I. IntroductionMeningococcal meningitis is a bacterial form of meningitis, a serious infection of the meninges that affects the brain membrane. It can cause severe brain damage and is fatal in 50% of cases if untreated.Several different bacteria can cause meningitis.Neisseria meningitidisis the one with the potential to cause large epidemics. There are 12 serogroups ofN. meningitidisthat have been identified, 6 of which (A, B, C, W, X and Y) can cause epidemics. Geographic distribution and epidemic potential differ according to serogroup.
TransmissionThe bacteria are transmitted from person-to-person through droplets of respiratory or throat secretions from carriers. Close and prolonged contact such as kissing, sneezing or coughing on someone, or living in close quarters (such as a dormitory, sharing eating or drinking utensils) with an infected person (a carrier) facilitates the spread of the disease. The average incubation period is 4 days, but can range between 2 and 10 days.Neisseria meningitidisonly infects humans; there is no animal reservoir. The bacteria can be carried in the throat and sometimes, for reasons not fully understood, can overwhelm the body's defenses allowing infection to spread through the bloodstream to the brain. It is believed that 10% to 20% of the population carriesNeisseria meningitidisin their throat at any given time. However, the carriage rate may be higher in epidemic situations.
SymptomsThe most common symptoms are a stiff neck, high fever, sensitivity to light, confusion, headaches and vomiting. Even when the disease is diagnosed early and adequate treatment is started, 5% to 10% of patients die, typically within 24 to 48 hours after the onset of symptoms. Bacterial meningitis may result in brain damage, hearing loss or a learning disability in 10% to 20% of survivors. A less common but even more severe (often fatal) form of meningococcal disease is meningococcal septicaemia, which is characterized by a haemorrhagic rash and rapid circulatory collapse.
DiagnosisInitial diagnosis of meningococcal meningitis can be made by clinical examination followed by a lumbar puncture showing a purulent spinal fluid. The bacteria can sometimes be seen in microscopic examinations of the spinal fluid. The diagnosis is supported or confirmed by growing the bacteria from specimens of spinal fluid or blood, by agglutination tests or by polymerase chain reaction (PCR). The identification of the serogroups and susceptibility testing to antibiotics are important to define control measures.
Meningococcal disease is potentially fatal and should always be viewed as a medical emergency. Admission to a hospital or health center is necessary, although isolation of the patient is not necessary. Appropriate antibiotic treatment must be started as soon as possible, ideally after the lumbar puncture has been carried out if such a puncture can be performed immediately. If treatment is started prior to the lumbar puncture it may be difficult to grow the bacteria from the spinal fluid and confirm the diagnosis.A range of antibiotics can treat the infection, including penicillin, ampicillin, chloramphenicol and ceftriaxone. Under epidemic conditions in Africa in areas with limited health infrastructure and resources, ceftriaxone is the drug of choice.
There are 3 types of vaccines available.1. Polysaccharide vaccines have been available to prevent the disease for over 30 years. Meningococcal polysaccharide vaccines are available in either bivalent (groups A and C), trivalent (groups A, C and W), or tetravalent (groups A, C, Y and W) forms to control the disease.2. For group B, polysaccharide vaccines cannot be developed, due to antigenic mimicry with polysaccharide in human neurologic tissues. The first vaccine against NmB, made from a combination of 4 protein components, was released in 2014.3. Since 1999, meningococcal conjugate vaccines against group C have been available and widely used. Tetravalent A, C, Y and W conjugate vaccines have been licensed since 2005 for use in children and adults in Canada, the United States of America, and Europe.The extended meningitis belt of sub-Saharan Africa, stretching from Senegal in the west to Ethiopia in the east (26 countries), has the highest rates of the disease. The 26 countries include: Benin, Burkina Faso, Burundi, Cameroon, Central African Republic, Chad, Cte dIvoire, Democratic Republic of Congo, Eritrea, Ethiopia, The Gambia, Ghana, Guinea, Guinea Bissau, Kenya, Mali, Mauritania, Niger, Nigeria, Rwanda, Senegal, South Sudan, Sudan, Tanzania, Togo and Uganda. The risk of meningococcal meningitis epidemics differs within and among these 26 countries.In December 2010, a new meningococcal A conjugate vaccine was introduced nationwide in Burkina Faso, and in selected regions of Mali and Niger (the remaining regions were covered in 2011), targeting persons 1 to 29 years of age. As of January 2015, 217 million persons have been vaccinated with this new vaccine in 15 countries (Benin, Burkina Faso, Cameroon, Chad, Cte dIvoire, Ethiopia, The Gambia, Ghana, Mali, Mauritania, Niger, Nigeria, Senegal, Sudan, and Togo).The MenA conjugate vaccine has several advantages over existing polysaccharide vaccines: it induces a higher and more sustainable immune response against group A meningococcus; it reduces the carriage of the bacteria in the throat and thus its transmission; it is expected to confer long-term protection not only for those who receive the vaccine, but on family members and others who would otherwise have been exposed to meningitis; it is expected to be particularly effective in protecting children under two years of age, who do not respond to conventional polysaccharide vaccines
II. Nursing Assessment1. Personal HistoryMy patient Rain Jey Dela Cruz, Male and is 10 days old. He is taken care of by his parents who are Renalyn Comedia and Jayson Dela Cruz. They live in District 6 Block 67 Lot 14 Pandacaqui, Mexico, Pampanga. His parents are both Filipino and they are Iglesia Ni Cristo. Rain Jey Dela Cruz was born in January 2, 2015 in Clinic Osme near their home. He was admitted to Jose B. Lingad Memorial Regional Hospital, January 3, 2015, 3:06pm due to a complaint of fair jerk and jitters. 2. Family HistoryRain Jey Dela Cruz is the only child of Renalyn and Jayson Dela Cruz. They live in a small house with concrete walls and with good ventilations. The father works as a construction worker and has enough wages to pay for their daily expenses and bills. There are no hereditary diseases that can be attributed from her mother side, but her father had a family health history of Hypertension. Other than the latter, no other hereditary diseases from both parents are within the patients parents knowledge. 3. History of Past IllnessPrior to His hospitalization, his parents denied in having any record or medical history of being admitted. They also confirmed that our patient has no allergies to food and drugs. 4. History of Present IllnessAfter a being born, Baby Rain Jey was healthy and didnt have any sign of abnormalities until the midwife gave him a bath the next day. The parents said that it stopped crying and didnt eat at all. The next day January 3, 2015, 3:06pm, He was admitted to Jose B. Lingad Memorial Regional Hospital with Positive jerky movement of extremities, upward rolling of the eyeballs, and poor sucking.
5. Physical Examination RR47
CR103
Temp35.1
Skinpinkish
Head-EENTCephalic edema
Lymph Nodes
ChestLungs :Cardiovascular:SCE, CR 1AP
Breast
AbdomenLeft, non-distended
RectumPatent
Genitalia
MusculoskeletalGood tone
Neurological
Admitting Impression T/C Septic Meningitis
ObjectivesNurse-Centered
After the completion of the case study, the nurse-researcher shall have: Discussed the statistics and current trends regarding the disease condition; Assessed the personal history, pertinent family health-illness history and past medical history in relation to the present disease condition and perform a comprehensive physical assessment/examination; Defined Meningitis and relate the modifiable and non- modifiable factors that contributed to the occurrence of the disease including the signs and symptoms Provided accurate health education to the patient and the significant others regarding the disease process and the importance of strict compliance to the treatment regimen; and, Formulated conclusions and recommendations based on the case presented.
Patient-Centered
After the completion of the case study, the patient shall have: Patients parents would have a better understanding of the disease process; Complied with the prescribed medical and pharmacologic regimen; Adhered to the health teachings provided; Engaged with the interventions that may prevent the occurrence of complications or further complications; Displayed improvement of the condition as evidenced by absence of further complications; and, Verbalized understanding on the advantages of having regular check-up for the baby and follow-up of the medical and nursing regimens.
III. Anatomy and Physiology Blood-Brain BarrierSince the brain is such a delicate organ, nature has taken extra measures toprotect the brain by creating the blood-brain barrier to limit the diffusion ofsubstances from the bloodstream into brain tissue selectively.
The blood-brain barrier mainlyconsists of tight junctions,which seals the endothelial cellsthat line the brain capillaries. Astrocytes, a type of neuroglia from the brain, closely attached to the endothelial cells and release chemicals to regulate the permeabilities of the tight junctions. The major sites of the blood brain barrier are the arachnoid membrane, choroid plexus epithelium, and the cerebral microvascular endothelium.
Only a few kinds water-soluble substance can move across the blood-brain barrier, such as glucose by active transport, urea, creatinine, and ions move across by slow diffusion. On the other hand, lipid-soluble substances can easily cross the blood-brain barrier, such as oxygen, carbon dioxide, alcohol, andmost anesthetic agents.
When bacteria break through the blood-brain barrier, an infection occurs in the cerebrospinal fluid.
Cerebrospinal FluidCerebrospinal fluid (CSF)is a colorless, transparent liquid that continuously circulates through the cavities of the brain and spinal cord, and as such, it acts as an internal circulation system to transport nutrients and wastes between the bloodstream and the brain and spinal cord. This reducdant circulation protects the brain and spinal cord from chemical injuries similar to the function of the blood-brain barrier. The CSF also protects the brain and spinal cord from physical injuries by acting as a shock absorber between the brain and spinal cord from the skeletal structures (cranium and vertebrae) [2].
CSF is produced in thechoroid plexuses, which are networks of capillaries in the ventricles. The choroid plexuses filter out blood plasma from the bloodstream, which is the main component of CSF. The choroid plexuses are covered by ependymal cells that are sealed together with tight junctions. These tight junctions forces the blood plasma to pass through these ependymal cells, which further filter out the blood plasma, producing CSF [2].
From the choroid plexuses of each lateral ventricle, CSF flows into thethird ventriclethrough theinterventricular foramina, which are two narrow oval openings. The choroid plexuses in the third ventricle adds more CSF. Then, CSF flows into thefourth ventriclethrought thecerebral aqueduct. Again, the choroid plexuses in the fourth ventricle adds more CSF. The fluid then enters the subarachnoid spacethrough the three openings in the roof of the fourth ventricle. These three openings are amedian apertureand a pair oflateral apertures. Then, CSF circultates in thecentral canal of the spinal cordand in thesubarachnoid spacearound the surface of the brain and spinal cord [2].
MeningesThemeningesare three connective tissue coverings thatencircle the spinal cord and brain. Thespinal meningessurround thespinal cord and are continuous with thecranial meninges,which encirclethe brain [2].
The meninges linedthe cranial and vertebral cavities to protect the brain and the spinal cord, and they are also attached to thecranial bones' inner surfaces, which facilitate the crainal bones tostabilize the positions of the brain, blood vessels, lymphaticvessels, and nerves [2].
These three connective tissue coverings areduramater, which is composed of dense, irregular connective tissue),arachnoidmater, which is composed of delicate collagen fibers and some elastic fibers in a spidersweb arrangement, andpiamater, which is athin transparent connective tissue layer consists of squamous to cuboidal cellswithin interlacing bundles of collagen fibers and some fine elasticfibers [2].
The most superficial of the three spinal meninges, theduramater, forms a sac from the level of the foramen magnum in the occipitalbone, where it is continuous with the dura mater of the brain, to the secondsacral vertebra. The spinal cord is also protected by a cushion of fat andconnective tissue located in theepidural space,a space between the duramater and the wall of the vertebral canal [2].
The middlemeninxis an avascular covering called thearachnoid mater. It is deep to the dura mater and is continuous with thearachnoid mater of the brain. Between the dura mater and the arachnoid mater isa thinsubdural space,which contains interstitialfluid [2].
The innermost meninx is thepia mater, which adheres tothe surface of the spinal cord and brain. Within the pia mater are many bloodvessels that supply oxygen and nutrients to the spinal cord. Between thearachnoid mater and the pia mater is thesubarachnoid space,whichcontains cerebrospinal fluid that serves as a shock absorber and suspensionsystem for the spinal cord and brain [2].
All three spinal meninges cover the spinal nerve roots, structures that connect spinal nerves to the spinal cord, up to the point wherethey exit the spinal column through the intervertebral foramina. Triangular-shaped membranous extensions of the pia mater suspend the spinal cordin the middle of its dural sheath. These extensions, calleddenticulate ligaments, are thickenings of the pia mater. They project laterally and fuse with the arachnoid mater and inner surface of the dura mater between the anterior and posterior nerve roots of spinal nerves on either side. Extending all along the length of the spinal cord, the denticulate ligaments protect the spinal cord against sudden displacement that could result inshock [2].
References[1]Netter, F. H. (2006).Atlas of Human Anatomy(4th ed.). Philadelphia: Saunders Elsevier.
[2]Simk, M., Fiedeler, U., Gazs, A., & Nentwich, M. (2010, December). Can nanoparticles end up in the brain?NanoTrust Dossiers(014en).
[3]Tortora, G. J., & Derrickson, B. (2009).Principles of Anatomy and Physiology(12th ed.). Danver, United States of America: John Wiley & Sons, Inc.
IV. Patient and His Illnessa. Pathophysiology Various bacteria including the major meningeal pathogens (e.g.,S. pneumoniae) undergo autolysis under harsh conditions such as exposure to antimicrobial agents and/or growth to stationary phase. Autolysis consists of self-digestion of the cell wall by peptidoglycan hydrolyases termed autolysins. At least 3 autolysins are recognized in pneumococci, but the major autolysin is theN-acetyl-muramoyl-l-alanine amidase (LytA) Activation of LytA and autolysis result in the release in subcapsular bacterial components including peptidoglycan, lipoteichoic acid, bacterial DNA, and pneumolysinMechanisms of immune activationVarious cell wall products of meningeal pathogens are well-known inducers of the inflammatory host response. The inflammatory response in the subarachnoid space characteristic of acute purulent meningitis can be reproduced by the intracisternal challenge with whole heat-killed unencapsulated pneumococci, their isolated cell walls, lipoteichoic acid, or peptidoglycan, but not by the injection of heat-killed encapsulated strains or isolated capsular polysaccharide. Exact mechanisms of immune activation by pneumococcal cell wall products remain poorly understood, but recent in vitro studies suggest that the first step in immune activation is binding of peptidoglycan and/or lipoteichoic acid to the pattern recognition receptor membrane CD14 (mCD14). mCD14 is not a transmembrane molecule and thus by itself cannot transmit the activating signal into the cellA second step in immune activation is necessary and this potentially occurs through the toll-like receptor-2 (TLR-2). Coexpression of CD14 and TLR-2 in Chinese hamster ovary fibroblasts confers responsiveness to pneumococcal peptidoglycan and heat-killedS. pneumoniaeas evidenced by inducible translocation of the nuclear transcription factor NF-B. These studies also suggest that pneumococci stimulate both a TLR-2dependent and a TLR-2independent pathway; however, in a model of pneumococcal meningitis, TLR-2deficient mice responded to live pathogens virtually to the same extent as wild type mice (Koedel et al., unpublished data). Leukocyte infiltration into the subarachnoid space and brain mRNA expression of proinflammatory cytokines and chemokines did not differ between TLR-2deficient and wild type mice inoculated with live pneumococci. It appears that mechanisms other than binding of pneumococcal cell wall products to TLR-2 play a central role in the induction of the host immune response during pneumococcal meningitis. It appears that both TLR-2dependent and independent (pneumolysin) pathways are sufficient to cause inflammation in the absence of the other, but in vivo both are likely activatedTLR-2independent immune activation may be mediated at least in part by the pneumococcal toxin pneumolysin. Pneumolysin stimulates the production of inflammatory mediators in vitro including tumor necrosis factor (TNF)-, interleukin (IL)-1, and IL-6. Pneumolysin is also an inducer and/or activator of enzymes such as phospholipase A2, COX-2, and inducibleNITRIC OXIDEsynthase (iNOS). However, in a rabbit meningitis model, a pneumolysin-deficient pneumococcal strain resulted in an inflammatory response similar to that induced by injection of the wild type strain, suggesting that pneumolysin is not essential for the induction of meningeal inflammation Another potential trigger of immune activation during acute meningitis is bacterial DNA released during bacterial autolysis. Bacterial DNA has substantial immune stimulatory effects on B, NK, and dendritic cells and on monocytes and macrophages. The activity of bacterial DNA is mediated by unmethylated CpG motifs, in particular base contexts. In fact, when mice or rats are injected intracisternally with bacterial DNA or unmethylated CpG oligonucleotides, meningitis developed within 12 h. Bacterial DNA appears to initiate CNS inflammation by stimulation of macrophages and proinflammatory products such as TNF-. TLR-9 is absolutely required for cellular responses to CpG DNA, and TLR-9deficient mice show no response to CpG DNA (inflammatory cytokine production from macrophages, maturation of dendritic cells, or proliferation of splenocytes) . TLR-9deficient mice are also completely resistant to the lethal effects of CpG DNA without production of serum proinflammatory cytokines. Thus, the role of the CpG DNATLR-9 pathway for immune activation in acute bacterial meningitis deserves further evaluation. In summary, subcapsular bacterial components act as inducers of the host inflammatory response in acute bacterial meningitis, but the host receptor systems and downstream elements of signal transduction are still largely unexploredIntracellular signal transduction pathwaysFor meningeal pathogens, the major inflammatory stimuli are lipopolysaccharide (LPS) and peptidoglycan for gram-negative and gram-positive organisms, respectively. These inflammatory stimuli activate I-B kinase NF-B pathways and 3 mitogen-activated protein kinase (MAPK) pathways: extracellular signal-regulated kinases (ERK) 1 and 2, c-Jun N-terminal kinase (JNK), and p38. As a result of activation of these signaling pathways, a variety of transcription factors are activated: NF-B (p50/p65) and activator protein-1 (cFos/cJun), which coordinate the induction of many genes encoding a variety of inflammatory mediators Soluble peptidoglycan strongly activates ERK-1 and -2 in the mouse macrophage cell line RAW264-7 and moderately activates JNK, while weak activation of p38 MAPK is observed. In contrast, LPS strongly activates all of these kinases, suggesting a similar but not identical activation of signal transduction pathways by these major inflammatory mediators of meningeal pathogens Pneumococcal cell wall components release inflammatory mediators by mouse microglia, which is dependent on both p38 and ERK-2/ERK-1 MAPK activities. These same MAPKs are also activated when rat or human astrocytes are stimulated with various pneumococcal cell wall fragments. In addition, pneumococci activate NF-B in undifferentiated human and mature murine monocytes. Although the signaling pathways involved in immune inactivation only recently became a major focus of research activity, a rat model of pneumococcal meningitis showed a marked increase in NF-B activity. Pharmacologic inhibition of NF-B led to a significant reduction of host inflammatory responses as evidenced by lower CSF leukocyte and IL-6 concentrations . It appears that NF-B is a central transcriptional activator of many genes that encode proteins, host factors, or both involved in the pathophysiology of pneumococcal meningitis, including cytokines, chemokines, and adhesion moleculesProinflammatory cytokinesMultiple cytokines play an important regulatory role in the control of inflammation. TNF-, IL-1, and IL-6 are major early response cytokines that trigger, often in synergy, a cascade of inflammatory mediators, including other cytokines, arachidonic acid metabolites, chemokines, and reactive nitrogen and oxygen intermediates. Multiple cell types within the CNS including cerebromicrovascular endothelial cells, astrocytes, and microglia produce all 3 cytokines. Increased concentrations of these cytokines have been detected in CSF samples from patients with acute bacterial meningitis and concentrations of IL-1, but not IL-6 and TNF-, are associated with significantly worse disease outcome or disease severity Brain mRNA and protein expression of IL-1, IL-6, and TNF- are markedly up-regulated in rodents during the acute stage of experimental pneumococcal meningitis. Recent studies with genetically engineered mice provide further insight into the role of acute phase cytokines in the pathophysiology of pneumococcal meningitis. For example, brain bacterial titers were not affected by either TNF- or TNF receptor deficiency in murine models of CNS infection. Furthermore, leukocyte recruitment into the subarachnoid space was not affected by TNF deficiency. In contrast, mice with targeted disruption of TNF receptors p55 and p75 had decreased meningeal inflammation. It appears that other TNF receptor ligands (e.g., lymphotoxin-) must contribute to the induction and/or maintenance of the inflammatory response during pneumococcal meningitis. Intracisternal inoculation of pneumococci caused a three-fold increase in CSF leukocyte concentrations in IL-6deficient mice when compared with wild type controls. Increased CSF pleocytosis is thought to result from higher brain expression of the potent neutrophil chemoattractant macrophage inflammatory protein (MIP)-2. These observations are similar to those in animal models of endotoxin-induced lung injury and endotoxemia, where IL-6 appears to control the extent of the inflammatory response by down-regulating the expression of chemokines and/or proinflammatory cytokines
Figure 1Mechanisms ofbrain damagein experimental pneumococcal meningitis. NF-B, a transcriptional activator of many genes involved in the pathogenesis of bacterial meningitis, encodes host factors including proinflammatory cytokines, chemokines (e.g., interleukin [IL]-8), and adhesion molecules. The proinflammatory cytokines IL-1 andtumor necrosis factor(TNF)- are synthesized as inactive precursors that are processed to mature active forms by proteases (casbase 1 [Casp1], also known as IL-1converting enzyme, and TNF-converting enzyme [TACE]). IL-1 and TNF- are potent activators of NF-B. This process may lead to the uncontrolled expression of proinflammatory mediators and the increased expression of adhesion molecules both on the endothelium (e.g., intercellular adhesion molecule [ICAM]-1) and on neutrophils, leading to subsequent massive influx of leukocytes into the subarachnoid space. Once present, activated leukocytes release a complex variety of potentially cytotoxic agents including oxidants and proteolytic enzymes (e.g., matrix metalloproteinases [MMP]), which may contribute to tissue destruction. Also, peroxynitrite may cause brain damage via a variety of independent mechanisms. The best studied are attack of polyunsaturated fatty acids, leading to lipid peroxidation, and an alternative pathway that involves oxidant-induced DNA strand breakage and subsequent poly (ADPribose) polymerase (PARP) activation, which initiates anenergy-consuming intracellular cycle that ultimately results in cellular energy depletion and cell death. Both mechanisms likely contribute to cell injury during pneumococcal meningitis. ECM, extracellular matrix; MIP, macrophage inflammatory protein
Figure 2Vicious cycle of pathophysiologic alterations leading to neuronal injury during bacterial meningitis. BBB, blood-brain barrier; CBV, cerebral blood volumeV. Medical ManagementThis Chapter is a summary of the management of care rendered to the patient, which was presented through a table.
DAYSJanuary 12, 2015January 13, 2015
SOURCECHART (7:35AM)CHART(12:00PM)CHART(7:35AM)CHART(12:00PM)
Blood Pressure
Temperature3736.53737.4
Pulse Rate120115118120
Respiratory Rate32484242
Clinical Chemistry Result Form
RBS9.92
Sodium134.6
Potassium4.07
Ionized Calcium1.04
Hematology Result Form
ABO Blood TypingA
RH TypingPositive
Hemoglobin131
Hematocrit0.39
WBC Count10.0
Neutrophils0.77
Lymphocytes0.17
Monocytes0.06
Platelet183
URINE AND STOOL
Stool 2 2
Urine 2 2
INTRAVENOUS FLUID
N10 x 12 hours at 8-9gtts/ hr
Drugs
Phenobarbital 60mgIVIVIVIV
Ampicillin 300mg IVIVIVIV
Cefuroxime 300mg IVIVIVIV
Meropenem 120mg with 10cc D5W in solventIVIVIVIV
Gentamyacin 15mg IVIVIVIV
TYPE OF DIET
Liquid Diet
VI. ConclusionWith early diagnosis and treatment, term infants are not likely to experience long-term health problems associated with neonatal sepsis; however, if early signs or risk factors are missed, mortality increases. Residual neurologic damage occurs in 15-30% of neonates with septic meningitis.Mortality from neonatal sepsis may be as high as 50% for infants who are not treated. Infection is a major cause of fatality during the first month of life, contributing to 13-15% of all neonatal deaths. Low birth weight and gram-negative infection are associated with adverse outcomes Neonatal meningitis occurs in 2-4 cases per 10,000 live births and contributes significantly to mortality from neonatal sepsis; it is responsible for 4% of all neonatal deaths.In preterm infants who have had sepsis, impaired neurodevelopment is a concern.Proinflammatory molecules may negatively affect brain development in this patient population. In a large study of about 6000 premature infants who weighed less than 1000 g at birth, preterm infants with sepsis who did not have meningitis had higher rates of cognitive deficits, cerebral palsy, and other neurodevelopmental disabilities than infants who did not have sepsis. Infants with meningitis may acquire hydrocephalus or periventricular leukomalacia. They may also have complications associated with the use of aminoglycosides, such as hearing loss or nephrotoxicity.That is why regular checkup and proper diet during pregnancy is a very important aspect for the babys outcome to be able to prevent any abnormalities at birth. Baby Rain Jeys parents should have a strict compliance to the medical treatment, health teachings and medical check up every now and then is advised. They should always keep their eyes and focus on the baby to help fasten the recovery.
SYSTEMS PLUS COLLEGE FOUNDATIONBalibago, Angeles CityCollege of Nursing
In partial fulfillment of the Requirements in NCM 102 CASE STUDY
SEPSIS MENINGITIS
Submitted to Mrs. Mary Anne S. De Dios
Submitted by Molina, Ruth Anne C.
February 4, 2014
