Early manifestations of sepsis in children

Early manifestations of sepsis in children

Pediatric sepsis can have a huge impact on the health of children, because it can cause infections in the feet, lungs, urinary tract and blood, trigger a systemic inflammatory response, and even cause changes in the function and metabolism of some important organs. Therefore, once this symptom is discovered, active treatment must be carried out. Below we will introduce some relevant knowledge about pediatric sepsis!

1. Primary infection lesions

Through careful inquiry into medical history and physical examination, primary infection lesions can be found in most patients. Common sites of infection are the feet, lungs, abdominal cavity, urinary tract and blood. However, some elderly, immunosuppressed patients may lack clear focal clinical symptoms.

2. Systemic Inflammatory Response

The most common symptom is fever, which is often accompanied by chills. The most common fever types are remittent fever, irregular fever and intermittent fever. The body temperature can be as high as over 40°C. The body temperature may not rise (<36.5°C) in the elderly, exhausted, and immunosuppressed patients.

The white blood cell count increases and the proportion of neutrophils increases. The proportion of immature white blood cells increases. In severe cases, toxic particles may appear; some patients with poor or exhausted immune function. The white blood cell count may also be reduced, but the proportion of neutrophils increases, so the classification of neutrophils in patients considered to be infected is sometimes more important in differential diagnosis than the white blood cell count itself.

In uncontrolled severe sepsis, platelet counts often decrease progressively, often dropping from normal to below 30×10^9/L within a few days.

3. Changes in organ function and metabolism

Patients with severe sepsis are prone to multiple organ dysfunction, which is mainly related to insufficient tissue and organ perfusion, systemic inflammatory response, and the effects of toxins, and are prone to metabolic changes.

(1) Respiratory system: The patient's breathing speeds up mainly due to the stimulation of the respiratory center by insufficient perfusion, toxins and humoral factors. In the early stage, it can lead to respiratory alkali poisoning. As the disease worsens, respiratory acidosis appears, indicating that the condition is critical. In elderly patients, tachypnea with mild respiratory alkali poisoning and altered mental status may be the only sign of early sepsis.

(2) Cardiovascular system: The heart rate increases, and acute heart failure may occur due to insufficient perfusion, myocardial inhibitory factors, and toxins.

(3) Liver: Transaminase levels are often slightly elevated. Patients with a long course of illness may develop mild enlargement of the liver and spleen or even metastatic or multiple liver abscesses.

(4) Kidney: Due to insufficient renal perfusion, the effects of cytokines and toxins on the kidneys, fever, poor food intake, etc., the patient often has oliguria. When systolic blood pressure is >10.7 kPa (80 mmHg), urine volume can be maintained at 30 ml per hour. A value lower than this is clinically considered oliguria. Due to hypermetabolism and insufficient blood volume, the patient's urea nitrogen often continues to increase. It decreases when the condition improves, but when it develops into septic shock, oliguria or anuria occurs and creatinine may progressively increase.

(5) Central nervous system: The patient will experience irritability, apathy, drowsiness, lethargy, and finally coma. The main causes are insufficient blood perfusion of the central nervous system, the effects of toxins and some humoral factors on the central nervous system, and the imbalance of water, electrolytes, and acid-base.

(6) Skin and mucous membranes: In the early stage, the skin and face become flushed due to fever, and the skin temperature of the extremities does not drop. The body surface is not moist. In the later stage, due to insufficient perfusion, subcutaneous veins may collapse or the filling time may be prolonged. The skin color becomes pale, cyanotic, and patterned, accompanied by a decrease in skin temperature, and the temperature difference between axillary and rectal temperatures increases (normal is 0.5°C). Because the sympathetic nerves stimulate the secretion of sweat glands, the skin appears damp and cold.

(7) Coagulation system: There are changes in plasma fibrinogen, FDP, D-dimer, etc. in the early stage. As the disease progresses, changes in PT, APTT, etc. will appear, and eventually DIC will form, resulting in skin, mucous membrane and visceral bleeding.

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