fluid resuscitation and/or vasoactive drug dependence, glucocorticoid therapy can be applied.
2.Glucocorticoids are preferred to intravenous hydrocortisone. The daily glucocorticoid dosage should not be greater than 300 mg of hydrocortisone or other preparations equivalent to 300 mg of hydrocortisone.
3.If hydrocortisone is not available and preparations without significant salt corticosteroid activity are used, fludrocortisone 50μg/d can be supplemented and taken orally.
4.The course of glucocorticoid is usually 7 days.
Anaphylaxis
Anaphylactic shock is a rapid systemic allergic reaction caused by specific allergens, with acute circulatory failure as the main cause.
Treatment principles
1.Immediately lie down and get rid of the possible allergens.
2, immediately intramuscular injection of 1: 1000 epinephrine 0.5 ~ 1.0ml, if necessary, 5-10 minutes after repeated use; can be combined with glucocorticoid therapy.
3. Rapid infusion should be given to replenish the effective circulating blood volume to maintain tissue perfusion.
4.To prevent the development of the disease, antihistamine drugs can be used.
5.For bronchospasm, use aminophylline 0.25g plus 10% glucose 20ml slowly intravenously.
6.Severe laryngeal edema requires tracheotomy.
Application of glucocorticoids
1, glucocorticoids have non-specific anti-allergic anti-shock effect, but the effect is slow, and cannot be used as the first choice of rescue measures, but can be used in combination with epinephrine.
2, need to use glucocorticoids, it is appropriate to use shock dose, generally with hydrocortisone or dexamethasone.
Traumatic shock
Traumatic shock is caused by a sharp decrease in the effective circulating blood volume due to important organ damage, hemorrhage and other reasons, with the involvement of severe pain, fear and other complex factors.
Treatment principles
1.Grab the first 10 minutes after the trauma to effectively control the active bleeding and prevent asphyxia.
2.Severe life-threatening trauma should be operated immediately; severe traumatic shock which is not yet life-threatening can be resuscitated while making preoperative preparation; trauma which can be observed and delayed operation should be operated after adequate preoperative preparation.
3. Fluid resuscitation strategy: fluid resuscitation should be performed according to the patient’s hemodynamic status. Delayed resuscitation” strategy should be adopted during the active bleeding period.
Application of glucocorticoids
In traumatic shock, the affinity of glucocorticoid receptors is reduced. Early application of glucocorticoids may lead to a decrease in synthesis and further decrease in affinity due to negative feedback regulation, which may affect the prognosis, so the application of glucocorticoids is not recommended.
Acute lung injury and/or ARDS
Acute lung injury and/or ARDS is an acute progressive hypoxemia and respiratory distress syndrome caused by damage to lung parenchymal cells during severe infections, shock, trauma and burns, mostly as part of MODS. Glucocorticoids have been introduced into the treatment because of their involvement in the regulation of inflammatory response, but they are controversial and should be used with caution.
Principles of treatment
1, control the etiological factors, including drainage of the infected foci and effective antibiotic therapy, etc.
2, regulation of the inflammatory response, glucocorticoids, prostaglandin E, etc. are currently available drug therapy.
3.Early active respiratory support. Pulmonary protective ventilation strategy should be used when mechanical ventilation is performed. Avoid circulatory volume overload.
4, Active extra-pulmonary organ function support, as well as nutritional and metabolic support, to prevent the occurrence and development of MODS.
5.Pulmonary surface active substance, extracorporeal membrane lung and other treatments can be given if necessary.
Application of glucocorticoids
1.The routine use of glucocorticoid therapy is not recommended. In the case of life-threatening hypoxemia and the ineffectiveness of other therapeutic measures, low-dose methylprednisolone ( 1 mg?kg-1?d-1) therapy can be considered.
2. During glucocorticoid therapy, arterial partial pressure of oxygen/inhaled gas oxygen content (PaO2/FiO2), pulmonary compliance, and arterial partial pressure of carbon dioxide (PaCO2) are assessed daily. If there is no improvement after 3 days of treatment, glucocorticoid therapy is considered ineffective; if there is improvement, it may be continued. Although the optimal duration of treatment is still unknown, 7 days of treatment is sufficient to improve oxygenation. Risk and benefit assessment should be performed for those who need continuous glucocorticosteroid treatment.
3. Systemic infections need to be ruled out before applying glucocorticosteroids, or ensure that the infection has been effectively treated; potential infections should be closely monitored during treatment.
4. Glucocorticoid therapy should not be considered for patients after 14 days of definitive diagnosis or for those who require or may require neuromuscular blocking agents.
Acute cerebral edema
Cerebral edema is a pathological phenomenon in which increased water in the brain leads to increased brain volume, which often leads to intracranial hypertension and brain tissue damage. It is classified into 4 categories according to the pathological pattern and pathogenesis, namely, vasogenic cerebral edema, cytotoxic cerebral edema, interstitial cerebral edema, and osmotic cerebral edema. Acute cerebral edema is mostly vasogenic cerebral edema, followed by cytotoxic cerebral edema, with the former prone to life-threatening brain herniation and the latter prone to brain function changes.
Treatment principles
1.When intracranial pressure increases sharply, dehydration treatment is the preferred emergency measure, commonly used methods are: (1) osmotherapy: intravenous rapid drip mannitol or glycerol fructose, etc.; (2) diuretic therapy: intravenous strong diuretics can be injected to increase sodium and water discharge and reduce extracellular fluid.
2.Decompression surgery is an emergency measure to relieve severe intracranial hypertension and prevent brain herniation, and is not a conventional treatment. For interstitial cerebral edema caused by infarct hydrocephalus, ventricular shunt should be performed in time, and the cerebral edema can subside soon after the operation.
3.Glucocorticoid treatment is controversial.
Application of glucocorticoids
1.Glucocorticoids can be used for vasogenic cerebral edema, but cerebral ischemia and traumatic cerebral edema are not recommended; they are not beneficial for cytotoxic cerebral edema.
2.The first choice is dexamethasone, which is less active than salt corticosteroids, usually with a starting dose of 10 mg, injected intravenously, followed by 4 mg, once every 6 h. It can be used continuously for several days and gradually reduced until it is withdrawn.
3.Glucocorticoid treatment can temporarily relieve cerebral edema, but attention should be paid to observation during the treatment process, do not delay the diagnosis and treatment of postoperative hemorrhage and intracranial hematoma.
4. Prevent upper gastrointestinal bleeding, infection and electrolyte balance imbalance, etc.
Organ transplant rejection
Immunosuppressive therapy is the main measure to prevent and treat organ transplant rejection. Glucocorticoids are an important part of the immunosuppressive treatment regimen for organ transplantation; however, high-dose glucocorticoids, especially when applied for a long time, have significant adverse effects and may even affect the long-term survival of organ transplant recipients.
Renal transplant rejection.
There are four types of rejection reactions after kidney transplantation: (1) hyperacute rejection; (2) accelerated rejection; (3) acute rejection; and (4) chronic rejection. Glucocorticoids play a more important role in the combined drug regimen for the prevention and treatment of rejection in kidney transplant recipients.
Principles of treatment
1, transplanted kidney rejection before treatment need to have sufficient basis and exclude drug nephrotoxic reaction, vascular factors and urinary tract obstruction, hemolytic-uremic syndrome (HUS), viral infection, etc., should be transplanted kidney pathology biopsy as an important basis for treatment.
2, glucocorticoids are usually used as the first choice of treatment drugs for acute rejection.
3, chronic rejection should be combined with transplanted kidney puncture biopsy and clinical condition, the comprehensive treatment of immunosuppressive scheme or dose adjustment.
Application of glucocorticoids
1, kidney transplantation perioperative application: in order to prevent early strong rejection after kidney transplantation, usually in transplantation surgery that high-dose intravenous drip program.
Usual dosing regimen: intravenous methylprednisolone 250~1000mg (5~15mg/kg) is given during renal transplantation (on the day of surgery); 250~500mg daily for 2 days on the next day after surgery, after which the dose is rapidly reduced to oral, and the daily oral maintenance amount of prednisone (Long) is 5~10mg or methylprednisolone 4~8mg for 1 month after surgery.
Early rapid dose reduction of glucocorticoids after transplantation should have the following conditions: (1) the transplant recipient is not an immune-risk patient; (2) antibody induction therapy was used in the perioperative period; (3) the target blood concentration of calcium phosphatase inhibitor has been achieved early. (4) Adequate doses of concomitant antiproliferative drugs (e.g., mycophenolate or azathioprine).
2. Acute rejection phase glucocorticoid shock therapy.
(1) Acute rejection is usually treated with high-dose glucocorticoid shock therapy. This method can reverse about 75% of the first rejection. Usually apply methylprednisolone 250-500mg/d or 6 mg?kg-1?d-1 intravenous drip for 30-60 minutes for 3-5 days. The dose can also be reduced if the rejection reaction is mild, and the shock dose should not be too large for combined diabetes, or the antibody therapy should be used directly. Later, the dose will be changed to oral and gradually reduced to the pre-shock dose.
(2) After the end of methylprednisolone shock treatment, the calcium phosphatase inhibitor should be increased by about 20% compared with the original dose, and the blood concentration of calcium phosphatase inhibitor should be located in the near upper limit of the “target treatment window” range; if it is located in the “target treatment window range” for a longer period of time, there is a risk of triggering another acute rejection. If it is below the “target therapeutic window” for a long time, it may induce another acute rejection reaction.
(3) For refractory acute rejection resistant to glucocorticoids, it is advisable to change to anti-thymocyte globulin (ATG) or monoclonal antibody (OKT3) therapy as soon as possible; if the pathology of transplant kidney puncture biopsy confirms antibody-mediated acute humoral rejection, ATG can be used as the first-line anti-rejection therapy and combined with other adjuvant therapy.
3, maintenance application after kidney transplantation: maintenance treatment is started after the initial treatment or antibody induction treatment period of kidney transplantation. It should be noted that acute rejection can occur at any time during the maintenance period. (1) In principle, glucocorticoids should be maintained at low doses, i.e. prednisone (Long) 5-10mg/d or methylprednisolone 4-8mg/d orally. (2) If acute rejection occurs, methylprednisolone shock therapy is still preferred, and the dose and method of application should be referred to “Corticosteroid shock therapy in acute rejection stage” above. (3) If chronic rejection, proteinuria or recurrence of original glomerular disease occurs, the glucocorticoid dosage can be adjusted upward, but attention should be paid to the monitoring of adverse reactions and weighing the pros and cons. Clinical practice has shown that long-term glucocorticosteroid application at higher doses does not improve the prognosis of patients. (4) The long-term effects of glucocorticoid withdrawal on the survival of the transplanted kidney are still controversial, so glucocorticoid withdrawal during the maintenance period should be done with caution.
Liver Transplant Rejection
Liver transplantation is currently the only effective treatment for various end-stage liver diseases. At present, acute rejection after liver transplantation can be effectively controlled by pharmacological treatment. Prevention of recurrence of the primary disease is a key factor for long-term survival after liver transplantation, while chronic rejection remains one of the important causes of chronic graft loss of function.
【Treatment principles
1, acute rejection must have sufficient diagnostic basis before treatment, pathological puncture biopsy of transplanted liver should be used as routine examination and exclude drug hepatotoxic reaction, vascular factors and biliary complications, viral infection and other lesions.
2.For moderate to severe acute rejection, glucocorticoid shock therapy can be preferred; however, for acute rejection resistant to glucocorticoids, it is recommended to switch to ATG or OKT3 therapy as soon as possible.
3, during and after acute rejection treatment, attention should be paid to adjusting the dose of calcium phosphatase inhibitor or mycophenolate lipid, especially adjusting the blood concentration of calcium phosphatase inhibitor to prevent the reoccurrence of acute rejection.
4. The treatment of chronic rejection of liver transplantation is more difficult, and glucocorticoid shock therapy does not significantly improve the efficacy and can increase its side effects.
5. Long-term application of glucocorticoids after liver cancer surgery is not conducive to the prevention of tumor recurrence, so patients with liver cancer should usually be rapidly reduced in the early stage after transplantation, and it is recommended to stop using them for 1 month. Hepatitis liver transplant recipients usually stop using it 3 months after transplantation. Postoperative glucocorticoid-free regimen for liver transplantation patients with hepatocellular carcinoma can be one of the recommended regimens.
Application of glucocorticoids]
1. Perioperative application of liver transplantation: intraoperative methylprednisolone 500 mg intravenous push, 240 mg on the first postoperative day, then decreasing by 40 mg daily. change to prednisone (dragon) or methylprednisolone oral administration on the 7th postoperative day. If necessary, prednisone (dragon) 5-10 mg/d (or methylprednisolone 4-8 mg/d) will be administered orally for 1 month after surgery for maintenance.
2.Acute rejection treatment: At present, there is no clear standard of shock therapy for acute rejection treatment in each transplantation center. It is recommended that the first day methylprednisolone 500-1000mg intravenous push shock, the dose decreases from the second day, to 5-7 days to oral prednisone 20mg / d maintenance, maintenance time depends on the condition.