Meningitis is inflammation of the membranes (dura, pia mater, and arachnoid) surrounding the brain and spinal cord. Bacterial meningitis most commonly results from seeding of the leptomeninges from a distant focus (hematogenous spread). It can also result from a direct extension from a contiguous focus (eg, sinusitis, otitis media, mastoiditis) or by direct invasion (eg, head trauma). Etiologies in the neonatal period include Group B streptococci, gram-negative enteric bacilli (Escherichia coli, Enterobacter spp.), and Listeria monocytogenes. Etiology from age 1 to 3 months includes Streptococcus pneumoniae, Neisseria meningitides, Haemophilus influenzae type b (Hib), and L monocytogenes. Etiology in infants >3 months include S pneumoniae, N meningitides, and Hib (unvaccinated children). In patients with ventriculoperitoneal shunts, coagulase-negative Staphylococcus epidermidis and Staphylococcus aureus are the pathogens. Tuberculous meningitis may present with a gradual onset over several weeks. Low-grade fever, weight loss, adenopathy, vomiting, lethargy, cranial nerve palsies, and coma are common presentations. Differential diagnosis includes other types of meningitis, subarachnoid hemorrhage (ruptured arteriovenous malformation [AVM]/aneurysm), parameningeal/paraspinal infection (eg, brain abscess, subdural or epidural abscess), retropharyngeal abscess, and trauma (eg, shaken impact syndrome, subdural or epidural hematoma).
Stabilize the patient and provide continuous cardiac and pulse oximetry monitoring, and fluid resuscitation with crystalloids for septic shock. If patient is not in shock, restrict intravenous (IV) fluid to basal requirement with 0.33% NaCl solution because of possible syndrome of inappropriate antidiuretic hormone (SIADH). Obtain cerebrospinal fluid (CSF) with lumbar puncture (LP). Head CT scan is not required routinely before LP when there is a clinical diagnosis of uncomplicated meningitis. If focal neurologic signs are present (eg, suspected complications like subdural effusion or empyema) or there is papilledema, begin antibiotics and obtain a CT scan before performing LP. Antigen detection tests (eg, latex agglutination) may help in partially treated meningitis. Order India ink stain for immunocompromised patients, and acid-fast stain when tuberculous meningitis is suspected. Order complete blood count, blood culture, serum electrolytes (monitoring for SIADH), glucose, and coagulation profile (disseminated intravascular coagulation). Place a 5–tuberculin unit purified protein derivative tuberculin test on the forearm of all patients with meningitis in areas where tuberculosis is endemic. Treat patients <4 weeks of age empirically with ampicillin and cefotaxime or ampicillin and an aminoglycoside (eg, gentamicin). Consider antiviral therapy if herpes is suspected. Treat patients >4 weeks of age empirically with vancomycin and cefotaxime or ceftriaxone. Offer antibiotic prophylaxis to close contacts for exposure to Hib and N meningitides. Dexamethasone (if given before or concurrently with the first dose of antibiotics) may help decrease hearing loss associated with Hib meningitis. Admit patients with a clinical diagnosis; admit those with septic shock requiring resuscitation to the ICU. Use standard and droplet precautions for the first 24 hours after institution of appropriate antibiotics.
Figure 13.1 ▪ Bacterial Meningitis Presenting with Purpura.
An adolescent patient with AIDS presented with high fever, neck stiffness, and signs of septic shock with purpuric lesions (photograph taken on second day of hospitalization). Both blood and cerebrospinal fluid cultures were positive for Streptococcus pneumoniae. (Photo contributor: Binita R. Shah, MD.)
Figure 13.2 ▪ Bulging Anterior Fontanelle as a Presenting Sign of Meningitis.
The anterior fontanelle is normally open in infants (usually closes between 9 and 18 months) and is pulsatile and slightly depressed in an infant in an upright position. The anterior fontanelle may appear full in an infant lying in a supine position or during crying. A bulging anterior fontanelle suggests increased intracranial pressure from any etiology (eg, meningitis, tumor, hydrocephalus). (Photo contributor: Binita R. Shah, MD.)
Figure 13.3 ▪ Hydrocephalus; Complication of Bacterial Meningitis.
A CT scan of the head shows moderate to severe hydrocephalus with periventricular transudation around the lateral ventricles and abnormal sulcal thickening along the parietal region due to subarachnoid exudates. This 10-month-old infant remained persistently febrile on amoxicillin for a presumed pneumonia. Her blood and cerebrospinal fluid cultures were positive for Streptococcus pneumoniae that showed intermediate resistance to penicillin and cefotaxime, but was sensitive to vancomycin. (Photo contributor: Binita R. Shah, MD.)
Figure 13.4 ▪ Neurological Sequelae; Bacterial Meningitis.
A noncontrast head CT scan shows multiple hypodense areas (left > right) over the frontal and parietal regions, with additional areas of hypodensity in the right deep white matter and basal ganglia indicative of multiple infarcts in an infant with Group B streptococcal meningitis. (Photo contributor: Binita R. Shah, MD.)
Figure 13.5 ▪ Severe Hydrocephalus; Complication of Bacterial Meningitis.
This autopsy photograph shows marked dilation of the ventricular system and prominent thinning of the cerebral mantle in a child who developed hydrocephalus requiring a ventriculoperitoneal shunt following Group B streptococcal neonatal meningitis. (Photo contributor: Chandrakant Rao, MD.)
Meningitis is a life-threatening medical emergency; maintain a high index of suspicion for all signs and symptoms.
Absence of meningeal signs in infants <18 months old does NOT exclude meningitis. In this age group, such signs are often not present, and when seen, usually represent a very late finding.
Stiff neck is a pathognomonic sign of meningeal irritation from a purulent exudate or hemorrhage in the subarachnoid space.
CSF examination is the gold standard for diagnosis; always perform LP when there is any suspicion of meningitis. Neutrophils may predominate early even in viral meningitis. Decreased CSF glucose may also occur in mumps and herpes meningoencephalitis.
Petechiae or purpura are seen in only 70% of cases of meningococcemia. Patients with meningococcal meningitis may also lack CSF abnormalities on initial LP even with a positive CSF culture. Consider infections caused by N meningitides even in the absence of skin lesions or CSF abnormalities.
Seizures are seen in about 20% to 30% of patients with bacterial meningitis; consider meningitis in children presenting with seizures associated with fever.
Avoid delays in initiating antibiotic therapy while awaiting completion of diagnostic studies.
Failure to diagnose meningitis early is a leading cause of malpractice litigation in pediatrics.
|
| Type of meningitis | Leukocytes (number) | Glucose | Protein | Gram’s stain |
|---|---|---|---|---|
| Bacterial | Neutrophils (hundreds to thousands) | Low | High | Often positive |
| Viral | Lymphocytes (hundreds) | Normal | Slightly high | Negative |
| Tuberculous | Lymphocytes (hundreds) | Low | High | Negative |
| Cryptococcal | Lymphocytes (few to hundreds) | Low | Normal or high | Negative |
| Parameningeal (brain abscess, subdural abscess) | Lymphocytes (few) | Normal | High | Negative |
The authors acknowledge the special contributions of Radha Giridharan, MD and Joseph A. Sykes, MD to prior edition.
Sustained elevations in intracranial pressure (ICP) may permanently retard normal brain function, especially in the developing brain. By volume, skull contents consist of brain (80%), blood (10%), and CSF (10%), and this volume is fixed. Increases in one component therefore must be compensated by a decrease in the others (Monroe-Kellie hypothesis); otherwise there will be an increase in ICP leading to brain compression. Normal values for ICP vary according to age and body position (normal <20 mm Hg). Patients with elevated ICP may be asymptomatic or present with nausea, headache, blurry vision, weakness, vomiting, or seizures. Clinical signs may be present, including tachycardia or bradycardia, bradypnea, hypertension, focal neurologic deficits, bulging fontanel (infants) or widening diathesis of cerebral sutures, doll’s eye, papilledema, retinal hemorrhages, and unequal pupils.
Figure 13.7 ▪ Epidural Hematoma with Herniation; Inflicted Head Trauma.
A noncontrast CT scan of the head shows a large right temporoparietal lenticular extradural hematoma with heterogenous density. There is a mass effect on the adjacent parieto-occipital lobe with evidence of subfalcine herniation, and a midline shift from right to left. This 4-month-old infant was brought to the ED with vomiting, inability to arouse, with vital signs showing Cushing triad. His mother subsequently confessed to shaking him violently and throwing him against the wall because he would not stop crying. (Photo contributor: Vikas S. Shah, MD.)
Figure 13.8 ▪ Hemorrhagic Stroke (Intraparenchymal Bleed) with Transtentorial and Subfalcine Herniation.
A noncontrast CT scan of the head shows left parieto-occipital intraparenchymal bleeding with left frontoparietal subdural hematoma (arrow). The basal cisterns are obscured with a significant mass effect with evidence of transtentorial and subfalcine herniation in an adolescent patient brought to the ED with Cushing triad. He was found unresponsive with mouth frothing and urinary incontinence in his bed. About 12 hours before this, he complained of a severe headache. He was intubated, hyperventilated, and given a dose of mannitol before this CT scan. (Photo contributor: Vikas S. Shah, MD.)
Figure 13.9 ▪ Brain Tumor Presenting with Increased Intracranial Pressure.
An axial head CT image shows a large right-sided cerebral hemisphere mass with vasogenic edema (black arrow), right to left subfalcine (white arrow), transtentorial, and right uncal herniation with obliteration of the right lateral ventricle in a 2-year-old child presenting with seizures, unsteady gait, and excessive sleepiness. (Photo contributor: Vikas S. Shah, MD.)
Figure 13.10 ▪ Brain Tumor Presenting with Increased Intracranial Pressure.
An axial head CT image shows a large lobulated supratentorial mass with calcifications (black arrows), surrounding vasogenic edema, a midline shift (white arrow), and compression of anterior horn of left lateral ventricle with hydrocephalus in a 2-year-old child presenting to ED with Cushing triad and lethargy. Subsequently, patient developed signs of herniation requiring intubation, mannitol, and ventricular drain by neurosurgeon. (Photo contributor: Vikas S. Shah, MD.)
Sustained ICP elevations (>20 mm Hg) need to be treated aggressively, and management is dependent on etiology. The factors contributing to ICP, including cerebral blood flow (CBF), cerebral perfusion pressure (CPP), mean arterial pressure (MAP), guide treatment. As CBF increases, ICP increases. CBF is autoregulated under a wide range of CPP and remains relatively constant. CPP is the difference between MAP and ICP. When ICP is not immediately available, central venous pressure (CVP) can be used instead of ICP to calculate CPP. In adolescents/adults, CPP ranges between 70 and 90 mm Hg when MAP is between 60 and 150 mm Hg. In children, the CPP is 50 to 70 mm Hg. From these relationships, to maintain constant CBF and ICP, constant CPP must be maintained.
Adhere to PALS and ATLS guidelines and mitigate any factors that may further compromise CPP. If ICP elevation is from trauma, immobilize the cervical spine and intubate trachea under rapid sequence protocol especially if Glasgow Coma Scale score is <8. Initiate mechanical ventilation and maintain normal ventilation (Paco2 between 35 and 40 mm Hg), optimize oxygenation by maintaining Pao2 > 110, and maintain normal acid-base status. Hyperventilation (Paco2 <35 mm Hg) and hypoventilation are to be avoided. Hypoventilation and hypoxemia cause vasodilation and lead to an increase in CBF, leading to increased ICP. Hyperventilation leads to vasoconstriction of the cerebral vasculature leading to ischemia from decreased blood flow. When maximizing oxygenation, minimize PEEP to avoid decreases in venous drainage, which increase ICP and reduces cerebral perfusion. Avoid hyperoxia (ie, Pao2 >110 mm Hg). Intubation raises ICP and negatively affects CPP. To minimize this, sedate the patient with fentanyl and etomidate and use lidocaine prior to intubation. Use short-acting drugs whenever possible to allow for accurate and frequent assessment of neurologic status. When a patient with increased ICP requires tracheal intubation, placement of an ICP monitor is recommended.
Figure 13.11 ▪ Traumatic Subarachnoid Hemorrhage with Increased Intracranial Pressure (ICP).
A noncontrast head CT scan shows extensive subarachnoid hemorrhage with obliteration of the basal CSF cisterns (red arrow) indicative of increased ICP in a 12-year-old boy brought to the ED with a penetrating brain trauma (a foot-long wooden stick into the left temporal region). Blood can also be seen around the foreign object penetrating the left temporal region (white arrows). (Photo contributor: Geetha Chari, MD.)
Figure 13.12 ▪ Intraventricular Drain and Hemicraniectomy; Increased Intracranial Pressure (ICP).
Noncontrast head CT scan shows a large left craniectomy, left ventricular drain (red arrow), bulging of the brain through the craniectomy site (white arrows), and a right frontal hematoma, in a 5-year-old boy who was struck by a motor vehicle. He was taken to the operating room from the ED for emergent treatment of raised ICP with hemicraniectomy and intraventricular drain. (Photo contributor: Vikas S. Shah, MD.)
Maximization of CPP is dependent on augmenting MAP and minimizing ICP and requires that central venous volume be optimized. If CVP is decreased, resuscitate the patient. Crystalloid is superior for initial resuscitation. If the CVP is adequate and the MAP remains low to maintain adequate CPP, then initiate inotropes and vasotropes. Femoral vein cannulation is preferable for central access as placement of catheter in the superior circulation may retard cerebral venous drainage and decrease CPP. Consult neurosurgery immediately. Order noncontrast head CT to aid in diagnosis and management. Address factors that worsen ICP (see Table 3.3).
| Brain | Traumatic brain injury | |
| Neoplasm | ||
| Seizure | ||
| Infection | Meningitis, Encephalitis, Brain Abscess | |
| Anoxic injury | ||
| Vasculitis | SLE | |
| Blood | Ruptured aneurysm | |
| Subdural hematoma | ||
| Epidural hematoma | ||
| Venous thrombosis | ||
| Cerebrospinal fluid | Aqueductal stenosis | |
| Decreased resorption | Arachnoid villi blockage | |
| Increased production | Choroid plexus tumor | |
| Additional factors | Fever, pain, inadequate sedation/agitation, increased CO2, acidosis |
If herniation is suspected (unequal pupil size, irregular respiration, hypertension, altered respirations and bradycardia, abnormal CT), prompt attention is warranted. In this case, implement the above recommendations and administer mannitol unless renal failure, severe dehydration, cerebral hemorrhage, or pulmonary edema are present. If an intraventricular catheter is in place, diversion of CSF externally may decrease ICP. Hyperosmolar therapy with 3% normal saline can be initiated in the emergency department (ED); however, goals may not be achieved until much later.
The Cushing triad (bradycardia, bradypnea, and hypertension) need not be present concomitantly in pediatric patients with increased ICP.
Goal of increased ICP management is to maintain adequate CPP.
Administer short-acting pharmaceuticals for sedation, analgesia, and paralysis whenever possible. Continuous propofol infusion is rarely indicated in children.
Alteration in the level of consciousness (LOC) is a common presentation in the ED and is a vague term that requires evaluation to be specified. Consciousness requires both cerebral hemispheres and the brainstem ascending reticular activating system to be functional. The spectrum of altered consciousness includes lethargy, confusion, delirium, obtundation, stupor, and coma, and causes of altered LOC include a wide spectrum of disorders.
Figure 13.13 ▪ Purpura and Septic Shock Presenting with Obtundation.
A 21-year-old adolescent patient presented with fever and rapidly spreading purpuric rash and shock (unresponsiveness to stimuli, hypotension, poor capillary refill with cold and clammy extremities, and decreased urine output). Her blood culture grew Neisseria meningitidis type B. This photograph was taken on the third day of the hospitalization. (Photo contributor: Binita R. Shah, MD.)
Figure 13.14 ▪ Epidural Hematoma Following a Trivial Fall.
A noncontrast head CT scan shows a biconvex hyperdense extra-axial collection in the right parietal region, characteristic of an epidural hematoma (black arrow), with edema of the white matter of the right cerebral hemisphere and midline shift (white arrows). This 2-year-old child presented to ED following a fall from a short flight of stairs with no loss of consciousness. After a lucid interval, he developed lethargy. (Photo contributor: Geetha Chari, MD.)
| Lethargy | Reduced wakefulness, lack of interest in environment; arousable and able to communicate |
| Confusion | Inattentiveness, mental slowness, dulled perception, and incoherence |
| Delirium | Confusion with hallucinations and motor abnormalities (such as tremors or myoclonus), agitation that may alternate with drowsiness |
| Obtundation | Severe blunting of awareness with decreased response to stimuli |
| Stupor | Unresponsiveness from which the individual can be aroused only temporarily by vigorous and repeated stimuli |
| Coma | Unresponsiveness from which the patient cannot be aroused by verbal, tactile, or painful stimuli |
| Mnemonic: COMATOSE PATIENT |
|
| Commonly Used Mnemonic: TIPS from Vowels |
|
Obtain a history and vital signs with attention to possible causes. Fever suggests infectious etiology (eg, encephalitis, meningitis). Hypothermia may indicate metabolic or toxic conditions. Tachypnea is seen in hypoxia, sepsis, acidosis, and toxins. Central nervous system (CNS) involvement with increased ICP and herniation will cause Cheyne-Stokes respiration. General examination may show signs of trauma and infection. A brief focused neurologic examination can reveal significant information. Use the Glasgow Coma Scale to measure LOC; using the parameter of motor response to pain helps to also determine any focal weakness. Obtain finger stick blood glucose, metabolic panel (electrolytes, blood urea nitrogen [BUN], creatinine, Ca, liver enzymes, Mg, PO4, etc), CBC, arterial blood gas analysis, and urinalysis. Monitor cardiorespiratory status and stabilize patient with evaluation and maintenance of ABCs (airway, breathing, and circulation). If trauma is suspected, immobilize cervical spine until cervical trauma is ruled out. Administer IV dextrose 25%, if finger stick glucose is not available to confirm hypoglycemia. Administer thiamine 100 mg IV to adolescents if alcohol intoxication or thiamine-deficient states are suspected. If clinically indicated, administer naloxone, for opioid intoxication. Order urgent head CT if symptoms and signs of raised ICP are present or if no metabolic cause is identified. Perform a lumbar puncture if infectious etiology is considered. Initiate specific therapy for various causes based on the assessment (eg, antibiotics for meningitis, anticonvulsants for seizures, correction of electrolyte and acid-base imbalance, antidote for toxic overdose). Obtain specific consultations depending on the etiology of the coma (eg, neurosurgery for intracranial bleed, poison control for toxic ingestion, neurology for stroke). After initial stabilization, admit to ICU for continuous monitoring and further management.
Altered mental status has a very wide differential diagnosis; it is essential to treat the underlying cause.
Pupillary assessment helps differentiate metabolic and structural causes of coma; reactive pupils suggest metabolic causes, while asymmetric or absent pupillary responses suggest trauma.
Features of increased ICP and herniation include headache, vomiting, altered mental status, Cushing triad (systolic hypertension, bradycardia, bradypnea) and unequal pupils.
Figure 13.15 ▪ Herpes Simplex Virus, Type 2 (HSV-2) Encephalitis.
A noncontrast CT scan of head shows acute hemorrhage in the left frontal/parietal region, with extension into the subarachnoid spaces (arrows) in an adolescent girl presenting with fever, headache, and lethargy, becoming comatose. She had perinatally acquired HIV with previous history of HSV-2 encephalitis during the postneonatal period. She was later diagnosed to have a recurrence of HSV-2 encephalitis. (Photo contributor: Geetha Chari, MD.)
Figure 13.16 ▪ Hemorrhagic Stroke (Intraparenchymal Hemorrhage).
A noncontrast axial CT image of the head shows a large area of hyperdensity (hematoma) involving the right parietal area with surrounding hypodensity (representing associated edema) and intraventricular extension to the right lateral ventricle. A mass effect with a significant right-to-left midline shift is also seen. This adolescent girl presenting with headache, stiff neck, and fever was diagnosed as aseptic meningitis (CSF: red blood cells 720/mm, white blood cells 11/mm, normal protein, and glucose with negative culture). With clinical improvement, she was discharged after 48 hours. Within 8 hours after discharge, she complained of severe headache followed by seizures. On arrival to the ED, she was comatose with these CT findings. (Photo contributor: Binita R. Shah, MD.)
Figure 13.17 ▪ Hypertensive Encephalopathy (Posterior Reversible Leukoencephalopathy Syndrome [PRES]).
(A) A noncontrast head CT scan reveals hypodensity in the posterior white matter of both hemispheres, in a 7-year-old girl with hypertensive encephalopathy with hemolytic uremic syndrome. These findings are characteristic of hypertensive encephalopathy. (B) Axial fluid-attenuated inversion recovery MRI shows hyperintensities in the occipital white matter (white arrows). (Photo contributor: Steve Pulitzer, MD.)
Figure 13.18 ▪ Currant-Jelly Stool; Intussusception Presenting with “Neurologic” Signs.
This currant-jelly stool was passed by an 8-month-old infant brought to the ED with vomiting, extreme lethargy, and intermittent episodes of crying. He responded with a very weak cry to any painful stimuli, and fell back to sleep as soon as stimulus was withdrawn. He had ileocolic intussusception that required surgical reduction. “Neurologic” signs of intussusception (often misdiagnosed as sepsis or a postictal state) include lack of interaction, extreme lethargy, coma or shock-like state, apnea, seizures and seizure-like activity, opisthotonic posturing, weak cry, hypotonia, or pinpoint pupils. (Photo contributor: Binita R. Shah, MD.)
Febrile seizures are an age-related phenomenon in which a child between 6 months to 5 years of age has fever and a generalized seizure not associated with CNS infection or any other definable cause (eg, metabolic abnormality) or previous history of afebrile seizures. Types of febrile seizures are listed in Table 13.7.
| Ictal Features | Duration | Postictal Features | Recurrence | |
|---|---|---|---|---|
| Simple | Tonic, clonic, tonic-clonic, rarely atonic | <15 min | None | None within 24 hours |
| Complex | Partial onset or focal features | >10–15 min | Within 24 hours | |
| Status epilepticus | Tonic, clonic, tonic-clonic, rarely atonic Partial onset or focal features | 30 min or longer or a series of short seizures, without regaining consciousness in between |
Strongly consider performing lumbar puncture in infants <12 months of age. Between ages 12 and 18 months, LP should be considered. After the age of 18 months, LP is not routinely warranted, but should be done if meningeal signs are present. Obtain laboratory studies (CBC, chemistry, etc) based on clinical evaluation. Treat ongoing seizure activity with benzodiazepine IV or rectally. The rectal preparation comes in a pre-dosed syringe (2.5, 5, 10, 15, and 20 mg), making it easy to deliver. Absorption is rapid and effective in interrupting seizure clusters or repetitive seizures. Give antipyretics to make the child more comfortable.
Figure 13.19 ▪ A Toddler Presenting to the ED with a Recent History of a Simple Febrile Seizure.
As seen in this toddler, most patients present with a history of a brief febrile seizure without any postictal neurologic deficits (the overwhelming majority of febrile seizures will have terminated before presentation to the ED). In the absence of clinical signs or symptoms suggestive of CNS infection, such patients can be safely discharged home (once the etiology of fever has been determined). Discharge instructions include fever management, education about the possibility of recurrence of febrile seizures, and first aid management of seizures. (Photo contributor: Toral Shah, BS, PA-C.)
Figure 13.20 ▪ Convulsion Associated with Fever; Intrauterine Cytomegalovirus (CMV) Infection.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
