Perinatal hypoxic-ischemic encephalopathy (EHIP)
Diagnosis
Issue diagnosis of hypoxic-ischemic encephalopathy is based on history and clinical examination of the newborn.
Anamnesis must establish:
- complications in pregnancy, labor, birth;
- cardio-fetal monitoring;
- fetal acid-base status;
- Apgar score at 5, 10, 20 minutes;
- placental pathology.
The cornerstone of diagnosis is clinical neurological assessment during the immediate post-natal period, which must include examination and identification of associated metabolic disorders, and evaluation of lesions in other organs.
Laboratory examinations include:
- measurement of intracranial pressure;
- measurement of cerebral blood flow by Doppler ultrasound;
- electroencephalogram (EEG);
- evoked potentials;
- computed tomography;
- Trans ultrasound;
- nuclear magnetic resonance.
Explorations biochemical investigations focused on the following: hypoglycemia, hypocalcemia, hyponatremia, hyperammonemia.
Exploring the diagnosis of acid-base metabolic acidosis.
Highlights the increased creatine enzyme markers in blood and cerebrospinal fluid (CSF).
Lumbar puncture performed to determine the presence of liquid high blood pressure, or bleeding xantocrom with proteinorahie over 1, 50 g% o.
Wednesday, March 9, 2011
Perinatal hypoxic-ischemic encephalopathy (EHIP) Clinical signs
Perinatal hypoxic-ischemic encephalopathy (EHIP)
Clinical signs
Depending on the severity of disease symptoms is diverse, being divided into three different levels.
Level I of disease shows the following symptoms: restlessness, normal tone, poor sucking, decreased Moro reflex, mydriasis, absence seizures.
Grade II of hypoxic-ischemic encephalopathy shows symptoms: lethargy or sleepiness, mild hypotonia, poor sucking or absent, weak Moro, miosis, focal or multifocal seizures.
Grade III of the disease is characterized by clinical signs: stupor that responds only to strong stimuli, placidity, cerebration intermittent sucking absent Moro absent pupillary light reflex decreased.
In mild (Grade I) electro encephalogram (EEG) is normal and duration of symptoms is less than 24 hours.
In mild form (grade II) show microvolt EEG delta and theta, with duration of symptoms between 2-14 days, and severe (Grade III) is suppressed brain power, duration of symptoms in weeks.
Clinical signs
Depending on the severity of disease symptoms is diverse, being divided into three different levels.
Level I of disease shows the following symptoms: restlessness, normal tone, poor sucking, decreased Moro reflex, mydriasis, absence seizures.
Grade II of hypoxic-ischemic encephalopathy shows symptoms: lethargy or sleepiness, mild hypotonia, poor sucking or absent, weak Moro, miosis, focal or multifocal seizures.
Grade III of the disease is characterized by clinical signs: stupor that responds only to strong stimuli, placidity, cerebration intermittent sucking absent Moro absent pupillary light reflex decreased.
In mild (Grade I) electro encephalogram (EEG) is normal and duration of symptoms is less than 24 hours.
In mild form (grade II) show microvolt EEG delta and theta, with duration of symptoms between 2-14 days, and severe (Grade III) is suppressed brain power, duration of symptoms in weeks.
Perinatal hypoxic-ischemic encephalopathy (EHIP)
Perinatal hypoxic-ischemic encephalopathy (EHIP)
* Introduction
* Clinical signs
* Diagnosis
* Treatment
Hypoxic-ischemic encephalopathy is one of the most common brain injury in the neonatal period and the most common cause of long-term neurological disability. Hypoxic-ischemic encephalopathy is actually a variety of clinical entities that share a decrease in oxygen for brain and neurological damage is defined by occurring in newborns due to cerebral hypoxia and ischemia secondary chronic or acute fetal distress.
Epidemiology:
The incidence of hypoxic-ischemic insult in newborns is 2-4% a newborn infant at term and higher incidence of premature infant who presents a serious risk of injury due to hypoxic-ischemic cardio-pulmonary instability, labile self-regulation of cerebral blood flow, increased frequency of sepsis and metabolic disorders. Hypoxic-ischemic insult occurs mostly in antepartum and intrapartum, and long-term neurological damage such as cerebral palsy may be associated with a rate of 10-15% with intrapartum hypoxic-ischemic insult.
Etiology:
Incriminated in the etiology of the disease are three types of factors: factors antepartum, intrapartum factors and neonatal factors. From vategoria antepartum factors include: pregnant toxemia, maternal diabetes, disease-specific obstetric incompetent cervix, placenta previa, abruptio placentae, polihidramnios, multiple pregnancy. Intrapartum factors may be the following: abnormal presentations, prolonged labor. Neonatal factors are prematurity, idiopathic respiratory distress syndrome, cardiopulmonary abnormalities, infectious diseases, hemolytic diseases, convulsions, ventilatory alkalosis.
Pathophysiology:
Brain injury is the result of an association of hypoxia with ischemia, which increases the rate of cellular anaerobic metabolism, with low-phosphate products produced macroergici and accumulation of anaerobic metabolism, lactic, As intracellular free radicals, excitatory neurotransmitters. Changing cerebral blood flow is the main change induced by asphyxia postasfixica. Normal cerebral blood flow varies between 80-100 ml/100 g tissue / minute and depends on the quantity of blood pumped by the heart, the pressure difference between arteries and veins of the cerebral vascular resistance of the vessels involved. Following the installation of asphyxia, cardiac output is redistributed compensatory response, which leads to increased cerebral blood flow. The relationship between cerebral perfusion pressure and cerebral blood flow is governed by the principle of self-regulation, which represents the tendency of the brain to maintain a steady flow in terms of variations in cerebral perfusion pressure. As the hypoxia persists, this mechanism is not effectively self leads to a decrease in cardiac output with systemic hypotension and decreased cerebral flow, cerebral lesions. In turn, acidosis, hypercapnia and hypoglycaemia can disrupt brain mechanisms of self-regulation.
* Introduction
* Clinical signs
* Diagnosis
* Treatment
Hypoxic-ischemic encephalopathy is one of the most common brain injury in the neonatal period and the most common cause of long-term neurological disability. Hypoxic-ischemic encephalopathy is actually a variety of clinical entities that share a decrease in oxygen for brain and neurological damage is defined by occurring in newborns due to cerebral hypoxia and ischemia secondary chronic or acute fetal distress.
Epidemiology:
The incidence of hypoxic-ischemic insult in newborns is 2-4% a newborn infant at term and higher incidence of premature infant who presents a serious risk of injury due to hypoxic-ischemic cardio-pulmonary instability, labile self-regulation of cerebral blood flow, increased frequency of sepsis and metabolic disorders. Hypoxic-ischemic insult occurs mostly in antepartum and intrapartum, and long-term neurological damage such as cerebral palsy may be associated with a rate of 10-15% with intrapartum hypoxic-ischemic insult.
Etiology:
Incriminated in the etiology of the disease are three types of factors: factors antepartum, intrapartum factors and neonatal factors. From vategoria antepartum factors include: pregnant toxemia, maternal diabetes, disease-specific obstetric incompetent cervix, placenta previa, abruptio placentae, polihidramnios, multiple pregnancy. Intrapartum factors may be the following: abnormal presentations, prolonged labor. Neonatal factors are prematurity, idiopathic respiratory distress syndrome, cardiopulmonary abnormalities, infectious diseases, hemolytic diseases, convulsions, ventilatory alkalosis.
Pathophysiology:
Brain injury is the result of an association of hypoxia with ischemia, which increases the rate of cellular anaerobic metabolism, with low-phosphate products produced macroergici and accumulation of anaerobic metabolism, lactic, As intracellular free radicals, excitatory neurotransmitters. Changing cerebral blood flow is the main change induced by asphyxia postasfixica. Normal cerebral blood flow varies between 80-100 ml/100 g tissue / minute and depends on the quantity of blood pumped by the heart, the pressure difference between arteries and veins of the cerebral vascular resistance of the vessels involved. Following the installation of asphyxia, cardiac output is redistributed compensatory response, which leads to increased cerebral blood flow. The relationship between cerebral perfusion pressure and cerebral blood flow is governed by the principle of self-regulation, which represents the tendency of the brain to maintain a steady flow in terms of variations in cerebral perfusion pressure. As the hypoxia persists, this mechanism is not effectively self leads to a decrease in cardiac output with systemic hypotension and decreased cerebral flow, cerebral lesions. In turn, acidosis, hypercapnia and hypoglycaemia can disrupt brain mechanisms of self-regulation.
Acute diarrhea in children Prevention
Acute diarrhea in children
Prevention
Measures to prevent transmission of infectious diarrhea:
Wash your hands with soap and water after using the toilet, after changing diapers and before the baby comes into contact with food
-keep dirty diapers in a separate container, where the reach of children or pets. The container should be washed daily with soap and water, and he has to put in a waste bag to be changed daily.
baby diaper-changing should not be done in the kitchen or eat in the room that
Prevention
Measures to prevent transmission of infectious diarrhea:
Wash your hands with soap and water after using the toilet, after changing diapers and before the baby comes into contact with food
-keep dirty diapers in a separate container, where the reach of children or pets. The container should be washed daily with soap and water, and he has to put in a waste bag to be changed daily.
baby diaper-changing should not be done in the kitchen or eat in the room that
Acute diarrhea in children Complications
Acute diarrhea in children
Complications
The severity of complications depend on patient age, the most common being:
- dehydration
- acidobazic disturbances (acidosis)
- bacteremia
- abscess formation in the gastrointestinal tract
- meningitis and osteomyelitis
- hemolytic-uremic syndrome
- exudative enteropathy
Complications
The severity of complications depend on patient age, the most common being:
- dehydration
- acidobazic disturbances (acidosis)
- bacteremia
- abscess formation in the gastrointestinal tract
- meningitis and osteomyelitis
- hemolytic-uremic syndrome
- exudative enteropathy
Acute diarrhea in children Treatment
Acute diarrhea in children
Treatment
Mild cases heal on their own without treatment, and laboratory testing to discover the causes of diarrhea are not necessary. But if the diarrhea is severe, persists for more than 14 days or is accompanied by severe abdominal pain, medical advice is required.
The child must ingest a sufficient amount of fluids to avoid dehydration.
In most cases of mild or moderate dehydration (less than 10% by weight), oral rehydration is recommended. Vein infusions are used when diarrhea is accompanied by vomiting, significant emission of seats, a carbohydrate malabsorption or if a significant dehydration (> 10% by weight).
Treatment of acute diarrhea is based on clinical examination, which allows assessment of hydration status. Electrolyte losses are characteristic of any diarrhea, especially in early and be replaced by oral rehydration. Once the electrolyte losses are replaced, go to replenish the child, which lowers the seat number and volume of diarrhea.
Anti-diarrheal drugs are recommended for children aged 2-3 years, and antibiotics are used in cases of bacterial diarrhea.
Treatment
Mild cases heal on their own without treatment, and laboratory testing to discover the causes of diarrhea are not necessary. But if the diarrhea is severe, persists for more than 14 days or is accompanied by severe abdominal pain, medical advice is required.
The child must ingest a sufficient amount of fluids to avoid dehydration.
In most cases of mild or moderate dehydration (less than 10% by weight), oral rehydration is recommended. Vein infusions are used when diarrhea is accompanied by vomiting, significant emission of seats, a carbohydrate malabsorption or if a significant dehydration (> 10% by weight).
Treatment of acute diarrhea is based on clinical examination, which allows assessment of hydration status. Electrolyte losses are characteristic of any diarrhea, especially in early and be replaced by oral rehydration. Once the electrolyte losses are replaced, go to replenish the child, which lowers the seat number and volume of diarrhea.
Anti-diarrheal drugs are recommended for children aged 2-3 years, and antibiotics are used in cases of bacterial diarrhea.
Acute diarrhea in children Laboratory examinations
Acute diarrhea in children
Laboratory examinations
The seat must be examined in terms of color, volume and consistency, but also for the presence of mucus, blood or leukocytes.
PH and glucose content of the seats are other clues for detecting the cause of diarrhea. If the pH is below 5.5 and glucose content is low, the causes noninfectious diarrhea (intolerance to disaccharides). An alkaline pH of the seats indicates the origin of bacterial diarrhea.
Stool is a diagnostic examination of germs that cause diarrhea. Examination may reveal seats for parasites Giardia lamblia, present in some outbreaks of diarrhea in the collectivity of children.
Fluorescence microscopy or ELISA (Enzyme Linked immuno Sorbent Assay) is used for rotaviruses.
Other tests that may be performed are abdominal ultrasound and coloscopiile are made in cases of severe diarrhea.
Laboratory examinations
The seat must be examined in terms of color, volume and consistency, but also for the presence of mucus, blood or leukocytes.
PH and glucose content of the seats are other clues for detecting the cause of diarrhea. If the pH is below 5.5 and glucose content is low, the causes noninfectious diarrhea (intolerance to disaccharides). An alkaline pH of the seats indicates the origin of bacterial diarrhea.
Stool is a diagnostic examination of germs that cause diarrhea. Examination may reveal seats for parasites Giardia lamblia, present in some outbreaks of diarrhea in the collectivity of children.
Fluorescence microscopy or ELISA (Enzyme Linked immuno Sorbent Assay) is used for rotaviruses.
Other tests that may be performed are abdominal ultrasound and coloscopiile are made in cases of severe diarrhea.
Acute diarrhea in children Causes
Acute diarrhea in children
Causes
The causes of acute diarrhea are:
1. viruses, bacteria or parasites
Rotavirus is the most common cause of diarrhea in pediatric patients and is responsible for 25% of cases of acute diarrhea, including cases associated with acute dehydration. Rotavirus gastrointestinal infection lasts between two and eight days and shows a high incidence in winter months. At age 2, children had antibodies against rotavirus, which proves that they have already suffered an infection with this virus.
Other enteric viruses are and Norwalk virus, which affects older children, pestivirus, astrovirusul, parvovirus, etc.. Enteric virus infection, occurs in children under two years, especially during the summer months and can last for 14 days.
Diarrhea is due to bacterial infections: Salmonella, Escherichia coli, Campylobacter pylori (affects children and young adults under one year) and Shigella, the leading cause of diarrhea outbreaks in nurseries.
Of the enteropathogens parasites, Giardia lamblia is the most common protozoan that causes diarrhea, with an increased incidence in the collectivity of children.
2. food poisoning
3. medicines, especially antibiotics
4. food allergies
5. enzyme deficiency (eg, lactose intolerance)
Causes
The causes of acute diarrhea are:
1. viruses, bacteria or parasites
Rotavirus is the most common cause of diarrhea in pediatric patients and is responsible for 25% of cases of acute diarrhea, including cases associated with acute dehydration. Rotavirus gastrointestinal infection lasts between two and eight days and shows a high incidence in winter months. At age 2, children had antibodies against rotavirus, which proves that they have already suffered an infection with this virus.
Other enteric viruses are and Norwalk virus, which affects older children, pestivirus, astrovirusul, parvovirus, etc.. Enteric virus infection, occurs in children under two years, especially during the summer months and can last for 14 days.
Diarrhea is due to bacterial infections: Salmonella, Escherichia coli, Campylobacter pylori (affects children and young adults under one year) and Shigella, the leading cause of diarrhea outbreaks in nurseries.
Of the enteropathogens parasites, Giardia lamblia is the most common protozoan that causes diarrhea, with an increased incidence in the collectivity of children.
2. food poisoning
3. medicines, especially antibiotics
4. food allergies
5. enzyme deficiency (eg, lactose intolerance)
Acute diarrhea in children
Acute diarrhea in children
* Introduction
* Causes
* Laboratory Examinations
* Treatment
* Complications
* Prevention
Diarrhea is defined as removing too quickly reduced to the consistency of stools. This common disease usually lasts only a few days. Diarrhea that lasts more than two weeks is called acute diarrhea. "
Children younger than three years generally suffer 1-3 episodes of diarrhea per year.
All of diarrheal pathogens are transmitted through fecal-oral route, but is not excluded as possible sources of contaminated water or food and no direct interpersonal contact (especially in nurseries, kindergartens, etc.).
Signs and symptoms
The main symptom of diarrhea is to remove the seats frequent, low and high volume consistency. In general, diarrhea episode lasting three days, but with increased symptoms of acute dehydration syndrome is installed.
Infectious diarrhea can be accompanied by fever, intestinal colic, vomiting, nausea.
* Introduction
* Causes
* Laboratory Examinations
* Treatment
* Complications
* Prevention
Diarrhea is defined as removing too quickly reduced to the consistency of stools. This common disease usually lasts only a few days. Diarrhea that lasts more than two weeks is called acute diarrhea. "
Children younger than three years generally suffer 1-3 episodes of diarrhea per year.
All of diarrheal pathogens are transmitted through fecal-oral route, but is not excluded as possible sources of contaminated water or food and no direct interpersonal contact (especially in nurseries, kindergartens, etc.).
Signs and symptoms
The main symptom of diarrhea is to remove the seats frequent, low and high volume consistency. In general, diarrhea episode lasting three days, but with increased symptoms of acute dehydration syndrome is installed.
Infectious diarrhea can be accompanied by fever, intestinal colic, vomiting, nausea.
Children with critical illness
Children with critical illness The most common life-threatening diseases that are accompanied by: respiratory failure, heart failure and neurological disorders. Rarely can occur: acute liver failure and acute renal failure.
Identifying the cause of organ failure may demand more time, physiological instability, but treatment should begin immediately. Provide for several steps. Detection of physiological instability is a simple assessment, but the consistency of the patient: close observation, rapid and complete clinical examination. It is preferable to lose a few minutes more by examination rather than inadequate treatment to begin. Observation begins by determining: - Lack of vivacity; - Low response to stimuli; - Decrease movement; - Muscle weakness; - Loss of voice. Next assessment of vital signs such as pulse and heart rate. Peripheral pulse is determined at different points (radial, femoral, preauricular, pedia, etc.). It is therefore, the frequency and amplitude. The follow proper fit physical signs: breathing, movements, cough, coloration of the skin. Increased pulse rate (tachycardia) may be associated with decreased stroke volume, decreased the amplitude that will cause poor perfusion and agitation. Bradycardia or pulse slowdown may signal a pre-cardiac arrest. Blood pressure (BP) defines a poor perfusion thus a decrease in systolic blood pressure (SBP). Organ perfusion is reflected in an infusion of good skin for this purpose is assessing skin temperature, Recolor time (2-3 seconds), pulse oximetry measures oxygen saturation of hemoglobin.
Work of breathing and gas exchange is suggested by this circulation, muscular nose wing beats, cornaj, wheezing, cyanosis.
Cardiac dysrhythmia is life-threatening emergency. In this category falls the infant bradycardia or asystole and ventricular fibrillation is more common in adolescent or adult. Is manifested by abnormal heart rhythm: - Collapse; - Shortness of breath; - Tachypnea; - Tachycardia; - Palpitations. Much attention is given asistoliei, manifest symptomatic tachycardia, bradycardia, it is very important recognition and timely intervention. Children who have higher risk and electrolyte imbalances.
Evaluation of pulmonary blood flow is also an urgent priority. Cardiac malformations associated with pulmonary hypertension and may occur in certain pathophysiological conditions of pulmonary hypertension crisis with clear risk for hypoxic or anoxic events.
Evaluation of metabolic status expressly provides tracking of two major disorders the critically ill child: acidosis and hypoglycemia.
Measurement of oxygen (O2) and carbon dixidului pressure (PCO2) of central venous blood (pulmonary artery) is performed by placing the child than Swan-Ganz probe. This is to assess if tissue perfusion is adequate and that anaerobic metabolism is increased, highlighting the high levels of lactic acid are suggestive in this regard. Current resuscitation guidelines underline the need assessment: airway, this ventilation, heart rate, peripheral perfusion adequate sodium bicarbonate before giving another agent or buffer.
Sodium bicarbonate (Na) is recommended: - Symptomatic hyperkalemia; - Hipermagneziemie; - Poisoning with tricyclic antidepressants; - Metabolic acidosis. Routine administration during resuscitation can be dangerous so be administered only in cases of documented metabolic acidosis by the gas meter. It is good to know that after prolonged respiratory arrest with resuscitation should be administered every 10 minutes.
Hypoglycemia is the decrease in glucose level values that can destabilize energy production. Brain activity is dependent on a normal level of glucose in the blood. Hypoglycaemia symptoms: fatigue, lethargy that can be followed by convulsions. Emergency resuscitation should include the administration of glucose in the amount of 250-500 mg / kg infused in minutes. Hypoglycaemia should be documented.
Evaluation function central nervous system (CNS) monitors its integrity based on the history and physical examination that investigates the possibility of trauma surgery: ingestion of toxic drugs, seizures, ischemia, intra-cranial lesions (Hemorrhage, tumors, abscesses, congenital malformations).
Assessment is by Glasgow scale: - Open eyes (total 4 points): Spontaneous (4 points), the Voice (3 points), pain (2 points), none (1 point); - Motor response (6 points): run (six points), localized pain (5 points), withdrawal of the member (4 points), flexion (3 points), extension (2 points), none (1 point); - Verbal response (5 points) in infants and young children: respond appropriately to words, smile and watch (5 points), slightly attenuated scream (4 points), to be continuously irritated (3 points), agitated without stopping (2 points) none (1 point). - Verbal response (5 points) in the older children: oriented (5 points), confused (4 points), inadequate (three points), incomprehensible (2 points), none (1 point).
Clinical staging of encephalopathy
Stage I is caraterizeaza by: lethargy, follow orders, reactive pupils, normal respiration and normal muscle tone. Stage II includes the following symptoms: psycho-motor agitation, confusion in the enforcement of controls, reacting difficult pupils, hyperventilation and diminished reflexes. Stage III shows the following symptoms: comatose, occasionally respond to commands, can be diverted eyes, irregular breathing and posture of the shelling. Stage IV is characterized by symptoms of coma, responds to pain, poor pupillary response, very irregular breathing, cerebration Stage V shows the following clinical signs: comatose, unresponsive to pain, pupil areactive, eclama mechanical ventilation, absence of reflexes.
Criteria for admission to the pediatric intensive care unit Receiving medical care in the intensive care unit patients who require invasive monitoring: central venous or arterial catheter, intracranial pressure, pulmonary arterial line. There also benifeciaza of medical care patients who have: respiratory failure, cardiovascular compromise, shock, hypotension or hypertension, acute neurological damage, coma, status epilepticus, intra-cranial pressure increased. Patients with acute renal failure (ARF) requiring dialysis and those with haematological disorders requiring massive transfusions.
Criteria for admission in the intermediate intensive care unit are: - Patients not requiring respiratory support for respiratory failure, but can claim a non-invasive monitoring by monitoring vital signs: blood pressure (BP), oxygen saturation (SaO2), transcutaneous measurement of oxygen (O2) and carbon dioxide (CO2) ; - Patients requiring non-invasive cardiovascular monitoring for early heart failure; - Patients with multiple organ dysfunction; - Patients with neurological injuries.
Identifying the cause of organ failure may demand more time, physiological instability, but treatment should begin immediately. Provide for several steps. Detection of physiological instability is a simple assessment, but the consistency of the patient: close observation, rapid and complete clinical examination. It is preferable to lose a few minutes more by examination rather than inadequate treatment to begin. Observation begins by determining: - Lack of vivacity; - Low response to stimuli; - Decrease movement; - Muscle weakness; - Loss of voice. Next assessment of vital signs such as pulse and heart rate. Peripheral pulse is determined at different points (radial, femoral, preauricular, pedia, etc.). It is therefore, the frequency and amplitude. The follow proper fit physical signs: breathing, movements, cough, coloration of the skin. Increased pulse rate (tachycardia) may be associated with decreased stroke volume, decreased the amplitude that will cause poor perfusion and agitation. Bradycardia or pulse slowdown may signal a pre-cardiac arrest. Blood pressure (BP) defines a poor perfusion thus a decrease in systolic blood pressure (SBP). Organ perfusion is reflected in an infusion of good skin for this purpose is assessing skin temperature, Recolor time (2-3 seconds), pulse oximetry measures oxygen saturation of hemoglobin.
Work of breathing and gas exchange is suggested by this circulation, muscular nose wing beats, cornaj, wheezing, cyanosis.
Cardiac dysrhythmia is life-threatening emergency. In this category falls the infant bradycardia or asystole and ventricular fibrillation is more common in adolescent or adult. Is manifested by abnormal heart rhythm: - Collapse; - Shortness of breath; - Tachypnea; - Tachycardia; - Palpitations. Much attention is given asistoliei, manifest symptomatic tachycardia, bradycardia, it is very important recognition and timely intervention. Children who have higher risk and electrolyte imbalances.
Evaluation of pulmonary blood flow is also an urgent priority. Cardiac malformations associated with pulmonary hypertension and may occur in certain pathophysiological conditions of pulmonary hypertension crisis with clear risk for hypoxic or anoxic events.
Evaluation of metabolic status expressly provides tracking of two major disorders the critically ill child: acidosis and hypoglycemia.
Measurement of oxygen (O2) and carbon dixidului pressure (PCO2) of central venous blood (pulmonary artery) is performed by placing the child than Swan-Ganz probe. This is to assess if tissue perfusion is adequate and that anaerobic metabolism is increased, highlighting the high levels of lactic acid are suggestive in this regard. Current resuscitation guidelines underline the need assessment: airway, this ventilation, heart rate, peripheral perfusion adequate sodium bicarbonate before giving another agent or buffer.
Sodium bicarbonate (Na) is recommended: - Symptomatic hyperkalemia; - Hipermagneziemie; - Poisoning with tricyclic antidepressants; - Metabolic acidosis. Routine administration during resuscitation can be dangerous so be administered only in cases of documented metabolic acidosis by the gas meter. It is good to know that after prolonged respiratory arrest with resuscitation should be administered every 10 minutes.
Hypoglycemia is the decrease in glucose level values that can destabilize energy production. Brain activity is dependent on a normal level of glucose in the blood. Hypoglycaemia symptoms: fatigue, lethargy that can be followed by convulsions. Emergency resuscitation should include the administration of glucose in the amount of 250-500 mg / kg infused in minutes. Hypoglycaemia should be documented.
Evaluation function central nervous system (CNS) monitors its integrity based on the history and physical examination that investigates the possibility of trauma surgery: ingestion of toxic drugs, seizures, ischemia, intra-cranial lesions (Hemorrhage, tumors, abscesses, congenital malformations).
Assessment is by Glasgow scale: - Open eyes (total 4 points): Spontaneous (4 points), the Voice (3 points), pain (2 points), none (1 point); - Motor response (6 points): run (six points), localized pain (5 points), withdrawal of the member (4 points), flexion (3 points), extension (2 points), none (1 point); - Verbal response (5 points) in infants and young children: respond appropriately to words, smile and watch (5 points), slightly attenuated scream (4 points), to be continuously irritated (3 points), agitated without stopping (2 points) none (1 point). - Verbal response (5 points) in the older children: oriented (5 points), confused (4 points), inadequate (three points), incomprehensible (2 points), none (1 point).
Clinical staging of encephalopathy
Stage I is caraterizeaza by: lethargy, follow orders, reactive pupils, normal respiration and normal muscle tone. Stage II includes the following symptoms: psycho-motor agitation, confusion in the enforcement of controls, reacting difficult pupils, hyperventilation and diminished reflexes. Stage III shows the following symptoms: comatose, occasionally respond to commands, can be diverted eyes, irregular breathing and posture of the shelling. Stage IV is characterized by symptoms of coma, responds to pain, poor pupillary response, very irregular breathing, cerebration Stage V shows the following clinical signs: comatose, unresponsive to pain, pupil areactive, eclama mechanical ventilation, absence of reflexes.
Criteria for admission to the pediatric intensive care unit Receiving medical care in the intensive care unit patients who require invasive monitoring: central venous or arterial catheter, intracranial pressure, pulmonary arterial line. There also benifeciaza of medical care patients who have: respiratory failure, cardiovascular compromise, shock, hypotension or hypertension, acute neurological damage, coma, status epilepticus, intra-cranial pressure increased. Patients with acute renal failure (ARF) requiring dialysis and those with haematological disorders requiring massive transfusions.
Criteria for admission in the intermediate intensive care unit are: - Patients not requiring respiratory support for respiratory failure, but can claim a non-invasive monitoring by monitoring vital signs: blood pressure (BP), oxygen saturation (SaO2), transcutaneous measurement of oxygen (O2) and carbon dioxide (CO2) ; - Patients requiring non-invasive cardiovascular monitoring for early heart failure; - Patients with multiple organ dysfunction; - Patients with neurological injuries.
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