Science, Technology and Medicine open access publisher.Publish, read and share novel research. Early Detection and Prevention of Neonatal SepsisKetevan Nemsadze[1] Georgian National Academy of Sciences, Georgia1.
Patient information: See related handout on lifestyle changes to manage type 2 diabetes, written by the authors of this article. This acute illness protocol is a guideline for healthcare professionals treating the sick infant or child who is known to have ornithine transcarbamylase deficiency (OTC deficiency). Metabolic crises in infants and children with urea cycle disorders are complex medical emergencies and must be treated as such to avoid death or serious brain injury.
OTC deficiency is one of the proximal urea cycle defects and is due to a complete or partial deficiency of the mitochondrial enzyme ornithine transcarbamylase (OTC) which combines ornithine and carbamylphosphate to form citrulline (as shown below).
Unlike fats and carbohydrates, protein is not stored in the body but rather exists in a balanced state of anabolism (formation) and catabolism (breakdown). Ammonia also circulates in the body as free ammonia or within glutamine which functions as a temporary “repository” for ammonia.
Hyperammonemic crises in neonates or infants with OTC deficiency are frequently precipitated by sepsis. Identify potential precipitant(s) of metabolic decompensation such as infection (presence of fever) or any other physical stressor (e.g. Plasma ammonia level is a direct index of CNS toxicity and is important to follow in acute management. Plasma amino acids should be drawn at presentation and should be monitored frequently thereafter. Other amino acids, including glutamate, glycine, asparagine, aspartate and lysine, may be elevated when there is an excess in waste nitrogen burden. Immediate treatment of hyperammonemia is crucial to prevent neurologic damage and avoid associated morbidity and mortality. Stop all protein intake (but do not withhold protein for longer than 36-48 hours as that can promote breakdown of endogenous proteins and hamper metabolic control). Prepare for probable hemodialysis by contacting the relevant renal and surgical specialists in anticipation of imminent need. There are two main ways to promote ammonia detoxification: hemodialysis and medications that facilitate ammonia excretion. Hemodialysis is the most effective way of rapidly disposing of excess ammonia and is far superior to other methods of dialysis (hemofiltration, peritoneal dialysis). Ammonia scavenger medications include IV Ammonul® (sodium benzoate and sodium phenylacetate).
Sodium should not be provided in supplemental IV fluids when IV Ammonul® is given since this solution contains sufficient amounts of sodium.
A metabolic decompensation in a patient with a UCD is often precipitated by an underlying illness such as an infection or dehydration which results in a state of catabolism.
Plasma ammonia levels do not always directly correlate with the presence or severity of clinical signs and symptoms and, thus, monitoring of clinical status and changes in that is crucial. There may be a “rebound” hyperammonemia initially as stored glutamine is metabolized to glutamate and ammonia, and with the efflux of intracellular ammonia into the ‘relatively’ ammonia-depleted blood while on treatment and, thus, it is important to continue closely monitoring plasma ammonia levels until they remain stable in the normal range. Cerebral edema: Oncotic agents such as albumin will increase the overall nitrogen load but may in selected cases be considered.
Neurologic status should be closely monitored for signs of CNS toxicity and cerebral edema while the patient is under treatment and in the recovery period. Avoid certain medications, such as valproic acid, as it interferes with urea cycle function and accentuates hyperammonemia. Once the patient is stabilized and improving, oral diet has been established, and the plasma ammonia level is stable in an acceptable range, oral scavenger medications (sodium benzoate, sodium phenylbutyrate) and oral arginine can be provided in place of their IV forms. The dose of sodium benzoate and sodium phenylbutyrate is determined based on either body weight or body surface area.
This Concept Map has information related to: Zoom-Tuberculosis-Rheumatic Fever, Tuberculosis is in Lungs, Parts of Body, Skin, Tuberculosis prevented by TB Vaccination, Nutritious Food, Don't eat & sleep closer to TB patient, Consult doctor (or Visit to Hospital) if cough lasts more than 2 weeks. When the heart beats, an electrical signal moves through the heart muscle in a coordinated way to fire the heart muscle contracting and pumping blood in an efficient manner. This normal path of electrical conduction, can be interepted for various reasons, but the most common is after injury to the heart, that leads to scarring or loss of tissue that formed this pathway. Prevention of Perinatal Group B Streptococcal DiseaseRevised Guidelines from CDC, 2010 [11]10.
IntroductionSepsis has been a burden to mankind for millions of years and will continue to plague man as long as microorganisms exist here on earth.
Insulin resistance, decreased insulin secretion, and increased hepatic glucose output are the hallmarks of type 2 diabetes, and each class of medication targets one or more of these defects. The American Diabetes Association recommends an A1C goal of less than 7 percent.7 Glycemic control requires the patient to have cognitive, visual, and motor skills to monitor and manage blood glucose levels, and identifying and minimizing barriers for effective self-management is an important first step to setting individualized goals. This protocol is only a guideline and should not be used for definitive treatment without metabolic consultation.
OTC deficiency is the most common urea cycle disorder and it is inherited in an X-linked manner. Among the six enzymes in the cycle, N-acetylglutamate synthase (NAGS), carbamyl phosphate synthetase 1 (CPS1) and ornithine transcarbamylase (OTC) are intramitochondrial whereas arginase, argininosuccinate synthetase (ASS) and argininosuccinate lyase (ASL) are cytosolic.
Protein excess beyond normal bodily requirements comes from either excess dietary protein intake or from protein breakdown through various catabolic processes (stress of the newborn period, infection, dehydration, injury, or surgery). Consequently, in a urea cycle defect not only does free ammonia rise (hyperammonemia) but glutamine is also elevated. Consequently, any neonate or infant with OTC deficiency who has clinical signs of a severe illness should be evaluated for a hyperammonemic crisis precipitated by infection or any other stressor. Glutamine, as an ammonia buffer, reflects the direction of control of the hyperammonemia and, therefore, it is a useful marker for monitoring of ammonia status. Cognitive outcome is inversely related to the number of days of neonatal coma in the urea cycle disorders.
Hemodialysis has the added benefit of removing amino acids such as glutamine and, in that way, disposing of additional waste nitrogen from the body.


Sodium benzoate conjugates with glycine to form hippuric acid and sodium phenylacetate conjugates with glutamine to form phenylacetylglutamine; both compounds are excreted in the urine, thereby removing the nitrogen (N) in glycine and glutamine which contribute to the hyperammonemia.
This may be controlled with antiemetic medications such as ondansetron, either prior to or during the infusion.
Citrulline (by mouth, NG or g-tube) may help pull aspartate into the urea cycle and, thus, increase nitrogen clearance. Diagnostic investigation and treatment aimed at this underlying precipitant is extremely important to optimize metabolic control of the decompensation and should be undertaken at the time of initial presentation and continued throughout the management phase of hyperammonemia. Clinical decisions on appropriate treatments should be based on the combination of clinical assessment and plasma ammonia levels.
On rare occasions it may be necessary to assess the magnitude of glutamine excess in brain tissue by performing brain magnetic resonance spectroscopy (MRS). Mannitol has been used but may not be as effective as hypertonic saline in alleviating cerebral edema due to hyperammonemia.
Close monitoring of the intake of calories is an essential part of treatment and monitoring of a patient with a urea cycle defect in crisis. The dose should be decided in conjunction with a metabolic physician if the patient does not have an up to date regimen. Consensus statement from a conference for the management of patients with urea cycle disorders. Use Govt DOTS programme as a part of RNTCP (Revised National TB Control Programme); Stop TB, Use DOTS! A This electrical signal originates in the SA node of the heart and is carried down the conduction pathways of the ventricles. Only recently the medical community has started celebrating the World Sepsis Day (WSD) which was established in 2012, yet a decade before, at the end of the 20th century the Anti-Sepsis Center was founded in Georgia. Metformin, which decreases hepatic glucose output and sensitizes peripheral tissues to insulin, has been shown to decrease mortality rates in patients with type 2 diabetes and is considered a first-line agent. Amino acids liberated from excess protein are broken down, releasing nitrogen which circulates in the body as ammonia (NH3).
Alanine (Ala) is another amino acid that accumulates as a result of hyperammonemia due to a urea cycle defect.
Rapid control of the hyperammonemia is crucial in preventing or lessening the degree of mental retardation. Overdoses (3-5x the recommended dose) of IV Ammonul® can lead to agitation, confusion and hyperventilation.
Other medications include sulfonylureas and nonsulfonylurea secretagogues, alpha glucosidase inhibitors, and thiazolidinediones.
Gastrointestinal symptoms associated with its use can be minimized by beginning with a low dose and titrating slowly. Girls can have a wide spectrum of clinical symptoms ranging from mild to severe depending on the degree of X-chromosome inactivation in different tissues and especially in the liver. Ammonia is then converted into urea via the urea cycle and disposed of in the urine.  An enzymatic block in the urea cycle defect results in the accumulation of excess ammonia which has toxic effects, most severe in the central nervous system causing cerebral edema.
These two amino acid elevations (glutamine, alanine) may precede hyperammonemia and the onset of clinical symptoms and can serve as useful biochemical markers of decompensation in a patient with a urea cycle defect. Central venous catheters should be placed in a critically ill patient in hyperammonemic crisis in anticipation of the potential for hemodialysis and the appropriate nephrology and surgical specialists should be alerted in advance for this potential need. Supplemental calories are added from a non-nitrogenous formula with vitamins and minerals (Ross formula Pro-Phree® or equivalent). Please note that as the patient’s condition improves and anabolic homeostasis is restored, it may be necessary to rapidly eliminate or reduce the rate of the insulin infusion as hypoglycemia may develop. Prolonged Treatment (1-2 years) to be cured completely, Medicines:- Streptomycin Inj- ection, Isoniazid, Rifampicin, Thiacet- azone, Ethambutol. To achieve this improvement requires a partnership between the public, parents, and healthcare professions. Insulin can be used acutely in patients newly diagnosed with type 2 diabetes to normalize blood glucose, or it can be added to a regimen of oral medication to improve glycemic control.
It is also critical to remember that the goal of treatment is not only to reduce A1C levels, but also to prevent premature mortality and morbidity.
Additional agents include sulfonylureas, nonsulfonylurea secretagogues, thiazolidinediones, and alpha-glucosidase inhibitors. The decision to hemodialyze is critical in preventing or minimizing irreversible CNS damage; when in doubt in the face of a markedly elevated ammonia level, the decision should be to hemodialyze as soon as possible. High IV dextrose solutions should not be decreased or stopped in the face of hyperglycemia. HIV-infected people are at high risk of TB, Tuberculosis is Contagious or Infectious, spread through air by a TB Patient, a serious illness, caused by Mycobacterium tuberculosis, Tuberculosis symptom Initial Symptoms:- (a) Chronic Cough especially after wake up, (b) Afternoon Fever (c) Night Sweating, (d) Chest Pain, (e) Weight Loss, (f) Weakness. A An irregular rhythm is the consequence of dis-coordination between the atria and the ventricles. Except in patients taking multiple insulin injections, home monitoring of blood glucose levels has questionable utility, especially in relatively well-controlled patients. Severe sepsis and septic shock are among the leading causes of death in infants and have an overall pediatric mortality rate of 8-10%.
Once fasting blood glucose approaches near-normal levels, postprandial glucose is addressed by increasing the dose of the current medications or by adding additional agents. Wide swings in glucose levels are not ideal and so plasma glucose should be kept within the above as best as possible.
Definitive diagnosis requires clinical identification of infection in a patient who also meets the clinical criteria for the Systemic Inflammatory Response Syndrome (SIRS). Sulfonylureas can cause weight gain; this effect is less common with nonsulfonylurea secretagogues.
However, progressive failure of the beta cells often occurs even with proper diet, exercise, and oral medications, so patients should be counseled that insulin is simply another management tool. Although insulin is typically introduced when glucose control is no longer possible with oral agents, it can also be used when contraindications to oral medications exist.
DefinitionNeonatal Sepsis – is a clinical syndrome which is a general reaction to infection.


Prolonged hyperglycemia can cause glucose toxicity, a potentially reversible impairment in glucose-stimulated insulin secretion. This can be corrected with aggressive insulin therapy, then oral medications can be added as insulin is tapered or discontinued.
Neonatal sepsis is an irreversible process which may cause mortality in cases of untimely detection and treatment. Rapid-acting or premixed preparations can be added if fasting blood glucose levels are persistently high or if A1C has plateaued at about 7.5 percent, which indicates that postprandial glucose levels are high. Adding more basal insulin in this setting usually will not help patients reach their target levels.24 Sliding-scale doses can be set by counting carbohydrate grams or by a preset scale (Figure 2).
Metformin is approved for use in children 10 years and older and sustained-release preparations are approved for use in persons 17 years and older who cannot maintain glycemic control with diet and exercise.7,27The increased prevalence of comorbid conditions in older adults requires careful consideration of medications. Serum creatinine levels are not always a reliable predictor of renal insufficiency in the elderly, so metformin should be used with caution. The high prevalence of heart failure in this population limits the use of thiazolidinediones. Nemsadze, Neonatology, 2010 [1]The frequency of early sepsis in infants with extremely low-birth-weight is 100 times higher than in full-term babies. Considering the fact that the number of children born at a gestational age greater than 35 weeks is much more common, the data shows that neonates with low birth weight are far more likely to be diagnosed with sepsis.
This form of clinical sepsis is one of main clinical problems characterized primarily by significantly premature babies.
Development of late sepsis in neonates of this group is associated with a significant increase in the frequency of complications, mortality and the prolonged hospitalization of neonates.In West Europe, North America and Australia – late sepsis frequency is up to 6 among 1000 neonates.
Among neonates of gestational age less of 25 weeks, late sepsis develops in 46% of them; among neonates of gestational age between 25-28 weeks, late sepsis develops in 29%. The frequency of nosocomial infections is inversely proportional to birth weight and gestational age of neonates.
This complication cannot only be explained by the prolonged hospitalization needs of extremely premature children. Etiology and epidemiology Etiological Structure of Sepsis in Developed CountriesFigure 3.J. Many factors impact the etiological structure, including the quality of life, cultural traditions, practice of antibiotic therapy and the possibility of distorted results caused by many neonates to die at home. PathophysiologyIn the presence of sepsis, the response of infection released anti-inflammatory mediators can’t localize anti-inflammatory process.
Cellular damage with discharge of anti-inflammators (IL1, IL6 TNF- Tumor Necrosis Factor) and anti-inflammatory mediators increase the probability of developing multi-organ failure. The cardiovascular system, pulmonary system, gastro-intestinal tract, kidneys and neurological system are most frequently damaged. Given mediators stimulate production of various proteins called as reagents of acute phase. Any kinds of inflammation stimulus, including infection, trauma and ischemia causes marginal extravasations and activation of granulocytes and monocytes with the simultaneous release of anti-inflammatory cytokines including interleukins IL1, IL6 TNF (Tumor Necrosis Factor) [7]Sepsis is caused by Systemic Inflammatory Response (SIR)It is widely known that sepsis educes as a result of Systemic Inflammatory Response (SIR). In the process of opsonization and macrophage phagocytosis pathogens cause the formation of various anti-inflammatory mediators (cytokines) which damage vessel endothelium the result of which is the release of tissue factors. In this phase the organism goes into a hyperactive state, which is particularly conditioned by a hyper inflammatory reaction. When among neonates with body temperature more than 38 °С, only 10% are expected to developed sepsis.7.
Consultation with obstetric providers is important to determine the level of clinical suspicion for chorioamnionitis. If signs of sepsis develop, a full diagnostic evaluation should be conducted and antibiotic therapy initiated. If 37 weeks’ gestation, observation may occur at home after 24 hours if other discharge criteria have been met, access to medical care is readily available and a person who is able to comply fully with instructions for home observation will be present. If any of these conditions are not met, the infant should be observed in the hospital for at least 48 hours and until discharge criteria are achieved.
It’s important to remember that listerias are potential agents for early infection of neonates. It is necessary to prescribe 2 antibiotics which cover a wide enough spectrum and at the same time resist a selection of antibiotic resistant bacteria.
In case of late hospital sepsis it is particularly important to affect staphylococcus and gram negative bacteria. Treatment of Sepsis should be started immediately after diagnosis, because the late start of treatment may endanger life. Sepsis diagnosed in children less than 1 month old is specified by the term “Sepsis of Newborn”. DefinitionNeonatal sepsis is a clinical syndrome which represents a general reaction to infection.
Observation of child will be conducted and blood analysis of the child will be done including tests known as ‘Blood Inoculation’.
These tests may determine the existence of infection in the blood.Frequently, there is need to conduct further laboratory testing in order to determine the existence of infection in different parts of body. Examples of some of these tests may be: Lumbar Puncture (During this procedure doctor inject a thin needle into the lower part of backbone to obtain a small amount of spinal fluid. Lumbar liquid helps diagnose disease in the brain and spinal cord), analysis of urine, X-ray of thorax.
What kind of treatment is conducted for newborns with sepsis?Most treatment is conducted in hospitals.
All material will be used for aerobic culture therefore anaerobic organisms rarely cause early neonatal sepsis. If there is a catheter, blood is obtained simultaneously from the central and peripheral catheter.



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