Definition of severe HFMD: 1. Patients with clinical manifestations of HFMD, accompanied by myoclonus or encephalitis, acute delayed paralysis, cardiopulmonary failure, pulmonary edema, shock, etc. 2. Infants and children in HFMD endemic areas without typical manifestations of HFMD, but with fever with myoclonus or encephalitis, acute delayed paralysis, cardiopulmonary failure, pulmonary edema, etc.
I. Clinical manifestations
Acute onset, fever, scattered herpes on the oral mucosa, maculopapular rash and herpes on the hands, feet and buttocks, inflammatory redness around the herpes, and less fluid in the herpes. It may be accompanied by cough, runny nose, loss of appetite, nausea, vomiting and headache. In a few cases, encephalitis, encephalomyelitis, meningitis, pulmonary edema, circulatory failure, etc. may occur.
1, the nervous system: poor mental health, drowsiness, headache, vomiting, easily startled, jumping, irritability, mania, delirium, limb tremors, myoclonus, muscle weakness or limb paralysis; physical examination can be seen in meningeal irritation, tendon reflexes are hyperactive or weak, or even disappear; critical cases may show frequent convulsions, coma, acute cerebral edema, brain herniation.
2. respiratory system: shallow and difficult breathing, altered respiratory rhythm, cyanosis of lips and mouth, spitting of white, pink or bloody foam (sputum); wet rales can be heard in the lungs.
3. circulatory system: pallor, increased or slow heart rate, increased pulse (flooded pulse), shallow speed, weakening or even disappearance, wet and cold extremities, cyanosis and marbling of skin and fingers (toes), prolonged capillary filling time, increased or decreased blood pressure.
4, other system corresponding symptoms such as gastrointestinal bleeding, liver and kidney function impairment, etc.
II. Laboratory tests
(a) Terminal blood leukocytes: elevated or decreased leukocyte count.
(b) Blood biochemical examination: some cases may have mildly elevated ALT, AST, CK-MB and elevated blood glucose.
(iii) Cerebrospinal fluid examination: clear appearance, increased pressure, normal or increased white blood cells, normal or mildly increased protein, normal sugar and chloride.
(iv) Pathogenic examination: positive for specific enterovirus nucleic acid or isolation of enterovirus.
(v) Serological examination: positive specific enterovirus antibody test.
(iii) Physical examination
(a) Chest radiograph: it may show increased texture of both lungs, grid-like, dot-like or large shadows, with some cases being unilateral and rapidly progressing to large bilateral shadows.
(b) MRI: brainstem and spinal cord gray matter damage is predominant.
(iii) EEG: no specific changes, may appear as diffuse slow waves, a few may appear spike (sharp) slow waves.
(d) Brainstem evoked potentials: abnormal.
(e) Transcranial multispectral: shows abnormal blood perfusion in the brain.
(f) Electrocardiogram: no specific changes. Sinus tachycardia or bradycardia with ST-T changes may be seen.
IV. Clinical diagnosis
Those who meet the above definitions are diagnosed as severely ill with HFMD.
V. Early detection of children with severe disease
Children with the following characteristics are likely to develop into severe cases within a short period of time, so they should be closely observed for changes in their condition, and the necessary auxiliary tests should be carried out to provide targeted treatment.
(a) Persistent high fever that does not subside.
(ii) Poor peripheral circulation.
(iii) shortness of breath, difficulty, change in rhythm, and marked increase in heart rate.
(iv) Psychoneurological symptoms.
(v) Increased or decreased peripheral blood white blood cell count.
(vi) Hyperglycemia.
(vii) Hypertension or hypotension.
VI. Clinical treatment
(a) General treatment: pay attention to isolation, avoid cross-infection, proper rest, light diet, good oral and skin care.
(ii) Symptomatic treatment.
1. Neurological involvement
(1) control intracranial hypertension: give 20% mannitol 2-5ml/kg?times every 3-6 hours, 20-30min intravenous injection, adjust the interval of drug administration and dose according to the condition, discontinue for impaired renal function. If necessary, add tachyphylaxis: 1~2mg/kg?times.
(2) 3% NaCl: 2~3ml/kg?times, dynamic observation of body fluid osmolality, maintain osmolality 285~310mOsm/Kg.
(3) Other treatments.
Active expansion: crystal: given immediately upon admission, 20ml/kg/group for poor circulation, drip within 20 minutes, re-evaluate after the first dose of fluid drip, repeat the drug for poor circulation improvement; colloid: 20% albumin diluted to 5% given 10-20ml/kg?times or plasma 10-20ml/kg? times.
Hypothermia: physical or pharmacological cooling, keeping the body temperature at about 36 degrees, using sub-cold temperature techniques if available.
Sedation and anti-stunning: Valium: 0.1-0.3 mg/kg?times; luminal: 4-6 mg/kg?times, if necessary, a loading dose: 10-20 mg/kg?times.
(4) Closely observe the change of condition, monitor closely, pay attention to serious complications, actively reduce intracranial pressure and cellular edema in case of cranial injury, keep SPO2 above 93% and MBP above 65 mmHg; elevate the body position 15-30 degrees, tilt the head back 15 degrees.
2.Cardiopulmonary failure
(1) Keep the airway unobstructed and administer oxygen; in case of respiratory dysfunction, promptly intubate the trachea using positive pressure mechanical ventilation (if the chest X-ray indicates pulmonary edema, even if it is unilateral, tracheal intubation and respiratory support should be considered). Suggested initial ventilator parameters: inhaled oxygen concentration 80% to 100%, PIP 20-30 cmH2O, PEEP 4-8 cmH2O, f 20-40 times/min, tidal volume about 6-8 ml/kg. In children with pulmonary edema, PEEP can be as high as 12 cmH2O under close monitoring and ensuring tidal volume, and later adjust ventilator parameters at any time according to blood gases.
(2) Ensure unobstructed venous access, monitor respiration, heart rate, blood pressure and oxygen saturation, capillary refill time. Central venous pressure and invasive arterial blood pressure monitoring are recommended if available.
(3) Elevation of head and shoulders 15-30 degrees, maintaining neutral position; insertion of gastric tube and catheterization (compression of bladder for urination is prohibited).
(4) Drug therapy.
Application of cranial pressure-lowering drugs.
Application of vasoactive and other drugs, dopamine, phentolamine, milrinone and scopolamine according to the changes in blood pressure and circulation.
Diuresis: tachyphylaxis 1 to 2 mg/kg?times.
Sodium fructose diphosphate: 70-160mg/kg?d; VitC: 100-300mg/kg, times.
Inhibition of gastric acid secretion: proton pump inhibitors: Loxac 0,8-1,0mg/kg?d, etc.
Antipyretic treatment.
Monitoring changes in blood glucose; if blood glucose continues to increase >15,0mmol/l, use insulin 0,03~0,1u/kg?h.
Administering sedative drugs in case of convulsions.
In case of combined bacterial infection, the use of effective antibiotics according to clinical manifestations.
Protect the function of vital organs.
(iii) Other treatments.
1.Intravenous immunoglobulin, total 1g/kg?times×2 days, 2g/kg?times×1 day.
2, application of glucocorticoid therapy, methylprednisolone general dose: 5-10 mg/kg?d, shock dose: 10-20 mg/kg?d; dexamethasone 0,2-0,5 mg/kg?d, divided into 1 or 2 times.
It is most critical to achieve early detection and treatment in severe cases; any treatment measures must be based on accurate and timely assessment of the disease.